Improving Women’s Health Across the Lifespan: (a volume in the Lifestyle Medicine series) 9780367627638, 9780367627621, 0367627639

Table of contents :
Cover
Half Title
Title Page
Copyright Page
Table of Contents
Acknowledgments
Editor Biographies
Contributors
Introduction
1 Optimal Nutrition for Women
Key Points
1.1 Introduction
1.2 Nutrition Basics
1.2.1 Energy
1.2.2 Nutrient Density
1.2.3 Macronutrients
1.2.4 Carbohydrates
1.2.5 Fats
1.2.6 Proteins
1.2.7 Micronutrients
1.2.8 Nutrients of Concern
1.2.9 Phytonutrients and Antioxidants
1.2.10 Water
1.3 Standard Nutrition Guidelines
1.3.1 National and Global Guidelines
1.4 Health-Promoting and Health-Harming Foods
1.5 The American College of Lifestyle Medicine’s Recommended Dietary Pattern
1.5.1 The American College of Lifestyle Medicine Dietary Position
1.5.2 The Dietary Spectrum
1.6 Nutrition Recommendations for Women
1.6.1 Women-Specific Health Risks
1.6.1.1 Weight Concerns, Body Image, and Eating Disorders
1.6.1.2 Women-Specific Cancers
1.6.1.3 Bone Health
1.6.2 Nutrients to Know for Women
1.6.2.1 Vitamin B12
1.6.2.2 Calcium
1.6.2.3 Vitamin D
1.6.2.4 Iron
1.6.2.5 Folate
1.6.2.6 Zinc
1.6.2.7 Iodine
1.6.2.8 Omega-3s
1.7 Brief Overview of Nutrition Needs Across The Lifespan
1.7.1 Nutrition and Fertility
1.7.2 Nutrition and Pregnancy and Lactation
1.7.3 Energy
1.7.4 Macronutrients
1.7.5 Micronutrients
1.7.5.1 Iodine
1.7.5.2 B12
1.7.5.3 Folate
1.7.5.4 Iron
1.7.5.5 Choline
1.7.5.6 Zinc
1.7.5.7 Calcium
1.7.5.8 Vitamin D
1.7.5.9 Other Nutrients
1.7.6 Nutrition and Menopause
1.7.7 Nutrition and Female Athletes
1.8 Practical Tools for Transitioning to a Whole Food Plant-Based Eating Pattern
1.8.1 The WFPB Plate
1.8.2 Tips for Transitioning
References
2 Physical Activity for Women
Key Points
2.1 Introduction
2.2 Children and Adolescents
2.3 Adults
2.3.1 PA Prescription
2.3.2 Measuring PA Intensity
2.3.3 Screening PA Participation
2.4 Preconception to Postpartum
2.4.1 PA Guidelines and Contraindications
2.4.2 PA Measurement
2.4.3 Postpartum
2.4.4 Improving Postpartum PA Screening
2.4.5 Future Considerations
2.5 Older Healthy Women
2.5.1 Menopause
2.6 Conclusion
References
3 Sleep and Women’s Health
Key Points
3.1 Introduction
3.2 Overview of Sleep Physiology and Circadian Biology
3.2.1 Sleep Need and Circadian Processes
3.2.2 Sleep Stages
3.2.3 Obstructive Sleep Apnea and Upper Airway Resistance in Women
3.3 Relationship Between Sleep and Health Outcomes
3.3.1 Sleep, Weight, and Cardiometabolic Risk
3.3.2 Sleep, Inflammation, and Immunity
3.3.3 Sleep and Mood
3.3.4 Sleep, Sex Hormones, and Gender
3.4 Sleep and Other Lifestyle Medicine Pillars
3.4.1 Diet and Sleep
3.4.2 Exercise and Sleep
3.5 Sleep and Life Stages in Women
3.5.1 Adolescents and Teenagers
3.5.2 Menstrual Cycles and Sleep
3.5.3 Pregnancy and Sleep
3.5.4 Mothers of Young Children
3.5.5 Sleep and the Menopause Transition
3.6 Conclusions
References
4 Emotional Wellness and Stress Resilience
Key Points
4.1 Introduction
4.2 Emotional Wellness Definition and Stress
4.3 Stress Response
4.4 Relaxation Response
4.5 General Adaptation Syndrome (Gas) Model of Stress
4.6 Consequences of Chronic Stress
4.7 Gender Is a Risk Factor for Stress
4.8 Stress Appraisal
4.8.1 A Growth Mindset and Self-Compassion Can Promote Resilience Against Stress
4.9 Positive and Adaptive Aspects of Stress: Coping
4.9.1 Positive Cognitive Restructuring
4.9.2 Gratitude
4.9.3 Mindfulness and Meditation
4.9.4 Clinician Burnout
References
5 Positive Psychology and Relational Connectedness
Key Points
5.1 Introduction to Positive Psychology
5.2 Positive Psychology, Gender, and Culture
5.2.1 Positive Psychology, Gender, and Sex
5.2.2 Positive Psychology and Culture
5.3 Positive Psychology Throughout the Lifespan
5.3.1 Adolescence
5.3.2 Pregnancy
5.3.3 Menopause
5.3.4 Aging
5.4 Positive Emotions, Healthy Lifestyles, and Well-Being
5.4.1 The Reciprocal Relationship Between Positive Emotions and Healthy Lifestyles
5.4.2 Positive Psychology Activities That Promote Positive Emotions
5.5 Types of Positive Psychology Interventions
5.5.1 The PERMA Framework
5.5.2 Mindfulness
5.5.3 Exposure to Nature
5.6 Practical Application of Positive Psychology Approaches in Health Care
5.6.1 Measures of Happiness and Related Constructs
5.6.2 Variety, Dosing, and Person-Activity Fit of Positive Psychology Interventions
5.7 Positive Psychology Approaches in Interactions With Patients
5.7.1 Coaching Health Behavior Change With Positive Psychology
5.7.2 Modeling Positive Psychology in the Exam Room
5.8 Positive Psychology Strategies For Health Care Workers’ Well-Being
5.8.1 Medical Practitioner Well-Being and Patient Care
5.8.2 Positive Psychology Interventions for Medical Practitioners
5.8.2.1 P – Positive Emotions
5.8.2.2 E – Engagement
5.8.2.3 R – Relationships
5.8.2.4 M – Meaning
5.8.2.5 A – Accomplishment
5.9 Positive Psychology Resources
5.9.1 Academic and Nonprofit Organizations
5.9.2 Positive Psychology Websites, Apps, and Programs
5.10 Summary and Conclusion
References
6 Avoiding Risky Substances and Environmental Exposures
Key Points
6.1 Introduction
6.1.1 Substance Use and Environmental Exposures
6.2 Substance Use and Women’s Health
6.3 Environmental EXPOSURES and Women’s Health
6.3.1 Air Exposures
6.3.2 Water Exposures
6.3.3 Soil Food Exposures
6.3.4 Personal Care Product Exposures
6.3.5 Plastics
6.3.6 Equity/Justice
6.7 Conclusion
6.7.1 Recommendations
Notes
References
7 Models of Care for Women and Families, Reimbursement, and Telemedicine
Key Points
7.1 In-Person Visit Structures
7.1.1 Individual Visits
7.1.2 Group Medical Visits
7.2 Telehealth
7.2.1 Televisits
7.2.2 Remote Patient Monitoring
7.3 Reimbursement Overview
7.3.1 Grants and Employer-Funded Programs
7.3.2 Analyzing Insurance Reimbursement
7.3.3 Optimizing Insurance Billing
7.3.4 A Deeper Look at Direct Payment
7.3.5 Membership Fees
7.3.6 Additional Services
7.4 Summary of Reimbursement
References
8 Adverse Childhood Events and Trauma-Informed Care
Key Points
8.1 Introduction
8.1.1 The Science: Allostasis in Women’s Health
8.2 Clinical Presentations: Aces and Trauma in Women’s Health
8.2.1 ACEs and Women’s General, Mental, and Physical Health
8.2.2 ACEs and Traumatic Experiences in the Pre- and Perinatal Period
8.2.3 ACEs and Women’s Lifestyle Pillars
8.3 Aces and Trauma Intervention and Response
8.3.1 Clinical Considerations for Therapy and Intervention Support
8.3.2 Responding With Resilience in Individuals and Communities
Conflict of Interest
9 Health Coaching, Motivational Interviewing, and Behavior Change in Women’s Health
Key Points
9.1 Introduction
9.2 Basic Behavioral Strategies
9.2.1 Medical Triggers
9.2.2 Evidence Review
9.2.3 Motivation Type
9.2.4 Evidence Review
9.2.5 Self-Efficacy
9.2.6 Evidence Review
9.3 Specific Behavioral Strategies
9.3.1 Pregnancy
9.3.2 Menopause
9.3.3 Cancer Survivorship
9.4 Advanced Behavioral Strategies
9.4.1 Motivational Interviewing
9.4.2 Health and Wellness Coaching
9.4.3 The 5 A’s
9.4.4 Referring Patients for Additional Support
9.4.5 Team-Based Approaches
9.4.6 Group Visits
9.6 Conclusion
10 Health Equity and Women’s Health in Underserved Communities
Key Points
10.1 Introduction
10.2 Lifestyle Medicine and Vulnerable Communities
10.2.1 Social Determinants of Health
10.2.2 Systemic Racism
10.2.3 Health Needs of Women in Under-Resourced Communities
10.3 Lifestyle Medicine: Women and Health Equity
10.3.1 Addressing Health Equity and SDOH
10.3.2 Cultural Competence and Responsiveness
10.3.3 Building Patient Self-Efficacy and Self-Management of Chronic Disease
10.4 Lifestyle Medicine: Cultural Responsiveness and Health Equity
10.4.1 Benefits of Increased Patient Self-Efficacy Among Women
10.5 Conclusion
11 Community Engagement and Women’s Health
Key Points
11.1 Introduction
11.2 Community Engagement Process
11.2.1 Checklist for Community-Engaged Lifestyle Medicine Prescription
11.2.2 A Model of Community Engagement
11.3 Adopting Community-Engaged Models
12 Lifestyle Medicine in the Care of Adolescent Girls
Key Points
12.1 Introduction
12.2 Nutrition
12.3 Physical Activity
12.4 Sleep
12.5 Stress Management
12.6 Social Connectivity/Relationships
12.7 Substance Use Prevention
12.8 Conclusion
13 Menstrual Health and Lifestyle Medicine
Key Points
13.1 Introduction
13.2 Dysmenorrhea
13.2.1 Physical Activity
13.2.2 Nutrition
13.2.3 Stress and Sleep
13.2.4 Caffeine, Alcohol, and Tobacco
13.3 Premenstrual Syndrome
13.3.1 Physical Activity
13.3.2 Nutrition
13.3.3 Caffeine, Alcohol, and Tobacco
13.3.4 Stress and Sleep
13.4 Uterine Fibroids
13.5 Conclusions
References
14 Women’s Sexual Health and Lifestyle Medicine
Key Points
14.1 Introduction
14.2 Lifestyle Medicine and Sexual Health
14.2.1 Nutrition
14.2.2 Physical Activity
14.2.3 Sleep
14.2.4 Stress
14.2.5 Positive Social Connections
14.2.6 Substance Use
14.2.6.1 Alcohol
14.2.6.2 Cigarettes
14.2.6.3 Cannabis/Marijuana
14.3 Conclusion
15 Polycystic Ovary Syndrome, Endometriosis, and Female Infertility
Key Points
15.1 Introduction
15.2 Polycystic Ovary Syndrome
15.2.1 Introduction
15.2.2 Clinical Presentation and Diagnostic Testing
15.2.3 Management of PCOS
15.2.4 Lifestyle Management of PCOS
15.2.5 Nutrition
15.2.5.1 Macronutrients
15.2.5.2 Food Types
15.2.6 Exercise
15.2.7 Sleep
15.2.8 Social Connection
15.2.9 Cessation of Risky Substances
15.2.10 Stress Management
15.2.11 Conclusion
15.3 Endometriosis
15.3.1 Introduction
15.3.2 Clinical Presentation and Diagnostic
15.3.3 Lifestyle and Endometriosis
15.3.3.1 Nutrition
15.3.3.2 Exercise
15.3.3.3 Sleep
15.3.3.4 Stress
15.3.3.5 Relationships
15.3.3.6 Substance Use
15.3.3.7 Conclusion
15.4 Unexplained Infertility
15.5 Conclusion
16 Lifestyle Medicine in Menopause and Bone Health
Key Points
16.1 Introduction
16.2 Impacts of Lifestyle On Menopause
16.2.1 Abnormal Uterine Bleeding
16.2.2 Vasomotor Symptoms
16.2.3 Mood Disorders/Psychological Symptoms
16.3 Using Lifestyle Medicine to Manage Menopausal Symptoms
16.3.1 Healthful Eating
16.3.2 Phytoestrogens
16.3.3 Physical Activity
16.3.4 Stress
16.3.5 Social Connectedness
16.3.6 Sleep
16.3.7 Avoiding Risky Substances
16.4 Pathophysiology of Bone Health
16.5 Lifestyle Recommendations for Prevention and Treatment of Osteoporosis
16.5.1 Healthful Eating
16.5.2 Physical Activity
16.5.3 Stress Management, Social Connectedness, Relationships, and Sleep
16.5.4 Substances
17 Preconceptual Health
Key Points
17.1 Introduction
17.2 Overview Of Preconceptual Care
17.2.1 Benefits of and Barriers to Preconception Care
17.2.2 Challenges and Opportunities
17.3 Teratogens and Risky Substances
17.3.1 What Is a Teratogen?
17.3.2 How Do We Study the Effects of an Exposure On Fetal Development?
17.3.3 Importance of Exposure Timing
17.3.4 Medication Risks and Benefits
17.3.5 Maternal Disease as a Teratogen
17.3.6 Maternal Lifestyle as a Teratogen
17.4 Preconception Nutrition
17.4.1 Dietary Patterns and Vitamin and Micronutrient Deficiencies
17.4.2 Eliminating High-Risk Food
17.4.3 Preventing Adverse Pregnancy Outcomes
17.4.4 Reversing Chronic Disease
17.5 Physical Activity
17.5.1 Physical Conditioning for Pregnancy
17.5.2 Impact On Gestational Weight Gain
17.5.3 Preconception Activity and Obstetric Outcomes
17.6 Sleep
17.7 Adverse Childhood Experiences and Stress
17.8 Emotional Wellness and Mental Health
17.8.1 The Relationship of Mental Illness With Preconception Care and Disease
17.8.2 Intimate Partner Violence and Mental Health
17.8.3 The Impact of Mental Health and Mental Health Treatment On Achieving Pregnancy
17.8.4 Screening for Anxiety and Depression
17.8.5 Optimizing Treatment for Mental Health Disorders Prepregnancy
17.9 Relational Connectedness
17.9.1 Preconception Social Support and Pregnancy Outcomes
18 Pregnancy
Key Points
18.1 Introduction
18.2 Developmental Origins of Health and Disease
18.3 Nutrition in Pregnancy
18.3.1 Dietary Patterns and Vitamin and Micronutrient Deficiencies
18.3.2 Foods to Avoid
18.3.3 Dietary Patterns and Adverse Pregnancy Outcomes
18.3.4 Excessive Weight Gain
18.3.5 Preterm Delivery
18.3.6 Gestational Diabetes
18.3.7 Gestational Hypertension and Preeclampsia
18.3.8 Reversing Chronic Disease
18.4 Physical Activity
18.4.1 Introduction
18.4.2 Safety of Exercise in Pregnancy
18.4.3 Benefits of Exercise in Pregnancy
18.4.4 Hypertensive Disease
18.4.5 Metabolic Disease
18.4.6 Labor and Delivery
18.4.7 Depression and Anxiety During Pregnancy and Postpartum
18.4.8 Impact of Pelvic Floor Muscle Training
18.4.9 A Prescription for Exercise
18.4.9.1 Frequency
18.4.9.2 Intensity
18.4.9.3 Type
18.4.9.4 Time
18.5 Sleep
18.5.1 Obstructive Sleep Apnea and Pregnancy Outcomes
18.5.2 Labor Outcomes
18.6 Stress
18.7 Emotional Wellness
18.7.1 Maternal Mental Health Disorders and Pregnancy Outcomes
18.7.2 Nutrition Interventions for Mental Health in Pregnancy
18.7.3 Toxic Emotions and Pregnancy Outcomes
18.7.4 Intimate Partner Violence and Pregnancy Outcomes
18.8 Avoiding Risky Substances
18.9 Relational Connectedness
18.10 Conclusions
19 Postpartum Health and Lactation
Key Points
19.1 The Fourth Trimester
19.2 Breastfeeding
19.2.1 Composition of Human Milk
19.2.2 Benefits of Breastfeeding
19.2.3 Barriers to Breastfeeding
19.2.4 Breastfeeding Support
19.3 The Lifestyle Medicine-Focused Postpartum Visit
19.4 Pillars of Lifestyle Medicine in the Fourth Trimester
19.4.1 Nutrition
19.4.2 Physical Activity
19.4.3 Sleep
19.4.4 Emotional Wellness
19.4.5 Avoiding Risky Substances
19.4.6 Positive Psychology and Connectedness
19.5 Reproductive Life Planning
19.6 Adverse Pregnancy Outcomes and Future Health
19.6.1 Cardiovascular Disease
19.6.2 Renal Disease
19.6.3 Type 2 Diabetes Mellitus
19.6.4 Offspring Effects
19.6.5 Screening and Interventions
19.7 Conclusion
20 A Lifestyle Medicine Approach to Breast Cancer
Key Points
20.1 Introduction
20.2 Nutrition and Primary Breast Cancer Prevention
20.2.1 Fiber
20.2.2 Carotenoids
20.2.3 Soy
20.2.4 Dairy
20.2.5 Osteoporosis
20.3 Physical Activity and Primary Breast Cancer Prevention
20.4 Obesity and Primary Breast Cancer Prevention
20.5 Sleep and Primary Breast Cancer Prevention
20.6 Psychological Stress and Primary Breast Cancer Prevention
20.7 Tertiary Breast Cancer Prevention
20.8 Nutrition and Tertiary Breast Cancer Prevention
20.8.1 Soy
20.9 Physical Activity and Tertiary Breast Cancer Prevention
20.10 Obesity and Tertiary Breast Cancer Prevention
20.11 Sleep and Tertiary Breast Cancer Prevention
20.12 Psychological Stress and Tertiary Breast Cancer Prevention
20.13 Loneliness and Tertiary Breast Cancer Prevention
20.14 Conclusion
21 Gynecologic Cancers and Lifestyle Medicine
Key Points
21.1 Lifestyle Factors Predispose to Gynecologic Cancers
21.1.1 Diet, Obesity, and Cancer Risk
21.1.2 Physical Activity and Gynecologic Cancer Treatment
21.2 Tobacco, HPV, and Cervical Cancer
21.3 Nutrition, Gut Microbiome, and Response Interplay
21.3.1 The Microbiome Affects the Immune System
21.3.2 Obesity and the Gut Microbiome
21.3.3 Impact of Diet On the Gut Microbiome and Carcinogenesis
21.3.4 Exercise Influences the Gut Microbiome
21.3.5 Gut Microbiome and Cancer
21.4 Other Cancers and Lifestyle Link
21.5 Conclusion
22 Lifestyle Medicine in Female Cancer Survivorship
Key Points
22.1 Introduction
22.2 Common Survivorship Challenges
22.2.1 Fatigue and Pain
22.2.2 Emotional Distress With a Focus On Depression
22.3 Lymphedema
22.4 Transitioning From Cancer Patient to Survivor
22.5 Conclusion
23 Cardiovascular Disease and Metabolic Syndrome
Key Points
23.1 Introduction
23.2 Cardiovascular Disease in Women
23.2.1 Cardiovascular Disease Burden in Women
23.2.2 Traditional Risk Factors
23.2.2.1 Metabolic Syndrome
23.2.2.2 Hypertension
23.2.2.3 Dyslipidemia
23.2.2.4 Diabetes/Obesity
23.2.2.5 Physical Inactivity
23.2.2.6 Tobacco Use
23.2.3 Sex-Specific Risk Factors
23.2.3.1 Pregnancy-Related Disorders
23.2.3.2 Lactation and Weight Gain After Pregnancy
23.2.3.3 Autoimmune Disorders
23.2.3.4 Breast Cancer and CVD
23.2.3.5 Menopause
23.3 Lifestyle Medicine and Cardiovascular Health
23.3.1 Nutrition
23.3.2 Physical Activity
23.3.3 Avoidance of Toxic Substances
23.3.4 Restorative Sleep
23.3.5 Stress Resilience
23.3.6 Positive Psychology
23.4 Conclusion
24 Diabetes, Overweight, and Obesity
Key Points
24.1 Introduction
24.2 Diabetes in Women
24.2.1 Incidence of Diabetes
24.2.2 Diagnosis of Diabetes
24.2.3 Risk Factors Across a Woman’s Lifespan for Diabetes
24.2.3.1 Type 1 Diabetes
24.2.3.2 Gestational Diabetes Mellitus
24.2.3.3 Type 2 Diabetes Mellitus
24.2.4 Prognosis of Diabetes in Women
24.2.5 Traditional Care Approach of Diabetes
24.2.6 Lifestyle Medicine Prevention, Treatment, Remission, and Reversal of Diabetes
24.2.6.1 Dietary Interventions
24.2.6.2 Physical Activity
24.3 Overweight and Obesity
24.4 Conclusion
25 Dementia
Key Points
25.1 Dementia and Women
25.2 Lifestyle Approaches
25.2.1 Nutrition
25.2.2 Sleep and Cognition
25.2.3 Physical Activity and Cognition
25.2.4 Stress and Cognition
25.2.5 Substance Use and Cognition
25.2.6 Socialization and Cognition
25.3 Conclusion
26 Autoimmune Disorders Across the Lifespan
Key Points
26.1 Autoimmune Disease, Sex Hormones, and Lifestyle Medicine
26.2 Rheumatoid Arthritis
26.3 Systemic Lupus Erythematosus
26.4 Autoimmune Thyroid Diseases
26.5 Multiple Sclerosis
26.6 Conclusion
27 Psychiatric Disorders in Women
Key Points
27.1 Introduction to Chronic Psychiatric Disorders in Women
27.2 Diet and Nutrition
27.2.1 The Gut Microbiome
27.2.2 Inflammation
27.2.3 Epigenetic Effects
27.2.4 Imbalances in Individual Nutrients
27.3 Exercise
27.4 Tobacco Use Cessation
27.5 Stress Management
27.6 Building Healthy Relationships
27.7 Healthy Sleep
27.8 Conclusion
Index

Citation preview

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Improving Women’s Health Across the Lifespan

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Improving Women’s Health Across the Lifespan (a volume in the Lifestyle Medicine series)

Edited by Michelle Tollefson, MD Professor of Lifestyle Medicine Metropolitan State University of Denver Executive Board Member: American College of Lifestyle Medicine Nancy Eriksen, MD Associate Professor Maternal Fetal Medicine Baylor College of Medicine Neha Pathak, MD Medical Editor Internal Medicine Board of Directors: American College of Lifestyle Medicine

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First edition published 2022 by CRC Press 6000 Broken Sound Parkway NW, Suite 300, Boca Raton, FL 33487-​2742 and by CRC Press 2 Park Square, Milton Park, Abingdon, Oxon OX14 4RN © 2022 selection and editorial matter, Michelle Tollefson, Nancy Eriksen, Neha Pathak; individual chapters, the contributors CRC Press is an imprint of Taylor & Francis Group, LLC Reasonable efforts have been made to publish reliable data and information, but the author and publisher cannot assume responsibility for the validity of all materials or the consequences of their use. The authors and publishers have attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if permission to publish in this form has not been obtained. If any copyright material has not been acknowledged please write and let us know so we may rectify in any future reprint. Except as permitted under U.S. Copyright Law, no part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers. For permission to photocopy or use material electronically from this work, access www.copyright.com or contact the Copyright Clearance Center, Inc. (CCC), 222 Rosewood Drive, Danvers, MA 01923, 978-​750-​ 8400. For works that are not available on CCC please contact [email protected] Trademark notice: Product or corporate names may be trademarks or registered trademarks and are used only for identification and explanation without intent to infringe. Library of Congress Cataloging-​in-​Publication Data A catalog record has been requested for this book ISBN: 9780367627638 (hbk) ISBN: 9780367627621 (pbk) ISBN: 9781003110682 (ebk) DOI: 10.1201/​9781003110682 Typeset in Times by Newgen Publishing UK

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Contents Acknowledgments......................................................................................................ix Editor Biographies.....................................................................................................xi List of Contributors..................................................................................................xiii Introduction........................................................................................... 1 Chapter 1 Optimal Nutrition for Women............................................................... 3 Kayli Anderson, Kaitlyn Pauly, Debra Shapiro, and Vera Dubovoy Chapter 2 Physical Activity for Women............................................................... 41 Ginger Garner and Wendy Farnen Price Chapter 3 Sleep and Women’s Health.................................................................. 63 Cindy Geyer Chapter 4 Emotional Wellness and Stress Resilience.......................................... 85 Gia Merlo, Ariyaneh Nikbin and Hanjun Ryu Chapter 5 Positive Psychology and Relational Connectedness......................... 105 Liana Lianov Chapter 6 Avoiding Risky Substances and Environmental Exposures.............. 125 Natasha DeJarnett and Neha Pathak Chapter 7 Models of Care for Women and Families, Reimbursement, and Telemedicine..................................................................................... 145 Haran Sivakumar, Megan Alexander, Allison Theberge, and Deepa Sannidhi Chapter 8 Adverse Childhood Events and Trauma-​Informed Care................... 155 Robin Ortiz Chapter 9 Health Coaching, Motivational Interviewing, and Behavior Change in Women’s Health............................................................... 167 Mark D. Faries, Alyssa Abreu, Sarah-​Ann Keyes, Tasnim El Mezain and Jessica A. Matthews v

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Contents

Chapter 10 Health Equity and Women’s Health in Underserved Communities..................................................................................... 185 Stacie Schmidt, Jada Bussey-​Jones, and Tracey L. Henry Chapter 11 Community Engagement and Women’s Health................................199 Cheryl True, Elisabeth Fontaine, and Erin Phillips Chapter 12 Lifestyle Medicine in the Care of Adolescent Girls.......................... 207 Neeta B. Agarwal and Michelle Dalal Chapter 13 Menstrual Health and Lifestyle Medicine......................................... 215 Kranti Dasgupta, Madeline Hardacre, and Michelle Tollefson Chapter 14 Women’s Sexual Health and Lifestyle Medicine.............................. 227 Megan Alexander, Shannon Worthman, Rashmi Kudesia and Michelle Tollefson Chapter 15 Polycystic Ovary Syndrome, Endometriosis, and Female Infertility............................................................................... 241 Mahima Gulati, Joy Brotherton, and Jill Chasse Chapter 16 Lifestyle Medicine in Menopause and Bone Health......................... 255 Amanda McKinney Chapter 17 Preconceptual Health......................................................................... 273 Nancy L. Eriksen, Kristi R. VanWinden, and John McHugh Chapter 18 Pregnancy.......................................................................................... 309 Nancy L. Eriksen, Kristi R. VanWinden, Anne Bingham, and John McHugh Chapter 19 Postpartum Health and Lactation...................................................... 347 Kristi R. VanWinden and Elizabeth Collins Chapter 20 A Lifestyle Medicine Approach to Breast Cancer............................365 Amber Orman, Dianne L. Johnson, Amy Comander, Nigel Brockton, Meghana Reddy, and Gautam Krishna Koipallil

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Chapter 21 Gynecologic Cancers and Lifestyle Medicine..................................389 Nathalie D. McKenzie, Nnamdi I. Gwacham, and Sarfraz Ahmad Chapter 22 Lifestyle Medicine in Female Cancer Survivorship.......................... 411 Amber Orman, Meghana Reddy, Gautam Krishna Koipallil, Nigel Brockton, Michelle Faris, and Michelle Tollefson Chapter 23 Cardiovascular Disease and Metabolic Syndrome............................ 425 Neha Pathak Chapter 24 Diabetes, Overweight, and Obesity................................................... 441 Jeni A. Shull Clayton Chapter 25 Dementia........................................................................................... 459 Kelly J. Freeman, D. Nicole Paddock, and Cristina H. Davis Chapter 26 Autoimmune Disorders across the Lifespan..................................... 469 Margaret A. Eagan Chapter 27 Psychiatric Disorders in Women....................................................... 477 Gia Merlo, Hanjun Ryu, and Ariyaneh Nikbin Index....................................................................................................................... 491

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Acknowledgments This book would not have been possible without the vision, dedication, hard work, and persistence of so many. We would like to thank James Rippe for his trailblazing work to advance the field of Lifestyle Medicine and educate future generations of health professionals through a robust evidence base. Thank you for the opportunity to participate in this work. We would also like to thank the publishing team at Taylor & Francis (CRC Press) for their guidance throughout the process of developing this textbook. To all the chapter authors who contributed their time and expertise to create immensely valuable content for the care of women and girls throughout the lifespan, words cannot express our gratitude. We also want to thank Meagan Grega and John Gobble for their thoughtful editorial assistance with Chapter 7 and Jeannine Gluck for her work with Chapter 15. The final product would not have been possible without the energy and passion of Amber Loomis, who helped us move forward every step of the way. We also wish to thank Mariyam Sohail for her detailed support in our final stages of review and Rashmi Kudesia for her aid with the online supplemental materials. Finally, we would not have been able to complete this consuming labor of love without the love and support of those most dear to us.

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Editor Biographies Michelle Tollefson, MD, FACOG, DipABLM, FACLM, is an obstetrician-​gynecologist in Denver, CO, and a professor in the Health Professions Department at Metropolitan State University of Denver where she created and oversees the Lifestyle Medicine Program and the Wellness Coaching and Lifestyle Medicine Pathway. Dr. Tollefson is a graduate of Creighton University, where she received both her Bachelor of Science and Doctor of Medicine degrees. She completed her obstetrics and gynecology residency at the University of Missouri in Kansas City. She is also board certified in Lifestyle Medicine and is a fellow of the American College of Lifestyle Medicine (ACLM). As an ACLM member for more than a decade, she founded and co-​chairs the Women’s Health Member Interest Group as well as the Pre-​Professional Lifestyle Medicine Education Member Interest Group. She serves as the ACLM Board Secretary and on the Education and Membership Committees. Dr. Tollefson has worked with Dr. James Rippe, Lifestyle Medicine Series Editor, on prior projects, including guest-​editorship of a special edition of the American Journal of Lifestyle Medicine. She is also a breast cancer survivor and thriver and facilitates PAVING the Path to Wellness online Lifestyle Medicine groups for breast cancer survivors. She lives in Colorado with her husband and three children, Kaitlyn, Luke, and Blake. Nancy Eriksen, MD, FACOG, DipABLM, is an associate professor of Maternal-​ Fetal Medicine in the Department of Obstetrics and Gynecology at Baylor College of Medicine in Houston, Texas. Dr. Eriksen is a graduate of the University of Miami in Miami, Florida, where she received her Bachelor of Science degree in Biology. She received her Doctor of Medicine degree and completed her residency in Obstetrics and Gynecology at Wright State University in Dayton, Ohio. She completed her fellowship in Maternal-​Fetal Medicine at the University of Texas Health Sciences Center in Houston, Texas. She is board certified in Obstetrics and Gynecology, Maternal-​Fetal Medicine, and Lifestyle Medicine. Dr. Eriksen is a member of the American College of Lifestyle Medicine (ACLM) Women’s Health Member Interest Group and co-​chair of the Pregnancy subcommittee. Dr. Eriksen lectures on a variety of topics related to Lifestyle Medicine and women’s health for local, regional, and national audiences. She has been a speaker for an ACLM webinar and at national meetings for ACLM and the American College of Obstetrics and Gynecology. Her most recent project is developing the Preconceptual Health and Nutrition and Pregnancy and Nutrition modules for the ACLM Food as Medicine CME course. Her clinical interests include the impact of a whole-​food plant-​based nutrition on improving preconceptual health and pregnancy outcomes. Neha Pathak, MD, DipABLM, is a physician and WebMD/​Medscape medical editor and writer. Dr. Pathak is an honors graduate of Harvard College. She received her Doctor of Medicine degree and completed her internal medicine degree at Weill xi

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Medical College of Cornell University in New York. She is board certified in both Internal Medicine and Lifestyle Medicine. Dr. Pathak began practicing Lifestyle Medicine within the Department of Veterans Affairs (VA) with the Whole Health program. She completed the VA Quality Scholar program, a VA-​sponsored quality improvement fellowship during which she developed and implemented a pilot program to improve care for vulnerable veterans utilizing interdisciplinary care, telehealth monitoring, and interventions focused on lifestyle and social determinants of health. Dr. Pathak serves on the board of directors of the American College of Lifestyle Medicine (ACLM) and is a member of the ACLM’s Women’s Health and Health Equity Achieved through Lifestyle Medicine (HEAL) member interest groups. She is also co-​chair of the ACLM’s Global Sustainability Committee. She is passionate about educating the public and health professionals about the benefits of Lifestyle Medicine not only to protect individual health, but also to improve community and planetary health. She lives in Atlanta with her husband and three daughters, Ishani, Kiran, and Vidya.

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Contributors Alyssa Abreu Texas A&M School of Public Health College Station, Texas Neeta B. Agarwal Indiana University School of Medicine Indianapolis, Indiana Sarfraz Ahmad AdventHealth Cancer Institute Gynecologic Oncology Program Orlando, Florida Megan Alexander Boston University School of Medicine Boston, Massachusetts Kayli Anderson American College of Lifestyle Medicine Kayli Anderson Nutrition Salida, Colorado

Elizabeth Collins Department of Gynecology and Obstetrics Emory University Atlanta, Georgia Amy Comander Massachusetts General Hospital Cancer Center Harvard Medical School Boston, Massachusetts Michelle Dalal University of Massachusetts Medical School Milford, Massachusetts Kranti Dasgupta Bloom Lifestyle Medicine Alamo, California

Anne Bingham Crescent Street OB/​GYN Middletown, Connecticut

Cristina Davis Oak Street Health Indianapolis, Indiana

Nigel Brockton American Institute for Cancer Research Arlington, Virginia

Natasha DeJarnett Christina Lee Brown Environment Institute University of Louisville Louisville, Kentucky

Joy Brotherton David Geffen School of Medicine at UCLA Los Angeles, California Jada Bussey-​Jones Department of Medicine Emory University School of Medicine Atlanta, Georgia Jill Chasse Department of Public Health William Paterson University Wayne, New Jersey

Vera Dubovoy Department of Obstetrics, Gynecology and Reproductive Sciences University of Texas Health Science Center Houston, Texas Margaret Eagan Virta Health San Francisco, California Tasnim El Mezain Point Loma Nazarene University San Diego, California xiii

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Nancy Eriksen Department of Obstetrics and Gynecology Maternal-​Fetal Medicine Baylor College of Medicine Houston, Texas Mark Faries Texas A&M AgriLife Extension Service Texas A&M School of Public Health College Station, Texas Michelle Faris UCHealth Physical Therapy and Rehabilitation Services The Wellness Place Fort Collins, Colorado Wendy Fernen Price Healthcore Lifestyle Medicine New Haven, Connecticut Elisabeth Fontaine Let’s Lead LLC, Plant Based Telehealth Swanton, Vermont Kelly Freeman Indiana University Indianapolis, Indiana Ginger Garner Living Well Institute EudeMOMia® Integrative Physical Therapy & Lifestyle Medicine Greensboro, North Carolina Cindy Geyer Ultrawellness Center Lenox, Massachusetts Mahima Gulati Middlesex Health Multispecialty Endocrinology Frank H. Netter MD School of Medicine, Quinnipiac University Middletown, Connecticut

List of Contributors

Nnamdi I. Gwacham AdventHealth Cancer Institute Gynecologic Oncology Program Orlando, Florida Madeline Hardacre Women’s Health Elevated Reno, Nevada Tracey L. Henry Department of Medicine Emory University School of Medicine Atlanta, Georgia Dianne L. Johnson MBB Radiology Jacksonville, Florida Sarah-​Ann Keyes School of Health Professions Baylor College of Medicine Houston, Texas Gautam Krishna Koipallil USF Morsani College of Medicine Tampa, Florida Rashmi Kudesia CCRM Fertility Houston Houston Methodist Hospital Houston, Texas Liana Lianov Global Positive Health Institute, Inc. HealthType, LLC. Sacramento, California Jessica A. Matthews Point Loma Nazarene University Department of Family Medicine and Public Health University of California San Diego San Diego, California John McHugh Department of Obstetrics and Gynecology Keck School of Medicine of USC, Huntington Hospital Pasadena, California

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Nathalie D. McKenzie AdventHealth Cancer Institute Gynecologic Oncology Program Orlando, Florida Amanda McKinney Doane University Crete, Nebraska Gia Merlo Rory Meyers College of Nursing, New York University Department of Psychiatry, NYU Grossman School of Medicine New York, New York Ariyaneh Nikbin Albert Einstein College of Medicine New York, New York Amber Orman Department of Radiation Oncology AdventHealth Cancer Institute Orlando, Florida Robin Ortiz National Clinician Scholars Program, University of Pennsylvania Children’s Hospital of Philadelphia Philadelphia, Pennsylvania D. Nicole Paddock Oak Street Health University of Indianapolis Indianapolis, Indiana Neha Pathak Board of Directors, The American College of Lifestyle Medicine Atlanta, Georgia Kaitlyn Pauly The American College of Lifestyle Medicine Spearfish, South Dakota Erin Phillips Program in Occupational Therapy Carlow University Pittsburgh, Pennsylvania

Meghana Reddy USF Morsani College of Medicine Tampa, Florida Hanjun Ryu Rice University Houston, Texas Deepa Sannidhi Department of Family Medicine UC San Diego Health San Diego, California Stacie Schmidt Department Medicine Emory University School of Medicine Atlanta, Georgia Debra Shapiro Premise Health South San Francisco, California Jeni A. Shull Clayton Well Life by Schneck Schneck Medical Center Seymour, Indiana Haran Sivakumar Department of Family Medicine UC San Diego Health San Diego, California Allison Theberge Department of Family Medicine UC San Diego Health San Diego, California Michelle Tollefson Lifestyle Medicine Program, Department of Health Professions Metropolitan State University of Denver Denver, Colorado Cheryl True True Lifestyle Medicine Clinic Davenport, Iowa

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Kristi R. VanWinden Department of Obstetrics and Gynecology Division of Maternal Fetal Medicine The Permanente Medical Group Oakland, California

List of Contributors

Shannon Worthman American College of Lifestyle Medicine Chesterfield, Missouri

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Introduction

The world has borne witness to a steep rise in noncommunicable diseases (NCDs) over the past three decades. Why? What is happening that has never happened before? Where is this rise coming from, and what can we do to protect ourselves from it? Cardiovascular disease, cancer, chronic respiratory disease, and diabetes now make up over 80% of global deaths, and take trillions of dollars out of our pockets each year. Also, for reasons not commonly discussed or addressed among the medical and scientific communities, NCDs disproportionally affect people of color. But here’s the thing: underlying causes of NCD are related to lifestyle and can be changed, modified, or stopped altogether to improve health and wellness! Poor diet, sedentary lifestyle, smoking, substance use, environmental exposures, chronic stress, insufficient sleep, poor emotional health, and adverse childhood events all play a role in the development of NCDs. As we write this book, the world is in the midst of a novel Coronavirus pandemic, with a surge in the number of Coronavirus disease 2019 (COVID-​19) cases throughout the United States. Not surprisingly, individuals who are at the greatest risk for becoming seriously ill, or worse, death, are those with underlying NCDs, with people from vulnerable communities suffering at a disproportionate rate. COVID-​19 has brought to the forefront the marked disparities affecting people of color in this country. If ever there was a time to incorporate lifestyle changes personally and professionally, it is now. It is understandable that Lifestyle Medicine has been focused on preventing and reversing chronic disease, the primary causes of death in general. This is natural, given our current state of health. But what about the role of Lifestyle Medicine for issues specific to women’s health? What are the specific benefits of positive lifestyle practices for gynecologic health, sexual health, and gynecologic cancer? Women have not only the added privilege, but also the responsibility of bringing the next generation into the world. With so much chaos, so much that feels out of our control, what choices can women be empowered with to easily improve maternal and fetal health? These are some of the questions that are explored in this book. This book seeks to provide the most comprehensive review of the application of Lifestyle Medicine to women’s health to date. The research and recommendations made in this book range from basic principles to practical application of Lifestyle DOI: 10.1201/9781003110682-1

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Medicine, gynecologic and obstetric health, cancer, and unique aspects of managing chronic conditions that occur in women. Every author has curated their experience and expertise to provide you with this text. So, whether you are a full-​time women’s care provider, a specialist, a dietician, a wellness coach, a training provider, or a psychologist, there is something in this book for you. It is our hope that you will not only become more knowledgeable about applying Lifestyle Medicine in your practice, and to your own health, but that you will become an advocate for transforming women’s health, and therefore their lives and the lives of their children, for the better!

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Optimal Nutrition for Women Kayli Anderson, MS, RDN, DipABLM, ACSM-​EP, Certified Intuitive Eating Counselor Kayli Anderson Nutrition Salida, CO

Kaitlyn Pauly, MS, RDN, DipABLM

The American College of Lifestyle Medicine Spearfish, SD

Debra Shapiro, MD, FACOG, DipABLM Premise Health South San Francisco, CA

Vera Dubovoy, MD, FACOG, DipABLM, Board Certified OBGYN

Department of Obstetrics, Gynecology and Reproductive Sciences University of Texas Health Science Center at Houston Houston, TX 1.1 Introduction........................................................................................................5 1.2 Nutrition Basics..................................................................................................6 1.2.1 Energy....................................................................................................6 1.2.2 Nutrient Density.....................................................................................7 1.2.3 Macronutrients.......................................................................................8 1.2.4 Carbohydrates.........................................................................................8 1.2.5 Fats.........................................................................................................9 1.2.6 Proteins.................................................................................................10 1.2.7 Micronutrients......................................................................................11 1.2.8 Nutrients of Concern............................................................................11 1.2.9 Phytonutrients and Antioxidants..........................................................12 1.2.10 Water....................................................................................................12 1.3 Standard Nutrition Guidelines..........................................................................13 1.3.1 National and Global Guidelines...........................................................13 DOI: 10.1201/9781003110682-2

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1.4 Health-​Promoting and Health-​Harming Foods................................................15 1.5 The American College of Lifestyle Medicine’s Recommended Dietary Pattern..................................................................................................16 1.5.1 The American College of Lifestyle Medicine Dietary Position...........16 1.5.2 The Dietary Spectrum..........................................................................17 1.6 Nutrition Recommendations for Women..........................................................17 1.6.1 Women-​Specific Health Risks..............................................................18 1.6.1.1 Weight Concerns, Body Image, and Eating Disorders...........18 1.6.1.2 Women-​Specific Cancers.......................................................19 1.6.1.3 Bone Health...........................................................................20 1.6.2 Nutrients to Know for Women.............................................................20 1.6.2.1 Vitamin B12...........................................................................20 1.6.2.2 Calcium..................................................................................21 1.6.2.3 Vitamin D...............................................................................21 1.6.2.4 Iron.........................................................................................21 1.6.2.5 Folate......................................................................................22 1.6.2.6 Zinc........................................................................................22 1.6.2.7 Iodine.....................................................................................22 1.6.2.8 Omega-​3s...............................................................................22 1.7 Brief Overview of Nutrition Needs Across The Lifespan................................23 1.7.1 Nutrition and Fertility...........................................................................23 1.7.2 Nutrition and Pregnancy and Lactation................................................23 1.7.3 Energy..................................................................................................24 1.7.4 Macronutrients.....................................................................................24 1.7.5 Micronutrients......................................................................................24 1.7.5.1 Iodine.....................................................................................24 1.7.5.2 B12.........................................................................................25 1.7.5.3 Folate......................................................................................25 1.7.5.4 Iron.........................................................................................25 1.7.5.5 Choline...................................................................................25 1.7.5.6 Zinc........................................................................................25 1.7.5.7 Calcium..................................................................................25 1.7.5.8 Vitamin D...............................................................................26 1.7.5.9 Other Nutrients.......................................................................26 1.7.6 Nutrition and Menopause.....................................................................26 1.7.7 Nutrition and Female Athletes..............................................................26 1.8 Practical Tools for Transitioning to a Whole Food Plant-​Based Eating Pattern...................................................................................................27 1.8.1 The WFPB Plate...................................................................................28 1.8.2 Tips for Transitioning...........................................................................28

KEY POINTS • Women’s health shapes the nutrition and health status of the entire society. They still do the majority of the food shopping, meal planning, and cooking; they are the primary victims of messaging that encourages unscientific dieting

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practices; and they have the responsibility of growing and birthing the next generation. Therefore, knowledge of women-​specific nutrition is critical for all clinicians. • A large body of evidence suggests that plant-​predominant dietary patterns have the power to prevent chronic diseases, and, when used as an intervention, can even treat and reverse certain diseases, including cardiovascular disease, obesity, and type 2 diabetes. • Women’s nutrition needs change throughout the lifecycle, and certain nutrients are of particular importance to women’s health, including vitamin B12, vitamin D, calcium, iron, folate, zinc, iodine, and omega-​3 fatty acids.

1.1  INTRODUCTION Humans make, on average, 221 food-​related decisions each day,1 and most people feel lost as to how to make the right decisions of what to eat.2 As the field of nutrition research grows, it becomes more apparent as how important each of those 221 decisions is to a person’s health. Seven of the ten leading causes of death in the United States are chronic diseases, and almost half of Americans live with at least one chronic disease.3 Poor diet is one of the most important modifiable risk factors for preventing these diseases, along with sedentary lifestyle and tobacco use.4 Making it even more challenging to establish healthful eating habits is the modern American food culture. Companies spend about 2 billion dollars per year marketing processed, packaged food products to children.5 Americans of minority races and ethnicities experience higher rates of many chronic diseases due to the social, economic, and environmental disadvantages they face,6 and it is estimated that more than 23 million Americans live in food deserts without ready access to nutritious foods.7 Although nutrition is such an important factor in human health, most medical school curricula still lack nutrition education.8 However, the tides are beginning to shift as more healthcare providers awaken to the importance of healthy eating habits. Women still do the majority of the food shopping, meal planning, and cooking, and, therefore, set the tone for their families’ eating habits.9 They are also the primary victims of cultural messaging about appearance that encourages unscientific dieting practices.10 Women also have the extraordinary responsibility of growing and birthing the next generation. The months fetuses spend developing in the womb are now understood to be some of the most critical periods. The developmental origins of health and disease hypothesis is now widely accepted in the scientific community and puts the importance of women’s health prior to and during pregnancy into clear focus.11 Gestational exposure to dietary factors,12 maternal emotional stress,13 and environmental exposures14 is now recognized as critical for influencing the future health of the generations that follow. Whether a woman is faced with feeding her family, nourishing herself in the climate of external pressures and expectations, or providing for her unborn child, her needs are unique, ever changing, and vital knowledge for every clinician caring for women.

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1.2  NUTRITION BASICS 1.2.1 Energy Foods and beverages contain energy that is measured in units known as calories. Each human needs a certain amount of calories to maintain basic metabolic functions like circulation, respiration, and mental processing, as well as daily activity. Physical traits, genetic variations, and lifestyle factors unique to each individual affect the amount of energy required. Several predictive formulas are used by researchers and clinicians to estimate caloric needs and make tailored nutrition recommendations. These formulas include sex, height, weight, age, and physical activity level. One of the most widely used formulas to estimate basal energy needs, also known as basal metabolic rate (BMR), is the Mifflin-​St. Jeor equation. BMR accounts for 60–​80% of total energy expenditure (TEE) and encompasses the energy required to perform basic metabolic functioning.15 Eq. 1.1 Mifflin-​St. Jeor16 Men BMR (kcal/day) = (10 × weight in kg) + (6.25 × height in cm) − (5 × age in years) + 5 Women BMR (kcal/day) = (10 × weight in kg) + (6.25 × height in cm) − (5 × age in years) − 161 While this formula calculates basal energy needs, other components of TEE must also be added for an accurate estimate of energy requirements. To account for the energy expended through daily activity, the BMR must be multiplied by an activity factor that approximates physical activity level. The following are general activity factor multipliers: • • • • •

Little to no exercise: BMR × 1.2 Light ­exercise 1–​3 days per week: BMR × 1.375 Moderate ­exercise 3–​5 days per week: BMR × 1.55 Heavy ­exercise 6–​7 days per week: BMR × 1.725 Very heavy exercise twice per day, extra heavy workouts: BMR × 1.9

Of the factors that contribute to TEE, the smallest and least variable is the thermic effect of food (TEF), or the increase in energy expenditure that occurs after a meal. TEF usually accounts for eight to twelve percent of TEE.17 Predictive equations for estimating energy needs have limitations. Older adults and ethnic minorities were underrepresented in both the development and validation process of most of the formulas. The equations also fail to take body composition into account, despite the fact that fat-​free mass (FFM) requires more energy to maintain than fat tissue. Unless indicated, predictive equations are also not accurate for underweight or obese body mass index (BMI) categories. Out of four predictive equations most commonly used in clinical practice, the Mifflin-​St. Jeor equation was found to be the most reliable, predicting caloric requirements within 10% of

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measured in non-​obese and obese individuals.18 Predictive equations for obese and underweight individuals do exist, but the literature cautions their use due to lack of accuracy.19,20 Estimated energy recommendation charts also exist for both adults and children and are often used in population health and policy guidelines.21 Specialized measurement tools like indirect calorimetry, direct calorimetry, doubly labelled water technique, bioimpedance scales, and dual-​energy X-​ray absorptiometry (DXA) bone scans more accurately estimate energy needs. However, they are generally expensive, time-​consuming, and impractical for most clinical encounters. Energy balance occurs when energy intake is equal to energy expenditure, which is the goal for maintaining body weight. When energy intake exceeds expenditure, a state of positive energy balance occurs followed by an increase in body mass, most of which is usually body fat. On the other hand, when energy expenditure exceeds intake, negative energy balance leads to a loss of body mass, which is also usually body fat.22 While overweight and obesity is generally considered to be a result of either excessive calorie intake or insufficient physical activity, body weight is incredibly complex, so the most effective strategies for achieving and maintaining a healthy body weight often employ many modalities including nutrition, physical activity, mental health, and others. While energy calculations can be a useful piece of information, energy needs vary from one person to another based on countless factors. The USDA Dietary Guidelines for Americans (DGA) state that the best way to determine whether an eating pattern contains the appropriate amount of energy is to monitor the trend of body weight over time and adjust intake and expenditure accordingly.23

1.2.2 Nutrient Density Nutrient density as described in the dietary guidelines is a: characteristic of foods and beverages that provide vitamins, minerals, and other substances that contribute to adequate nutrient intakes or may have positive health effects, with little or no solid fats and added sugars, refined starches, and sodium. Ideally, these foods and beverages also are in forms that retain naturally occurring components, such as dietary fiber.23

Nutrient-​dense foods include foods that are in their most whole form with little to no refinement, such as whole vegetables and fruits, whole grains and products made from whole grain flours, beans, lentils, nuts, and seeds. In recent decades, human diets have become more highly processed, even sparking a new category of food known as ultra-​processed foods (UPFs) in the NOVA food classification system. UPFs are defined as ready-​ to-​ consume and ready-​ to-​ heat formulations, made by combining substances derived from foods with cosmetic additives, typically through a series of industrial processes.24 UPFs often contain high amounts of calories, added sugars, fat, and sodium, and low amounts of vitamins, minerals, and fiber. In recent years, UPFs have become a significant food source in high-​income countries including the United States.24 There is mounting evidence of major health consequences related to the consumption of UPFs.25

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Globalization of processed food trends has led to a shift away from traditional nutrient-​dense diets toward those linked with diet-​related noncommunicable chronic disease.26 In the report titled “Ultra-​processed foods, diet quality, and health using the NOVA classification system,” the authors state that the significance of the effects of industrial food processing on human health has been underestimated.24 Due to the delayed nature of scientific evidence and the subsequent delay of that translation of public health policy, it is yet to be known what the long-​term health implications will be of UPFs.

1.2.3 Macronutrients Foods are made up of combinations of energy-​containing macronutrients and non-​ energy-​containing micronutrients. Essential macronutrients include carbohydrates, proteins, and fats. Alcohol is also an energy-​containing macronutrient, but it is not considered essential to human health. It is common to see foods categorized by the nutrient that is most prominent in them. For example, pasta and bread get classified as carbohydrates, and most Americans associate orange juice with vitamin C. This reductionist approach to food neglects to consider variances among foods, synergistic actions of nutrients, and the entire nutrient package of a food, all of which influence or determine the protective or harmful impacts of whole foods and food products and, most importantly, dietary patterns as a whole.27 Nutrition reductionism, as it is sometimes termed, is evident in nutrition research and results in the belief that randomized control trials (RCTs) that attempt to isolate the effects of singular nutrients on specific outcomes are the most reliable approach to establish causal relationships between diet and disease. However, this approach fails to acknowledge the larger context of how specific nutrients fit into an overall eating pattern over time. A more holistic approach to nutrition is to think in terms of dietary patterns and the relationship of those patterns with human, environmental, and global health. While the need to see the big picture in nutrition science and its application is imperative, it is still valuable to understand the basics of food components because each has different functions in the body, offers various amounts of energy by volume, and impacts health differently.

1.2.4 Carbohydrates Carbohydrates are the primary and preferred source of energy for the body’s cells, particularly the brain. Each gram of carbohydrate supplies 4 kilocalories (kcals) of energy. Monosaccharides consist of one sugar unit such as glucose or fructose. Disaccharides like sucrose, lactose, and maltose have two sugar units. The term “sugars” is usually used to describe both mono-​and disaccharides, which in food production serve to sweeten and preserve foods. Oligosaccharides have 3–​10 sugar units and are usually by-​products of polysaccharides that have more than 10 sugar units. These larger combinations of sugar units are often referred to as starches and are found in both whole plant food sources and added to food products per their functional properties.28

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Within the category of carbohydrate-​rich foods, there are varying levels of nutrient densities and subsequently different health effects. Carbohydrates are found abundantly in whole plant foods, including fruits, vegetables, whole grains, beans, and legumes, and to a smaller extent in nuts and seeds. Carbohydrate-​rich foods found in their whole, unprocessed forms come packaged with beneficial vitamins, minerals, dietary fiber, water, phytonutrients, and antioxidants. Dietary fiber is a type of carbohydrate that is neither digested nor absorbed in the small intestine. Fiber is found exclusively in plant food or can be synthesized and added to food products. It is characterized by its level of solubility in water. Soluble fiber dissolves in water, forming a gel-​like material that helps to sweep cholesterol from the intestine and slow the speed of digestion which can lower blood glucose. It is found in oats, peas, beans, apples, carrots, barley, citrus fruits, and psyllium. Insoluble fiber does not dissolve in water and increases stool volume, allowing movement of fecal matter through the digestive tract. It is known for its ability to help with constipation and feed the bacteria of the gut. Whole wheat foods, bran, nuts, beans, cauliflower, green beans, and potatoes all contain insoluble fiber. Higher intakes of dietary fiber are associated with reduced risk for several chronic diseases, including cardiovascular disease, cancer, type 2 diabetes, and obesity.29 More recently, dietary fiber and its relationship with gut microbiome diversity demonstrate its anti-​inflammatory and immunomodulatory effects, which bolster support about its important role in the human diet. The Dietary Reference Intake (DRI)s use 14 g of fiber per 1,000 kcal as a reference for adequate intake.23 Refined carbohydrates are found abundantly in manufactured foods, such as breads and pastas made from refined flour, white rice, donuts, cakes, pastries, soda, juice, candy, crackers, and beverages, which often fall into the ultra-​processed food category. In processing, these foods have beneficial components removed (i.e., outer bran of grain), and less health-​promoting components added (i.e., fat and sugar), usually to change texture, taste, or shelf stability. These processing techniques make refined carbohydrates relatively high in energy, added fats, sugars, and sodium, and low in healthful nutrients. These processing techniques result in food products that are very palatable, making it easy for the hedonic centers of the body to override homeostatic satiety signaling.30 Refined carbohydrate intake is positively associated with negative health benefits and increased risk of several chronic diseases.31 National and global dietary guidelines recommend that the majority of energy comes from a variety of carbohydrate food sources and that most of those foods should be as minimally processed as possible.

1.2.5 Fats Dietary fat is used for energy and for absorption of fat-​soluble vitamins A, D, E, and K. Dietary fat has the most energy by volume, offering 9 kcal per gram. The structure and function of dietary fatty acids can vary greatly depending on chain length: number of double bonds –​saturated with no double bonds, monounsaturated, or polyunsaturated; and whether the double bonds are positioned on the same side or opposite side.32 Fat is categorized as unsaturated or saturated, but most food sources of fat have a mixture of both saturated and unsaturated fats.

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Polyunsaturated fats, which include both omega-​3 and omega-​6 fatty acids, have important structural and physical functions. These fat types are considered essential and must be obtained from the diet because they are not synthesized in the body.32 Whole food sources of polyunsaturated fatty acids (PUFAs) include walnuts, pine nuts, sesame, sunflower, pumpkin flax seeds, and salmon, trout, herring, tuna, and mackerel. Refined sources of PUFAs include sunflower, corn, soybean, and cottonseed oil.23 Monounsaturated fatty acids (MUFAs) intake is associated with positive health benefits but is not considered essential. MUFAs are found in whole food forms in avocados, peanut butter, and most nuts. Refined MUFAs are found in olive, canola, peanut, sunflower, and safflower oils. MUFAs are also part of most animal fats such as fats from chicken, pork, beef, and wild game.23 Saturated fats have been shown to raise low-​density lipoproteins (LDL) cholesterol in the body, leading to the inference that dietary intake of saturated fat directly promotes the development of coronary heart disease.32 Saturated fat is found in animal products, such as pork, egg, chicken, beef, and dairy foods, as well as in some plant sources such as coconuts and other nuts. Refined saturated fat sources include coconut and palm kernel oils.23 Trans fats are unsaturated fats found primarily in partially hydrogenated vegetable oils and foods containing these oils. Their intake has been associated with deleterious impacts on human health, leading to an attempt to remove them from the US food supply by regulating their use by food manufacturers. There is a considerable amount of controversy in the research over how dietary fats influence health outcomes and chronic diseases. However, most public health guidelines universally advocate for reducing the intake of total and saturated fat, with the emphasis shifting away from total fat recommendations and toward the recommendations to replace saturated fat with polyunsaturated and monounsaturated fats and to completely eliminate trans fat.32 The DRI for fat is 25–​35% of total calories.23

1.2.6 Proteins Dietary proteins are the building blocks of DNA and cells. Protein is found in many types of foods including plant and animal sources and contains 4 kcal per gram. Like carbohydrates and fats, proteins are packaged in foods with many other nutrients. Protein found in plant-​based foods is packaged with beneficial nutrients including dietary fiber, phytonutrients, vitamins, and minerals. Proteins from plant sources are also lower in fat, particularly saturated fat, and contain little to no cholesterol. Protein found in animal foods is packaged with higher amounts of total and saturated fat, sodium, and cholesterol and does not contain beneficial fiber or phytonutrients. Protein-​rich plant food sources include legumes and beans, soy and soy products, nuts, and seeds as well as some whole grains. Animal sources of protein include meat (i.e., beef, lamb, pork, veal), poultry (i.e., chicken, turkey), eggs, dairy (milk, yogurt, cheese), and fish. The source of protein is important for health outcomes. High animal protein intake is positively associated with cardiovascular mortality, whereas high plant protein

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intake is inversely associated with all-​cause and cardiovascular mortality.33 Recent data from large cohorts have confirmed that high total and animal protein intakes are associated with the risk of cardiovascular disease and diabetes, even in models that are largely adjusted for lifestyle and dietary or nutritional factors. There is variability depending on the type of animal protein, with processed red meats being the most harmful.34 The DGA recommends consuming a variety of plant and animal protein foods and offer estimated amounts needed within estimated calorie ranges. Global recommendations that take human health and environmental sustainability into account often recommend replacing animal-​based protein sources with plant sources in comparison with the US government.35 The recommendation in the United States is to get 10–​30% of calories from protein.23

1.2.7 Micronutrients While much of dietary advice focuses on macronutrients, micronutrients in the form of vitamins and minerals are essential for human health. Micronutrients do not offer any calories but do play significant roles as cofactors in physiologic processes. Vitamins include biotin, choline, folate, niacin, pantothenic acid, riboflavin, thiamin, vitamin A, vitamin B6, vitamin B12, vitamin C, vitamin D, vitamin E, and vitamin K. Minerals include calcium, chloride, chromium, copper, iodine, iron, magnesium, manganese, molybdenum, phosphorus, potassium, selenium, sodium, and zinc. The Institute of Medicine (IOM) establishes DRIs for micronutrients. They serve as a guide for good nutrition and provide the scientific basis for the development of food guidelines in both the United States and Canada. Food sources of micronutrients are the preferred and recommended sources. Because micronutrients are found in varying amounts, have varying levels of absorption, and are found in various plant and animal foods, most nutrition professionals and dietary guidelines recommend eating a variety of foods to ensure adequate intakes. The Food and Drug Administration (FDA) does not regulate the dietary supplement industry; therefore, if a supplement is needed to obtain adequate levels of micronutrients, it is important to choose trusted manufacturers. Specific micronutrients of importance will be discussed later in this chapter.

1.2.8 Nutrients of Concern The DGA recognize calcium, potassium, dietary fiber, and vitamin D as nutrients of public health concern because low intakes are associated with health concerns. For young children, women capable of becoming pregnant, and women who are pregnant, low intake of iron is also a public health concern.23 Micronutrient deficiencies, while much less common in the United States today, are of importance to monitor in clinical practice as they often lead to damaging and sometimes irreversible health conditions. Plant-​based diets contain an abundant source of vitamins and minerals. However, plant-​based, vegan, vegetarian, and plant-​exclusive diets are often characterized

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by their association with micronutrient deficiencies rather than their abundance of micronutrients, especially when they are poorly planned. However, it is the position of the Academy of Nutrition and Dietetics that appropriately planned vegetarian and vegan diets are healthful, nutritionally adequate, and may provide health benefits for the prevention and treatment of certain diseases, including heart disease, type 2 diabetes, hypertension, certain types of cancer and obesity.36 Plant-​exclusive diets need to contain reliable sources of vitamin B12 because it is the only nutrient not directly available from plant foods.37

1.2.9 Phytonutrients and Antioxidants Phytonutrients are phytochemicals present in certain foods and play a role in the maintenance of human health and prevention of diseases. Their regular and adequate intake may offer protection from major chronic diseases, including cardiovascular and neurodegenerative diseases, and cancer. There are over 25,000 phytonutrients from different phytochemical classes including anthocyanins, carotenoids, coumarins, flavonoids, diarylalkanoids, lignans, phenolic acids, polyphenols, sterols, and terpenes, which have been found exclusively in plant foods.38 Antioxidants are natural substances that may prevent or delay some types of cell damage. Several decades of dietary research findings suggest that consuming greater amounts of antioxidant-​rich foods might help to protect against diseases. Accumulating epidemiological evidence has demonstrated the association between both antioxidants and antioxidant-​rich foods intake and human health. For example, recent meta-​analysis and cohort studies showed that high consumption of antioxidants and antioxidant-​rich foods is associated with decreased risk of “overall and cardiovascular disease (CVD) related” mortality,39 certain cancers,40 and CVD.41 Antioxidants are found in large amounts in fruits and vegetables, as well as in other plant-​derived foods like tea, coffee, and cocoa. There are currently no guidelines for the consumption of phytonutrients or antioxidants. However, due to their demonstrated health benefits, their intake is strongly encouraged. A variety of plant foods, which are the only source of naturally occurring phytonutrients and antioxidants, are recommended to be eaten in abundance at each meal. Although antioxidants are available in supplement form, it is healthiest and safest to consume them in whole food form.

1.2.10 Water Water plays a very important role in the body. Almost all of the body’s major functions depend on it. Not only does water play a role in the regulation of body temperature, it also moistens and protects organs and tissues, carries nutrients and oxygen, lubricates joints, flushes waste products, and helps in digestion and absorption. Because of its numerous benefits to human health and because of lack of added calories, water is the best fluid source for humans. Water is also prevalent in large quantities in fruits and vegetables. Numerous factors can impact fluid needs, including age, physical activity level, caloric intake, body composition, and health status. While there are many ways to

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assess calorie and micronutrient needs, there are less established ways to assess and make recommendations for fluid needs. Assessments based on a per body weight basis are most common in clinical settings. Fluid needs calculated on a per body weight basis and stratified by age category are as follows42: • 30–​35 mL/​Kg Body Weight (adults >30 years old) • 40–​60 mL/​Kg (adolescents) • 35–​40 mL/​Kg (16–​30 years old) Recommendations are often adjusted depending on medical conditions such as heart failure, liver or kidney disease, and medication use. In summary, whole foods can be reduced and classified by their nutrient components and value that exists in understanding the scientific basis underpinning individual nutrient recommendations, and the focus of dietary advice should be on the consumption of whole foods and overall dietary patterns.

1.3  STANDARD NUTRITION GUIDELINES There has been much interest in studying the diets of human ancestors to see what the human body might be most suited for, given that the human jaw, teeth, and digestive tract have not changed for millions of years. Research has shown that human Paleolithic ancestors and closest living primate relatives both ate a diet that consisted mostly of plants.43–​45 Discussions of evolution aside, today the government and other national and global organizations develop nutrition guidelines and recommendations to guide Americans in what to eat for health.

1.3.1 National and Global Guidelines In the United States, there is a history of government-​ sponsored research and recommendations dating back to over 100 years.46 The first nutrition guidance was published in 1894 in the form of food composition tables and dietary standards.47 Initial guidelines were concerned with food storage and safety, getting adequate macronutrients from basic foods groups, and consuming certain crucial vitamins and minerals. The enduring themes for the first 100 years of nutrition guidance were variety, moderation, and balance. These guidelines have come a long way, as the field of nutrition research has grown. As the idea of food groups evolved and the understanding of nutrition science and its relationship with human health deepened, government recommendations evolved and became more precise. In 1977, Senator George McGovern led the first US Senate Select Committee on Nutrition and Human Needs, and the resulting McGovern Report became the incentive for the DGA. The report explicitly laid out the connection between excessive intake of added salt, fat, and sugar and the non-​ communicable diseases that were starting to plague Americans such as heart disease, cancer, and stroke. The McGovern Report contained recommendations that were controversial both in the food industry and for scientists and were the impetus behind

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the publication of the first DGA in 1980, based partly on the 1979 publication by the Surgeon General titled “Healthy People, The Surgeon General’s Report on Health Promotion and Disease Prevention.”48 There was already concern about soaring healthcare costs and the United States’ unfavorable comparison with the health of other nations like Sweden and Japan, as well as the gap in health outcomes between white Americans and Americans of other races and ethnicities. In 1983, Congress mandated that a more neutral advisory committee should be formed to assist in the preparation of future DGA. This committee has become known as the Dietary Guidelines Advisory Committee (DGAC) and is composed of researchers and scientists from the fields of nutrition, medicine, and public health. The DGA is jointly issued by the US Department of Agriculture (USDA) and the Department of Health and Human Services (HHS). Despite the effort to include this neutral committee in the process, the dietary guidelines have been criticized for being influenced by the interests of the food industry. After experts create the Dietary Guidelines Advisory Committee Scientific Report, the secretaries of Agriculture and Health and Human Services take public comments and consider both the evidence and public comment in crafting the final DGA. Therefore, the DGA can include discrepancies between what the Dietary Guidelines Advisory Committee (DGAC’s) scientific report recommended and what the final guidelines ultimately recommend. The guidelines are mandated by the National Nutrition Monitoring and Related Research Act of 1990, requiring the secretaries of the USDA and HHS to review and release the DGA every 5 years. Initial recommendations to restrict salt, saturated fat, and sugar in the 1980s were replaced in the 1990s with the concept of moderation to set a more positive tone. Recommendations for physical activity to balance caloric intake were added in 1995. One of the more memorable shifts occurred in 2011 with the change from the food pyramid graphic to the plate graphic called MyPlate, as a visual diagram of what to eat. The 2020 Dietary Guidelines Advisory Committee Report is the first to extensively review the period from birth to age 24 months, as well as to fully integrate evidence reviewed on pregnancy and lactation. This will be the first US dietary guidelines in which the USDA and HHS take a full life-​span approach in its recommendations.49 Although the dietary guidelines can serve as a helpful starting point for nutrition recommendations and are an improvement upon the standard American diet, it is important to recognize what these guidelines are not. According to the DGA, “Its recommendations are ultimately intended to help individuals improve and maintain overall health and reduce the risk of chronic disease—​its focus is disease prevention. The dietary guidelines are not intended to be used to treat disease.”23 Canada’s most recent dietary guidelines show what can happen when industry influence is eliminated. In their exclusion criteria for identifying scientific reports for their 2020 guidelines, they excluded any reports that were “commissioned by industry or an organization with a business interest.”50 Some of the notable updates to their guidelines include meat and dairy no longer being represented as distinct food groups, the recommendation to choose protein foods that come from plants more often, and water replacing the dairy group on their plate graphic.

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One pressing issue that is not addressed in the most recent DGAC report is the intersection of dietary choices and environmental sustainability. The “EAT-​Lancet Commission on Healthy Diets from Sustainable Food Systems,” published in 2019, directly addresses this relevant topic from a global standpoint, including their own dietary recommendations for human and planetary health.51 The goal of this report is to define a healthy eating pattern that could be shared worldwide to feed all of the expected 10 billion people by 2050 with sustainable food systems in mind. The results of their extensive research into healthful diets and sustainability concluded that a diet rich in plant-​based foods and with fewer animal source foods is prudent for both improved human health and environmental benefits. More specifically, they call for the global consumption of fruits, vegetables, legumes, and nuts to double, and for the consumption of foods like red meat and added sugar to be reduced by 50%.51

1.4  HEALTH-​PROMOTING AND HEALTH-​HARMING FOODS When determining what foods and dietary patterns are health promoting and what are health harming, it is beneficial to begin by recalling which nutrients in the typical American diet are too high or too low in foods. According to the DGA report, Americans consume too much added sugars, saturated fats, sodium, trans fat, refined grains, and cholesterol.52 Therefore, the optimal dietary pattern should minimize foods high in these nutrients. These nutrients are found in ultra-​processed foods, red and processed meats, poultry, dairy, and eggs. According to the report, Americans are getting too little fiber, calcium, magnesium, potassium, and vitamins C, A, D, E, and K.52 Therefore, the optimal dietary pattern should emphasize foods high in these nutrients, which include vegetables, fruits, herbs and spices, legumes, whole grains, nuts, and seeds. Nutrition research is fraught with many challenges –​one of the most significant being that it is incredibly difficult to perform RCTs, considered the gold standard in research on lifetime dietary patterns. As previously discussed, it is the overall dietary pattern that primarily shapes one’s health. Later chapters in this book will narrow in on findings, many of them from RCTs that connect the consumption of specific nutrients to various health conditions. This section briefly examines some of the key studies that support the consumption of the most health-​promoting foods: vegetables, fruits, legumes, whole grains, nuts, and seeds. The Adventist Health Studies, AHS and AHS-​2, are large prospective cohort studies.53–​68 These studies follow individuals who identify as Seventh Day Adventists and engage in many positive lifestyle behaviors rooted in their religious beliefs, with most avoiding alcohol and smoking, being physically active, prioritizing spiritual and family connection, and consuming a predominantly plant-​based diet. In these studies, those who identified as vegetarians had lower risk of cardiovascular disease; lower disease risk factors including hypertension, high cholesterol and triglycerides; lower prevalence of diabetes; lower incidence of cancers including ovarian, colon, prostate, lung, and bladder cancers; and less degenerative arthritis and soft tissue disorders. Furthermore, almost all risk factors and disease incidences were further improved with a 100% plant-​based diet compared to those who ate eggs and dairy.

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Another large key study, the European Prospective Investigation into Cancer and Nutrition (EPIC) study, found that the overall incidence of all cancers was lower in vegetarians than in meat eaters, and vegans and lacto-​ovo vegetarians (vegetarians who include dairy and eggs) have 32% less chance of developing cardiovascular disease than even health conscious meat or fish eaters.69 A smaller prospective cohort, The Oxford Vegetarian Study, found that vegetarians had lower “all-​cause mortality” compared to meat eaters.70 It also found that those eating a plant-​ exclusive diet had lower total cholesterol and LDL cholesterol concentrations compared to meat eaters, and meat and cheese consumption was positively associated with total cholesterol while fiber intake was inversely associated. The Nurses’ Health Study, which includes many important findings related to women’s health,71 and the Health Professionals’ Follow-​ Up Study72 found that participants had an increased risk of type 2 diabetes with meat consumption, particularly with the intake of processed meats, and with consuming more than five eggs per week.73 These are some of the largest observational studies that shape the understanding of health-​promoting and health-​harming eating patterns. An eating pattern centered on whole plant foods is also reflected in the recommendations of major medical organizations. In their 2019 Guideline on the Primary Prevention of Cardiovascular Disease recommendations, the American Heart Association and the American College of Cardiology recommended that: All adults should consume a healthy diet that emphasizes the intake of vegetables, fruits, nuts, whole grains, lean vegetable or animal protein, and fish and minimizes the intake of trans fats, red meat and processed red meats, refined carbohydrates, and sweetened beverages.74

In the American Diabetes Association’s 2019 Nutrition Therapy for Adults with Diabetes or Prediabetes: A Consensus Report, recommendations for diabetes prevention, they highlight plant-​centric eating patterns including a Mediterranean diet, vegetarian, and vegan diets, and the DASH diet for reduction of diabetes risk.75 Finally, the American Institute for Cancer Research recommends that at least two-​thirds of the diet should be composed of whole, plant-​based foods, with animal protein limited to only one-​third or less for cancer prevention.76 All of these findings point to the increased consumption of a predominantly whole food, plant-​based diet for lower rates of chronic disease, improved cardiovascular health, and longevity.

1.5  THE AMERICAN COLLEGE OF LIFESTYLE MEDICINE’S RECOMMENDED DIETARY PATTERN 1.5.1 The American College of Lifestyle Medicine Dietary Position The American College of Lifestyle Medicine (ACLM) is the medical professional society for those dedicated to the advancement and clinical practice of Lifestyle Medicine as the foundation of a transformed and sustainable healthcare system. Lifestyle Medicine is the use of evidence-​based lifestyle therapeutic approaches, such as a predominantly whole food, plant-​based diet, regular physical activity, adequate sleep, stress management, avoidance of risky substance use, and other

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non-​drug modalities, to prevent, treat, and oftentimes reverse a disease. In 2018, the ACLM published its official statement on the role of diet in Lifestyle Medicine. The statement reads, “For the treatment, reversal and prevention of lifestyle-​related chronic disease, the ACLM recommends on eating plant based predominantly on a variety of minimally processed vegetables, fruits, whole grains, legumes, nuts, and seeds.”77 An abundance of evidence exists to suggest that plant-​predominant dietary patterns have the power to prevent chronic disease, and when used as an intervention, can even treat and reverse certain diseases, including cardiovascular disease, obesity, and type 2 diabetes.37,78–​79 A key distinction of the ACLM dietary statement is the emphasis on consuming a diet of predominantly minimally processed whole plant foods. Whole plant food consumption is globally associated with beneficial population health outcomes, chronic disease risk reduction, and reduced all-​cause mortality. These food groups are encouraged to be the predominant energy sources in most national and global nutrition recommendations. Consistent consumption of innate health-​ promoting compounds found in whole plant foods and the reduction of exposure to harmful substances in highly processed foods and animal food products are likely the reason for their powerful associations with decreased “overall and heart disease” mortality,80,81 medication needs,82 obesity,83 and related inflammatory markers,84 hyperglycemia,85 hypertension,86 and hyperlipidemia.87 The food groups emphasized in the ACLM dietary statement include vegetables, fruits, whole grains, legumes, nuts and seeds due to their abundance of energy, dietary fiber, vitamins, minerals, phytonutrients, water, and antioxidants, as well as lack of harmful components and the strong evidence demonstrating their power to treat and even reverse chronic diseases that are currently the leading causes of death in the United States. The ACLM also offers a plate graphic that embodies their dietary position statement, which emphasizes a whole food, plant-​based eating pattern for disease prevention, treatment, and reversal (Figure 1.1). The ACLM plate recommends fiber and antioxidant-​rich plant foods, a variety of fruits and vegetables covering a rainbow of colors, a variety of plant proteins, whole grains, and staying hydrated with water.

1.5.2 The Dietary Spectrum While many members of the ACLM recognize whole food plant based (WFPB) eating as the north star of chronic disease treatment and reversal, they also recognize that each person is on their own health journey and encourage any progression across the dietary spectrum from a standard American eating pattern to a WFPB eating pattern.

1.6  NUTRITION RECOMMENDATIONS FOR WOMEN Women have unique needs that warrant variances in certain nutrition requirements. Biologically, the needs of several nutrients like calcium, folate, and iron fluctuate as women progress through different stages of life, including puberty, pregnancy, breastfeeding, and menopause. Many of the DRIs list specific nutrient requirements for women. Women also tend to require a higher body fat percentage to maintain normal reproductive function. Certain conditions are either unique to women, like

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FIGURE 1.1  Whole food plant-​based food plate. (Reprinted with permission from the American College of Lifestyle Medicine, www.lifestylemedicine.org.)

female-​specific cancers, or impact women uniquely, like skeletal health. Mentally and emotionally, women face unique nutrition-​related challenges in the form of societal pressures to look a certain way and higher susceptibility to developing eating disorders. The next section addresses some of the nutrition-​related topics that are unique to women’s health.

1.6.1 Women-​Specific Health Risks  1.6.1.1  Weight Concerns, Body Image, and Eating Disorders Dieting in the name of weight loss is pervasive in our culture, and the business of fad dieting disproportionately targets women. However, dieting practices have not proven to be effective health improvement or long-​term weight loss strategies. About

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95% of all dieters will regain any lost weight within 1–​5 years.88,89 Chronic dieting has been associated with increased risk of premature death, increased risk of CVD, decreased metabolism, propensity for retaining more fat, binge eating and atrophied satiety cues, eating disorders, and damage to self-​efficacy and self-​esteem.90,91 Women are frequently discriminated against based on their weight or body size,92 including healthcare settings where weight stigma is ubiquitous.93,94 Higher weight women avoid seeking healthcare more than thinner women, and this avoidance is linked to experienced and internalized weight stigma, body-​related shame, and related stress around healthcare.95 Furthermore, experiencing weight stigma, regardless of BMI, is associated with increased mortality rate, systemic inflammation, and increased risk of anxiety and mood disorders, and it is predictive of future weight gain.91 Providers can safeguard female patients from the detrimental effects of weight bias in healthcare settings by focusing on positive health behaviors instead of on dieting and weight loss. Shifting the focus to health is associated with improvements in blood pressure, lipids, physical activity, and healthy body image.96–​99 When women emphasize the functionality of their bodies over appearance, they are more inclined to eat according to their biological hunger and fullness cues.100 In other words, they eat intuitively, and intuitive eating has been linked to a more diverse diet, lower BMI, improved blood pressure, lipids, diet quality, and better psychological health.101 Clinicians trained in these frameworks can assist patients in adopting sustainable health behaviors and avoiding the consequences of chronic dieting. It is advisable for all health professionals to seek training in weight-​inclusive care. Eating disorders are the second deadliest mental illness, and the practice of dieting is one of the most prominent precursors to developing an eating disorder.102 According to the National Eating Disorders Association, 35% of normal dieters progress to pathological dieting and as many as 25% of those dieters develop eating disorders.103 The prevalence of eating disorder is 4.5 times higher among women than among men,104 and 25% of female college athletes present with a subclinical eating disorder.105 Other risk factors include a family history of eating disorders, mental illness, anxiety, dieting, experiencing weight stigma, acculturation or internalization of an appearance standard, social isolation, and trauma history.106 People in larger bodies and from minority racial and ethnic groups are less likely to be screened, diagnosed, and treated for an existing eating disorder.107,108 Less than 6% of individuals diagnosed with an eating disorder are considered underweight by BMI standards.109,110 The three main types of eating disorders include anorexia nervosa, bulimia nervosa, and binge eating disorder. Patients may also present with subclinical disorders such as orthorexia nervosa, a pathologic fixation with eating healthy, or disordered eating that does not fit all criteria for other categories.111 Clinicians should screen for eating disorders and disordered eating behaviors and refer patients to eating disorder specialists when signs are present, as well as refrain from healthcare practices known to catalyze or exacerbate eating disorders, such as the promotion of dieting. 1.6.1.2 Women-​Specific Cancers Breast cancer is the most common cancer in women in the United States. Over 250,000 new cases of breast cancer are diagnosed annually.112 Endometrial cancer is the most

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common cancer in women’s reproductive organs and the fourth most common cancer among women.113 Over 57,000 new cases are diagnosed annually.112 Cervical cancer is the most common gynecologic cancer in women worldwide.114 Most cases stem from infection with high-​risk strains of human papillomavirus (HPV), a sexually transmitted disease. In the United States, ovarian cancer accounts for more deaths than any other gynecologic malignancy.115 Over 14,000 deaths are related to ovarian cancer each year.112 Environmental, lifestyle, dietary, and genetic factors play a role in all of these women-​specific cancers (read more in the supplemental materials for this chapter). 1.6.1.3 Bone Health Bone disease is generally associated with advancing age and menopause. However, almost all bone mass in the axial skeleton will be accumulated in young women by late adolescence, so the years immediately following menarche are especially important. Adequate calcium in prepubertal and pubertal girls improves bone accrual.116 Accordingly, osteoporosis prevention ideally begins in adolescence. Osteoporosis risk factors include weight less than 127 pounds, smoking, having three or more alcoholic drinks a day, low calcium intake, high caffeine intake, vitamin D insufficiency, high salt intake, inadequate physical activity, excess vitamin A, and certain medical conditions including depression, rheumatoid arthritis, and diabetes mellitus.117 Lifestyle measures are vitally important for the prevention of osteoporosis, as most fractures occur in individuals with a bone mineral density (BMD) above the cutoff of 2.5 standard deviations from the mean. For more about the relationship between nutrition and bone health, read the supplemental materials.

1.6.2 Nutrients to Know for Women A well-​planned plant-​exclusive diet is healthy for women throughout the lifecycle, with some attention to certain nutrients including protein, zinc, iron, vitamin B12, and omega-​3 fatty acids.36 1.6.2.1 Vitamin B12 Vitamin B12 should be supplemented in a plant-​based diet, as it is almost exclusively found in animal foods. Vitamin B12 is synthesized from microorganisms; it is not made by animals. There are some claims that certain plant-​based foods naturally contain B12, but it is more likely that these foods actually contain inactive B12 analogues that are inaccessible to humans and, therefore, are unreliable sources. B12 deficiency is common in older adults due to the decrease in gastric acid production and B12 absorption that occurs with aging. All women consuming a predominantly plant-​based diet should aim to consume 25–​100 μg/​day from daily intake of fortified foods or a supplement. Menopausal women who consume animal products are less likely to absorb vitamin B12 from food and should follow this advice as well. Commonly prescribed medications including metformin, oral contraceptives, aspirin, histamine-​H2 receptor blockers, and proton pump inhibitors can lead to a deficiency of vitamin B12.118

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1.6.2.2 Calcium Calcium is considered a nutrient of concern for the general population with respect to bone health, particularly for women and older adults. Plant sources of calcium include leafy green vege­tables –​especially bok choy, broccoli, napa cabbage, collard greens, and kale –​as well as fortified plant milks, calcium-​set tofu, sesame seeds and tahini, almonds and almond butter. Some calcium-​rich foods contain oxalates, which interfere with calcium absorption. High-​oxalate vegetables include Swiss chard, spinach, and beet greens. Other leafy green vegetables like kale, on the other hand, have low oxalates, and the absorption of calcium is greater than milk.119 If supplemental calcium is needed, it is best to take multiple small doses of calcium, as absorption is inversely related to intake.120 1.6.2.3 Vitamin D The prevalence of vitamin D deficiency is high especially in older adults. Vitamin D3 decreases mortality in older adults living independently or in institutional care.121 The optimal serum 25-​hydroxyvitamin D level is unknown, but a level of 30–​40 ng/​mL is considered normal range. Vitamin D is necessary for calcium, phosphate, and magnesium absorption and acts with vitamin K to stimulate bone mineralization. Vitamin D can be obtained through full-​body direct sun exposure for 10–​15 minutes for light skin, 20 minutes for darker skin, and 30 minutes for older adults without sunblock at appropriate latitude and season.121 If adequate sun exposure cannot be achieved, supplementation is recommended. The Endocrine Society recommends at least 600 IU of vitamin D per day for all women aged 19–​50 years, and intakes as high as 1,500 to 2,000 IU per day may be necessary to raise blood levels to the appropriate amount if deficiency is present.122 1.6.2.4 Iron Iron deficiency is common in women of reproductive age, with a prevalence of 9–​16% in women aged12–​49 years, due to menstrual bleeding, pregnancy, and childbirth.123 Women who are at high risk of iron deficiency (e.g., low or no meat intake, high physical activity, low socioeconomic status, and immigrants from developing countries) should be screened. There are two types of dietary iron: heme and nonheme iron. Heme iron is found solely in animal foods, while nonheme iron is found primarily in plant-​ based foods. Heme iron is more readily absorbed than nonheme iron, which is not necessarily a positive characteristic since it is possible to absorb heme iron in excess. Excess heme iron has been associated with an increased risk of coronary heart disease, breast cancer, esophageal cancer, and stomach cancer.123–​125 Therefore, plant-​based iron sources may be safer since the body is able to regulate its nonheme iron better. Many factors affect the absorption of nonheme iron, such as other foods it is eaten with and a person’s current iron status. Plant foods rich in iron include leafy green vegetables, beans, and whole grains. Iron-​rich foods should ideally be eaten with vitamin C-​rich foods to enhance absorption. Certain foods interfere with iron absorption, like coffee and tea, which contain tannins, and calcium supplements.120

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1.6.2.5 Folate It is recommended that all women who can become pregnant should take 400 mg of folic acid each day.120 Folate is found in dark green, leafy vegetables and legumes. Folic acid is the form of folate that has been tested and shown to decrease the risk of a neural tube defect (NTD), such as spina bifida in the fetus. Folic acid is also used in many supplements because it is highly stable and absorbed more efficiently than naturally occurring folate in food. 1.6.2.6 Zinc Zinc is commonly found in seafood, dairy, and meats. It is less available in plant foods, but it can be found in whole grains, wheat germ, wheat bran, legumes, peanuts, nuts, and seeds. Diets high in phytates can inhibit zinc absorption and increase zinc requirements.126 Therefore, it is important for women consuming plant-​exclusive diets to ensure adequate zinc intake. 1.6.2.7 Iodine Iodine content varies greatly in foods because it is dependent on the soil content that the food was grown in. Dairy foods are often thought to be good sources of iodine; however, dairy foods only contain iodine because dairy cows are given iodine supplements or the iodine-​based cleaning solutions used on dairy farms leech into the milk. In other words, dairy is not naturally high in iodine. Plant-​exclusive diets can be low in iodine, with 63% of female vegans having low iodine.127 Sea vegetables like nori, wakame, arame, kelp, and kombu contain iodine. Their iodine content, however, can be somewhat unreliable with the risk of toxicity. In the early 20th century in the United States, iodine deficiency was a common issue, so iodine was added to some table salts, called iodized salt. Women can meet needs with a varied plant-​based diet plus just a 1/​4 teaspoon of iodized salt a day, which contains about half of the recommended daily iodine intake and equates to just 580 mg of sodium. If a woman is avoiding salt, iodine needs can be met by consuming seaweed a few times per week or by taking an iodine supplement.128 1.6.2.8 Omega-​3s Omega-​3 fatty acids are important for the development and maintenance of the brain, retina, and cell membranes; healthy pregnancy; and are associated with a lower risk of cardiovascular disease and other chronic diseases. Omega-​3s include alpha-​linolenic acid (ALA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA). ALA fatty acids are found in plant-​based foods such as flaxseeds, chia seeds, hemp seeds, and walnuts. ALA requirements can be met by consuming one tablespoon of ground flaxseeds or chia seeds or about 1/​4 cup of walnuts per day. Although the body can convert ALA to the long-​chain forms EPA and DHA, conversion rates are affected by individual factors and other components of the diet.129 Therefore, some women may require a direct dietary source of EPA and DHA. Fish is the main dietary source of EPA and DHA; however, farmed fish has lower contents than wild fish and contamination is a concern with fish consumption, especially for pregnant women. A microalgae supplement is a safe, effective way to obtain adequate EPA and DHA.

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1.7  BRIEF OVERVIEW OF NUTRITION NEEDS ACROSS THE LIFESPAN 1.7.1 Nutrition and Fertility About 12% of US women experience difficulty in getting pregnant or sustaining a pregnancy.130 Healthy lifestyle factors, including a healthy diet, are associated with a 69% lower risk of ovulatory disorder infertility.131,132 Food is not a panacea for fertility issues, but good nutrition can certainly play a role in increasing the odds of successful conception for some women. Several studies have shown associations between healthy eating and improved fertility, both in unassisted pregnancies and in assisted reproductive technologies. The common themes among the researched diets that support fertility include an emphasis on protein from plant-​based foods in place of animal-​based sources, antioxidant-​rich fruits and vegetables, low-​glycemic whole grains, monounsaturated fats, and omega-​ 3 fatty acids.133,134 On the other hand, unhealthy eating patterns have been linked to lower fertility, including consumption of sugar-​sweetened beverages,134 high amounts of fast-​food,135 trans fats, saturated fats, and red and processed meats.132 In the Nurses’ Health Study, for each serving of animal protein that was replaced with plant-​based protein, the risk of ovulatory infertility decreased by more than 50%.136 The Nurses’ Health Study also found that women who consume more than two sodas per day were 50% more likely to experience infertility.137 Many specific nutrients also play important roles in fertility health. Adequate intake of vitamin B12 and folate has both been associated with improved fertility.132 Iron is another nutrient of importance for fertility. Specifically, plant-​based iron sources have been shown to support normal ovulation, which in turn supports fertility.131 Monounsaturated fats like avocado may reduce ovulatory infertility,133 and higher intakes of omega-​3 fatty acids may improve fertility, particularly EPA and DHA.132 Because of this, it may be wise for women eating a primarily plant-​based diet to take an algae-​based EPA/​DHA supplement. A diet rich in antioxidants, found primarily in plant-​based foods like fruits and vegetables, may also be helpful. Women experiencing unexplained fertility and conditions like Polycystic Ovary Syndrome (PCOS)and endometriosis that can cause infertility tend to have high markers of oxidative stress, which may be improved with an antioxidant-​rich diet.138,139 Both ends of the weight spectrum, low weight and high weight, are associated with lower fertility; therefore, lifestyle habits that support healthy weight may enhance fertility.140,141

1.7.2 Nutrition and Pregnancy and Lactation During pregnancy and lactation, women eat to nourish their babies in addition to themselves. Researchers have identified the first 1,000 days of a child’s life, beginning with conception, as extremely important for their future health.142 One of the first signs of pregnancy is often nausea or vomiting which is thought to be related to the direct effects of the hormone beta-​hCG on the chemoreceptor trigger center of the brain. Another theory is that nausea and vomiting developed as a way to

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protect women and their babies from harmful toxins and microorganisms in foods.143 Because about 70% of women suffer from nausea and vomiting of pregnancy (NVP), proper nourishment before pregnancy can be very beneficial.144 Ginger, vitamin B6, acupressure and acupuncture, as well as the prescription medications doxylamine and antiemetics, have all been used to treat NVP.145

1.7.3 Energy During the first trimester, no additional calories are required. In the second trimester, calorie needs increase to about 340 additional kcals per day, and about 450 additional kcals per day in the third trimester. The additional calories needed significantly depend on individual factors such as activity level, prepregnancy body weight, and age.146 While breastfeeding, women require an estimated 500 additional kcals per day compared to pre-​pregnancy caloric intake. Again, this is an estimate and individual factors must be considered.146

1.7.4 Macronutrients During pregnancy, there are specific recommendations women should follow regarding protein and fat intake. First, it is recommended that pregnant women obtain at least 20% of total calories from fat. This is best accomplished by including whole foods that contain both healthy, unsaturated fats and micronutrients that are important for pregnancy. Because many micronutrient needs increase with pregnancy, it is important to try to maximize the nutrient-​density of all additional calories consumed. Nuts, seeds, and avocados are all good choices.146 In addition to total fat, meeting omega-​3 needs is particularly important. For most pregnant women, this can be achieved by consuming an additional tablespoon of ground flaxseeds or chia seeds or an additional two tablespoons of walnuts per day in addition to taking an algae-​ based supplement of 200–​300 mg EPA/​DHA per day. While energy needs only rise by about 15% in the second and third trimesters, protein requirements increase by 50% after 12 weeks. During the second and third trimesters of pregnancy, an additional 28 g of protein per day is recommended. This means that pregnant women should aim to eat protein-​rich foods at every meal and snack.146

1.7.5 Micronutrients Whether a woman chooses to meet micronutrient needs with a prenatal vitamin supplement or by carefully monitoring food intake in conjunction with supplements as needed, the specific micronutrient needs are briefly outlined below. 1.7.5.1 Iodine Adequate iodine is critical for fetal development. Iodine requirements increase to 220 μg during pregnancy and increase again to 290 μg when breastfeeding.146 While it is possible to obtain adequate iodine from a combination of food sources and

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iodized salt, during pregnancy and breastfeeding it is most prudent to take an iodine supplement ideally beginning pre-​conception. 1.7.5.2 B12 Vitamin B12 needs increase slightly to 2.6 μg during pregnancy and 2.8 μg during lactation.146 Most prenatal vitamins contain small amounts of vitamin B12; however, they may not contain adequate amounts for women eating a plant-​exclusive diet. It is recommended to take a separate vitamin B12 supplement to ensure adequate intake and absorption. 1.7.5.3 Folate Folate is very important for the health of the developing embryo. It is recommended that women take 400 μg of folic acid pre-​pregnancy, 600 μg during pregnancy, and 500 μg while breastfeeding.146 It is recommended that all women who are planning to become pregnant take a daily supplement of 400–​800 μg of folic acid beginning at least one month before conception and continuing through the first 2–​3 months of pregnancy.146 There has even been an increase in birth defects seen specifically due to low-​carbohydrate diets and resulting low-​folate intake in pregnant women.147 1.7.5.4 Iron In pregnancy, iron needs increase greatly, from 18 μg to 27 μg per day.146 The IOM recommends that vegetarians and vegans aim for one point eight times that amount due to the decreased bioavailability of non-​heme iron, which equates to an iron requirement of 48 point 6 μg per day for pregnant women consuming a plant-​exclusive diet. Just like vitamin B12, folate, and iodine, it is important to have adequate iron stores at conception. During lactation, iron requirements decrease dramatically below pre-​ pregnancy needs to 9 μg per day until menstruation resumes. 1.7.5.5 Choline Choline is a more recently recognized nutrient of importance for the developing embryo, fetus, and infant. Maternal choline intake affects neurodevelopment, epigenetic programming, and placental function. Choline intake should be at least 450 μg per day while pregnant and 550 μg per day while breastfeeding.148 Grains and pseudograins such as quinoa, cruciferous vegetables like broccoli, shiitake mushrooms, legumes, and soy are excellent sources of plant choline. 1.7.5.6 Zinc Zinc is critical for cellular replication, and its deficiencies can lead to preterm delivery, low birth weight, and short stature throughout life. During pregnancy, zinc requirement increases to 11 μg per day. During breastfeeding, they increase again to 12 μg per day.146 1.7.5.7 Calcium Calcium requirements during pregnancy and lactation are unchanged from pre-​ pregnancy levels: 1000 μg a day is recommended.146 A supplement may be useful for women who were not meeting the recommended intake pre-​pregnancy.

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1.7.5.8 Vitamin D Similarly, vitamin D requirements remain consistent during pregnancy and lactation, but supplementation should be considered if pre-​pregnancy needs are not being met. 1.7.5.9 Other Nutrients Of the fat-​soluble vitamins, only vitamin A needs increase in pregnancy, from 700 μg RAE to 750 μg RAE in pregnancy and 1300 μg RAE while breastfeeding.149 There are also small increases in amounts of other B vitamins, vitamin C, copper, and magnesium.150,151 However, a varied plant-​based diet with adequate calories should easily fulfill these recommendations.

1.7.6 Nutrition and Menopause The ideal diet for women in menopause and postmenopause should focus on plenty of vegetables, fruits, legumes, whole grains, nuts and seeds, and essential fatty acids.152 Ideally, the diet should reduce saturated fat, sugar, and salt.152 Insulin resistance increases with age; therefore, menopausal women should consume complex carbohydrates with a low glycemic index. The early phases of the menopause transition are characterized by relative hyperestrogenism and hypoprogesteronism.153 The standard of care of treatment for symptoms of menopause including vasomotor symptoms is hormone replacement therapy. Some dietary interventions may help with vasomotor symptoms like hot flashes and night sweats. Flaxseeds may modulate the metabolism of endogenous estrogen and may improve hot flashes.154 Phytoestrogens, found in flaxseeds and legumes, can provide additional symptomatic benefits for menopausal women.152 Vitamin C with flavonoids may also relieve menopausal hot flashes.154 Vitamin B12 is also commonly deficient in menopausal women and should be supplemented as needed. To preserve bone health, menopausal women should achieve 1200 mg calcium and at least 800 IU vitamin D with a large variety of minerals to complement calcium. Keep in mind that absorption of Vitamin D decreases with age and many women require a higher dose of Vitamin D than the RDA (800 IU). The Endocrine Society recommends 1,500–​2,000 IU per day to prevent Vitamin D insufficiency; however, higher doses may be needed if the patient is obese or has malabsorption issues.122 Perimenopausal women should have adequate protein intake (0.8–​1.2 g/​kg divided throughout the day).21 Adequate omega-​3 fatty acids are also important for menopausal women.153 Coffee often increases symptoms of hot flashes in menopausal women and should be avoided.153 Hot beverages can exacerbate hot flashes; therefore, cool drinks are recommended. Additionally, moderate-​ intensity exercise resets the threshold for sweating and is a proven nonpharmacological treatment of hot flashes.155

1.7.7 Nutrition and Female Athletes The nutrition needs of women engaging in intense or prolonged physical activity and sports training require some special attention related to increased energy and nutrient

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needs. A diet rich in antioxidants, which is characteristic of a WFPB diet, may provide benefits to female athletes in the form of faster recovery and fewer injuries.156 In other words, very active women cannot only thrive on a WFPB diet, they might even have an advantage. With increased energy expenditure through physical activity come increased energy needs. Serious health consequences occur if these higher energy needs are not met. The relationship between female bone health, menstrual function, and the amount of energy available for normal body functions after energy has been expended through activity is referred to as the female athlete triad.157 Low energy availability, or a circumstance where there is an energy deficit, can lead to menstrual irregularity, amenorrhea, and loss of bone mass. Inadequate energy intake is especially common in weight-​sensitive sports like distance running, cycling, dance, gymnastics, and rowing.158 It may be intentional and connected to disordered eating, but it may also be unintentional. It is advisable for all female athletes to meet with a registered dietitian to ensure they are meeting energy needs and consuming a diet that supports normal menstrual function and bone health. There are certain macronutrient considerations for female athletes. High-​ carbohydrate diets are shown to be beneficial for athletes, especially during short-​ term intense exercise. It is recommended that female athletes consume about 2.7–​3.2 g of carbohydrate per kilogram of bodyweight. Adequate fat intake is also imperative for female athletes. Those eating a low-​fat plant-​based diet may be at higher risk of impaired recovery and menstrual irregularity, especially if fat intake falls below 15% of total calories. There is some controversy around protein requirements for athletes, especially those eating a plant-​based diet. The American College of Sports Medicine (ACSM), the Academy of Nutrition and Dietetics, and Dietitians of Canada recommend “1.3 to 1.8 g/​kg/​day” for vegetarian athletes.159 A registered dietitian with experience in plant-​based sports nutrition can assist individuals with determining appropriate macronutrient needs and planning meals to meet those needs. One final nutrient of importance for female athletes is iron. Iron is critical for energy production, hemoglobin, and oxygen-​carrying capacity. Low iron stores are the most common nutrient deficiency among female athletes, and even a mild deficiency can impair performance. Active women, especially those in endurance sports, lose additional iron through perspiration and training impact, which destroys red blood cells. Low iron stores may also be the result of inadequate energy intake or a poorly planned diet. Iron recommendations for female athletes are 70% higher than the RDA for nonathletes. The ACSM recommends periodically screening all female athletes for sufficient iron stores. In women experiencing iron deficiency, supplementation paired with nutrition therapy with a registered dietitian is advised.156

1.8  PRACTICAL TOOLS FOR TRANSITIONING TO A WHOLE FOOD PLANT-​BASED EATING PATTERN Beginning anything new can be both scary and exciting, and changing eating habits is no different. With a foundational understanding of the pillars of a WFPB diet paired with practical steps to making the transition, WFPB eating can be transformed from something new into an intuitive part of daily life.

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1.8.1 The WFPB Plate The ACLM developed the WFPB Plate to make it easier to envision what balanced, wholesome, WFPB meals look like (see Figure 1.1). Guidelines for the WFPB Plate: • Focus on whole fruits and vegetables and eat a rainbow of color. • Vegetables: dark leafy greens (spinach, kale, arugula, etc.), broccoli, squash, zucchini, carrots, tomatoes, beets, peppers, mushrooms, onions, celery, cauliflower, cucumbers, white and sweet potatoes, green peas, cabbage, whole plant fats (avocados and olives), and more. • Fruits: apples, bananas, grapes, citrus fruit, berries, peaches, pears, pineapple, kiwi, plums, watermelon, starfruit, mangoes, and more. • Drink water for hydration. • Eat a variety of plant proteins. • Legumes: peas and beans, including kidney beans, pinto beans, white beans, black beans, lima beans, black-​eyed peas, garbanzo beans (chickpeas), split peas and lentils, edamame, tempeh, tofu. • Nuts and seeds: almonds, pistachios, walnuts, pecans, nut butters, pumpkin/​ sunflower/​chia/​flax seeds, and more. • Choose whole grains. • Amaranth, barley, brown rice, buckwheat, bulgur, millet, popcorn, rye, quinoa, whole oats, whole-​grain bread/​tortillas/​cereals/​flours, to name a few. • Add herbs and spices for flavor and antioxidant power. • Basil, cilantro, rosemary, parsley, thyme, dill, cumin, chili powder, pepper, turmeric, ginger, cinnamon, fennel, paprika, and many more. Additional guidelines for balanced nutrition: • Eat three to four servings of legumes each day. • Meet omega-​3 needs with daily consumption of ground flaxseeds, chia seeds, hemp seeds, or walnuts. • Consider an algae-​based EPA/​DHA supplement. • Pair iron-​rich plant-​based foods with vitamin C-​rich foods. • Eat plenty of calcium-​rich, plant-​based foods. • Take a vitamin B12 supplement. • Meet iodine needs with a varied plant-​based diet plus 1/​4 tsp iodized salt or an iodine supplement. • Take a vitamin D supplement if sun exposure is inadequate.

1.8.2 Tips for Transitioning • Focus on additions instead of subtractions. Focusing on which foods to add instead of which foods to avoid sets a positive tone and encourages exploration and discovery of the abundant world of plant-​based foods. It also helps to naturally crowd out less healthy foods without much effort.

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• Start with simple swaps. Many popular foods have plant-​based counterparts that can be swapped in with little notice. For example, swap cow’s milk for soymilk or swap beef broth for vegetable broth. There are also simple recipes for WFPB versions of many ingredients. One tablespoon of ground flaxseed mixed with three tablespoons of water can stand in 1:1 for an egg in baked goods; and blitzing cashews, nutritional yeast, and a pinch of salt in a food processor makes an excellent substitute for Parmesan cheese. • Plan ahead. Use meal planning apps or a simple calendar to plan meals in advance. Look at the upcoming week’s schedule and determine how many meals are needed. Plan quick meals or leftovers for the busiest days. Set aside time each week to batch cook ingredients like dried beans, grains, steamed or roasted vegetables, sauces, and dressings so meals can be thrown together quickly on busy weeknights. Soups, chilies, casseroles, and bean burgers all bode well in large batches and extras can be frozen for meals in a pinch. • Make the healthy choice the obvious choice. Keep the foods to eat more often in plain sight and easily accessible. Store fresh produce in a bowl on the counter and at eye-​level in the refrigerator, and stock the pantry and freezer with staple ingredients that make for quick meals like quick-​cooking lentils and quinoa, canned beans, whole grain pasta, and frozen vegetables. • Reimagine the meal blueprint. Plant-​based meals often look different from meals that are centered around meat; therefore, it is beneficial to browse plant-​ based recipes websites and cookbooks to get a feel for the types of blueprints used in plant-​based cooking. For example, oatmeal topped with berries, nuts, and soymilk; bowls built from grains, beans, roasted vegetables, and a sauce; or a sandwich spread with hummus and piled with raw veggies all make delicious meals. • Add umami. Umami is the fifth flavor, along with sweet, salty, bitter, and sour. It is characterized as a savory flavor and is the flavor associated with meat and animal products. Adding umami can help boost satisfaction with plant-​based meals. Sun-​dried tomatoes, tomato sauce, tomato paste, mushrooms, miso paste, olives, nutritional yeast, and vinegars all contain umami. • Include the whole family. A support network helps prevent relapse, and other members of the household can be an ideal source of support in shopping for, cooking, and meals together. Pique children’s interest by allowing them to pick a new fruit or vegetable to try each week. Start a tomato plant or small herb garden, and have children water and take care of it. Assign age-​appropriate kitchen tasks to everyone in the family or have each family member take turns choosing and cooking a new plant-​based recipe. If family support is not an option, enlist friends or search for local plant-​based meetup groups. • Prepare for challenges. Feeling prepared is another key to preventing relapse. Plan in advance for how to handle challenging situations like social events, travel, or eating well on extremely busy days. When dining out, check menus ahead of time, pair side dishes together to create a hearty meal, ask if the kitchen is willing to make a dish with lots of vegetables, beans, and whole grains. When traveling, pack meals and snacks. Wraps, dried soups that only require hot water, fruits with durable skins, sliced raw vegetables, and nuts are all portable. When traveling by car, stop at grocery stores instead of fast-​food restaurants.

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• Nourish yourself. Understanding nutrition needs and how to meet those needs through plant-​based foods and certain supplements sets the stage for thriving and avoiding energy or nutrient deficiencies. For women, in particular, it is important to pay attention to how nutrient needs change through different stages of life and how women’s needs differ from that of men. • Focus on progress, not perfection. Remember that eating is a lifelong journey, and sustainable habits are built through small, incremental steps. Missteps, experiments, and trial and error are all part of the journey. Try this three-​step approach: • Enjoy: Identify plant-​based meals you already enjoy, and put them in your meal rotation more often (smoothies, lentil soup, bean burritos, etc.). • Adapt: Give some of your favorite recipes a plant-​based makeover with additions and simple swaps (swap ground beef for beans in tacos or add tofu to veggie fried rice). • Explore: Begin exploring new plant-​based foods and recipes. Find some favorites that are both delicious and easy to prepare so they become part of your meal rotation.

REFERENCES 1. Wansink B, Sobal J. Mindless eating: The 200 daily food decisions we overlook. Environ Behav. 2007;39(1):106–​123. doi: 10.1177/​0013916506295573. 2. IFIC Foundation. Food & health survey (Rep.). IFIC Foundation. 2018. https://​ foodinsight.org/​wp-​content/​uploads/​2018/​05/​2018-​FHS-​Report-​FINAL.pdf. 3. Centers for Disease Control and Prevention: Preventing chronic diseases and reducing health risk factors. CDC. 2013. www.cdc.gov/​nccdphp/​dch/​programs/​ healthycommunitiesprogram/​overview/​diseasesandrisks.htm. Published October 25, 2013. Accessed August 20, 2020. 4. World Health Organization. Chronic diseases and health prevention: Part two. The urgent need for action. WHO. 2005. www.who.int/​chp/​chronic_​disease_​report/​part2_​ ch1/​en/​. Accessed August 20, 2020. 5. Institute of Medicine. Food Marketing to Children and Youth: Threat or Opportunity? Washington, DC: The National Academies Press. 2006. doi: 10.17226/​11514. 6. Krueger PM, Reither EN. Mind the gap: race/​ethnic and socioeconomic disparities in obesity. Curr Diab Rep. 2015;15(11):95. doi: 10.1007/​s11892-​015-​0666-​6. 7. Diaz de Villegas C, Rodriguez K. Medley Food Desert Project (PDF). Florida International University Department of Biological Sciences. 2017. https://​ 19january2017snapshot.epa.gov/ ​ s ites/ ​ p roduction/​ f iles/​ 2 016-​ 0 5/​ d ocuments/​ floridainternationaluniversitymedleyfooddesertproject.pdf. 8. Crowley J, Ball L, Hiddink GJ. Nutrition in medical education: A systematic review. Lancet Planet Health. 2019;3(9):e379–​e389. doi: 10.1016/​S2542-​5196(19)30171-​8. 9. Silverstein MJ, Sayre K. The female economy. Harv Bus Rev. 2009;87. https://​hbr.org/​ 2009/​09/​the-​female-​economy. September 2009. Accessed August 20, 2020. 10. Grogan S. Age, social class, ethnicity and sexuality. In: Body Image: Understanding Body Dissatisfaction in Men, Women and Children, 2nd ed. London: Routledge; 2016:136–​191. 11. Heindel JJ, Vandenberg LN. Developmental origins of health and disease: A paradigm for understanding disease cause and prevention. Curr Opin Pediatr. 2015;27(2):248–​ 253. doi: 10.1097/​MOP.0000000000000191.

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12. Lee HS. Impact of maternal diet on the epigenome during in utero life and the developmental programming of diseases in childhood and adulthood. Nutrients. 2015;7(11):9492–​9507. doi: 10.3390/​nu7115467. 13. Laplante DP, Brunet A, Schmitz N, Ciampi A, King S. Project ice storm: Prenatal maternal stress affects cognitive and linguistic functioning in 5 1/​2-​year-​old children. J Am Acad Child Adolesc Psychiatry. 2008;47(9):1063–​1072. doi: 10.1097/​ CHI.0b013e31817eec80. 14. Bommarito PA, Martin E, Fry RC. Effects of prenatal exposure to endocrine disruptors and toxic metals on the fetal epigenome. Epigenomics. 2017;9(3):333–​350. doi: 10.2217/​epi-​2016-​0112. 15. Psota T, Chen K. Measuring energy expenditure in clinical populations: Rewards and challenges. Eur J Clin Nutr. 2013;67:436–​442. doi: 10.1038/​ejcn.2013.38. 16. Mifflin MD, St Jeor ST, Hill LA, Scott BJ, Daugherty SA, Koh YO. A new predictive equation for resting energy expenditure in healthy individuals. Am J Clin Nutr. 1990;51(2):241–​247. doi: 10.1093/​ajcn/​51.2.241. 17. Calcagno M, Kahleova H, Alwarith J, Burgess NN, Flores RA, Busta ML, Barnard ND. The thermic effect of food: A review. J Am Coll Nutr. 2019;38(6):547–​551. doi: 10.1080/​07315724.2018.1552544. 18. Frankenfield D, Roth-​Yousey L, Compher C. Comparison of predictive equations for resting metabolic rate in healthy nonobese and obese adults: a systematic review. J Am Diet Assoc. 2005;105(5):775–​789. doi: 10.1016/​j.jada.2005.02.005. 19. Marra M, Cioffi I, Sammarco R, Montagnese C, Naccarato M, Amato V, Contaldo F, Pasanisi F. Prediction and evaluation of resting energy expenditure in a large group of obese outpatients. Int J Obes (Lond). 2017;41(5):697–​705. doi: 10.1038/​ijo.2017.34. 20. Cancello R, Soranna D, Brunani A, Scacchi M, Tagliaferri A, Mai S, Marzullo P, Zambon A, Invitti C. Analysis of predictive equations for estimating resting energy expenditure in a large cohort of morbidly obese patients. Front Endocrinol (Lausanne). 2018;25(9):367. doi: 10.3389/​fendo.2018.00367. 21. Trumbo P, Schlicker S, Yates AA, Poos M, Food and Nutrition Board of the Institute of Medicine, The National Academies. Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein and amino acids [published correction appears in J Am Diet Assoc. 2003;103(5):563]. J Am Diet Assoc. 2002;102(11):1621–​ 1630. doi: 10.1016/​s0002-​8223(02)90346-​9. 22. Hill JO, Wyatt HR, Peters JC. Energy balance and obesity. Circulation. 2012; 126(1):126–​132. doi: 10.1161/​CIRCULATIONAHA.111.087213. 23. U.S. Department of Health and Human Services and U.S. Department of Agriculture. 2015–​2020 Dietary Guidelines for Americans. 8th ed. December 2015. http://​ health.gov/​dietaryguidelines/​2015/​guidelines/​. 24. Monteiro CA, Cannon G, Lawrence M, da Costa Louzada ML, Machado PP. Ultra-​Processed Foods, Diet Quality, and Health Using the NOVA Classification System. Rome: Food and Agricultural Organization of the United Nations. 2019. www.researchgate.net/ ​ p rofile/ ​ G eoffrey_ ​ C annon/ ​ p ublication/ ​ 3 34945695_ ​ FAO_​ Ultra-​processed_​foods_​diet_​quality_​and_​health_​using_​the_​NOVA_​classification_ ​ system/​links/​5d45a462a6fdcc370a79b7aa/​FAO-​Ultra-​processed-​foods-​diet-​quality-​ and-​health-​using-​the-​NOVA-​classification-​system.pdf. Published August 3, 2019. Accessed August 20, 2020. 25. Elizabeth L, Machado P, Zinöcker M, Baker P, Lawrence M. Ultra-​processed foods and health outcomes: A narrative review. Nutrients. 2020;12(7):1955. doi: 10.3390/​ nu12071955. 26. Baker P, Friel S. Processed foods and the nutrition transition: Evidence from Asia. Obes Rev. 2014;15(7):564–​577. doi: 10.1111/​obr.12174.

32

32

Kayli Anderson et al. 27. Fardet A. Towards a more holistic vision of human nutrition to prevent from diet-​related chronic diseases: The reductionist drift. Int J Food Sci, Nutr Diet. 2016;5(1e):1–​2. doi: 10.19070/​2326-​3350-​160005e. 28. Institute of Medicine (US) Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington (DC): National Academies Press (US); 1997. doi: 10.17226/​5776. 29. Anderson JW, Baird P, Davis RH Jr, Ferreri S, Knudtson M, Koraym A, Waters V, Williams CL. Health benefits of dietary fiber. Nutr Rev. 2009;67(4):188–​205. doi: 10.1111/​j.1753-​4887.2009.00189. 30. Lee PC, Dixon JB. Food for thought: Reward mechanisms and hedonic overeating in obesity. Curr Obes Rep. 2017;6(4):353–​361. doi: 10.1007/​s13679-​017-​0280-​9. 31. Ludwig DS, Hu FB, Tappy L, Brand-​Miller J. Dietary carbohydrates: Role of quality and quantity in chronic disease. BMJ. 2018;361:k2340. doi: 10.1136/​bmj.k2340. 32. Forouhi NG, Krauss RM, Taubes G, Willett W. Dietary fat and cardiometabolic health: Evidence, controversies, and consensus for guidance. BMJ. 2018;361:k2139. doi: 10.1136/​bmj.k2139. 33. Song M, Fung TT, Hu FB, et al. Association of Animal and Plant Protein Intake with All-​ Cause and Cause-​ Specific Mortality [published correction appears in JAMA Intern Med. 2016 Nov 1;176(11):1728]. JAMA Intern Med. 2016;176(10):1453–​1463. doi: 10.1001/​jamainternmed.2016.4182. 34. Mariotti F. Animal and plant protein sources and cardiometabolic health. Adv Nutr. 2019;10(Suppl_​4):S351–​S366. doi: 10.1093/​advances/​nmy110. 35. Willett W, Rockström J, Loken B, Springmann M, Lang T, Vermeulen S, Garnett T, Tilman D, DeClerck F, Wood A, Jonell M, Clark M, Gordon LJ, Fanzo J, Hawkes C, Zurayk R, Rivera JA, De Vries W, Majele Sibanda L, Afshin A, Chaudhary A, Herrero M, Agustina R, Branca F, Lartey A, Fan S, Crona B, Fox E, Bignet V, Troell M, Lindahl T, Singh S, Cornell SE, Srinath Reddy K, Narain S, Nishtar S, Murray CJL. Food in the Anthropocene: The EAT-​Lancet Commission on healthy diets from sustainable food systems. Lancet. 2019;393(10170):447–​492. doi: 10.1016/​ S0140-​6736(18)31788-​4. 36. Melina V, Craig W, Levin S. Position of the Academy of Nutrition and Dietetics: Vegetarian diets. J Acad Nutr Diet. 2016;116(12):1970–​1980. doi: 10.1016/​ j.jand.2016.09.025. 37. Hever J, Cronise RJ. Plant-​based nutrition for healthcare professionals: Implementing diet as a primary modality in the prevention and treatment of chronic disease. J Geriatr Cardiol. 2017;14(5):355–​368. doi: 10.11909/​j.issn.1671-​5411.2017.05.012. 38. Nahar L, Xiao J, Sarker SD. Introduction of phytonutrients. In: Xiao J, Sarker S, Asakawa Y (eds) Handbook of Dietary Phytochemicals, Singapore: Springer; 2019:1–​17. 39. Grosso G, Micek A, Godos J, Pajak A, Sciacca S, Galvano F, Giovannucci EL. Dietary flavonoid and lignan intake and mortality in prospective cohort studies: Systematic review and dose-​response meta-​analysis. Am J Epidemiol. 2017;185(12):1304–​1316. doi: 10.1093/​aje/​kww207. 40. Grosso G, Godos J, Lamuela-​Raventos R, Ray S, Micek A, Pajak A, Sciacca S, D’Orazio N, Del Rio D, Galvano F. A comprehensive meta-​analysis on dietary flavonoid and lignan intake and cancer risk: Level of evidence and limitations. Mol Nutr Food Res. 2017;61(4). doi: 10.1002/​mnfr.201600930. 41. Hooper L, Kroon PA, Rimm EB, Cohn JS, Harvey I, Le Cornu KA, Ryder JJ, Hall WL, Cassidy A. Flavonoids, flavonoid-​rich foods, and cardiovascular risk: A meta-​analysis

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Optimal Nutrition for Women

33

of randomized controlled trials. Am J Clin Nutr. 2008;88(1):38–​50. doi: 10.1093/​ajcn/​ 88.1.38. 42. Nelms MN, Sucher K, Lacey K, Habash D, Nelms GR, Hansen-​Petrik M, LaSalle C, Pujol TJ, Barnes TJ, Mattfeldt-​Beman M, Heuberger RA, Irwin KJ, Bergman EA, Hawk SN, Cohen DA, Lee RD, Jurecki E, Maloney S, Wong J. Nutrition Therapy and Pathophysiology. 3rd ed. Boston: Cengage Learning; 2016. 43. IUCN 2020. The IUCN Red List of Threatened Species. Version 2020-​3. www. iucnredlist.org. Accessed February 5, 2021. 44. Eaton SB. Paleolithic nutrition: Twenty-​five years later. Nutr. Clin. Pract. 2010; 25(6):594–​602. doi: 10.1177/​0884533610385702. 45. Lambert J. Primate digestion: Interactions among anatomy, physiology, and feeding ecology. Evol Anthropol. 1998 doi: 10.1002/​ (SICI)1520-​ 6505(1998)7: 13.0.CO;2-​C. 46. Jahns L, Davis-​Shaw W, Lichtenstein AH, Murphy SP, Conrad Z, Nielsen F. The history and future of dietary guidance in America. Adv Nutr. 2018;9(2):136–​147. doi: 10.1093/​advances/​nmx025. 47. Atwater WO. Principles of Nutrition and Nutritive Value of Food. 1910. https://​ archive.org/​details/​CAT87202134/​page/​n1/​mode/​2up. 48. United States Public Health Service Office of the Surgeon General, United States Office of the Assistant Secretary for Health. Healthy People: The Surgeon General’s Report on Health Promotion and Disease Prevention, 1979. Rockville: United States Public Health Service. 1979. https://​collections.nlm.nih.gov/​ext/​document/​101584932X92/​ PDF/​101584932X92.pdf. Published July 1979. Accessed February 5, 2021. 49. Dietary Guidelines Advisory Committee. Scientific Report of the 2020 Dietary Guidelines Advisory Committee: Advisory Report to the Secretary of Agriculture and the Secretary of Health and Human Services. U.S. Department of Agriculture, Agricultural Research Service. Washington, DC; 2020. www.dietaryguidelines.gov/​sites/​default/​ files/​2020-​07/​ScientificReport_​of_​the_​2020DietaryGuidelinesAdvisoryCommittee_​ first-​print.pdf. Published July 15, 2020. Accessed February 5, 2021. 50. Government of Canada. Canada’s Food Guide. Food-​Guide.Canada.ca; 2020. https://​ food-​guide.canada.ca/​en/​. Published January 22, 2019. Accessed July 7, 2020. 51. EAT-​Lancet Commission. Food Planet Health: Healthy Diets from Sustainable Food Systems. Stockholm: EAT-​Lancet Commission Summary Report; 2019. https://​ eatforum.org/ ​ c ontent/ ​ u ploads/ ​ 2 019/ ​ 0 7/ ​ E AT- ​ L ancet_ ​ C ommission_ ​ S ummary_​ Report.pdf. 52. US Department of Health and Human Services, US Department of Agriculture. Dietary Guidelines Advisory Committee. Dietary Guidelines for Americans, 2010 (No. 232). Washington, D.C.: GPO; 2010. www.dietaryguidelines.gov/​sites/​default/​ files/​2019-​05/​DietaryGuidelines2010.pdf. Published December 2010. Accessed February 5, 2021. 53. Fraser GE. Associations between diet and cancer, ischemic heart disease, and all-​cause mortality in non-​Hispanic white California Seventh-​day Adventists. Am J Clin Nutr. 1999;70(3 Suppl):532S–​538S. doi: 10.1093/​ajcn/​70.3.532s. 54. Hailu A, Knutsen SF, Fraser GE. Associations between meat consumption and the prevalence of degenerative arthritis and soft tissue disorders in the Adventist Health Study, California U.S.A. J Nutr Health Aging. 2006;10(1):7–​14. https://​pubmed.ncbi. nlm.nih.gov/​16453052/​. Accessed February 5, 2021. 55. Kiani F, Knutsen S, Singh P, Ursin G, Fraser G. Dietary risk factors for ovarian cancer: The Adventist Health Study (United States). Cancer Causes Control. 2006;17(2):137–​146. doi: 10.1007/​s10552-​005-​5383-​z.

34

34

Kayli Anderson et al. 56. Melby CL, Toohey ML, Cebrick J. Blood pressure and blood lipids among vegetarian, semivegetarian, and nonvegetarian African Americans. Am J Clin Nutr. 1994;59(1):103–​109. doi: 10.1093/​ajcn/​59.1.103. 57. Vang A, Singh PN, Lee JW, Haddad EH, Brinegar CH. Meats, processed meats, obesity, weight gain and occurrence of diabetes among adults: Findings from Adventist Health Studies. Ann Nutr Metab. 2008;52(2):96–​104. doi: 10.1159/​000121365. Epub 2008;18. Erratum in: Ann Nutr Metab. 2010;56(3):232. 58. Fraser G, Katuli S, Anousheh R, Knutsen S, Herring P, Fan J. Vegetarian diets and cardiovascular risk factors in black members of the Adventist Health Study-​2. Public Health Nutr. 2015;18(3):537–​545. doi: 10.1017/​S1368980014000263. 59. Japas C, Knutsen S, Dehom S, Dos Santos H, Tonstad S. Body mass index gain between ages 20 and 40 years and lifestyle characteristics of men at ages 40–​60 years: The Adventist Health Study-​2. Obes Res Clin Pract. 2014;8(6):e549–​e557. doi: 10.1016/​ j.orcp.2013.11.007. 60. Le LT, Sabaté J. Beyond meatless, the health effects of vegan diets: Findings from the Adventist cohorts. Nutrients. 2014;27;6(6):2131–​2147. doi: 10.3390/​nu6062131. 61. Orlich MJ, Singh PN, Sabaté J, Jaceldo-​Siegl K, Fan J, Knutsen S, Beeson WL, Fraser GE. Vegetarian dietary patterns and mortality in Adventist Health Study 2. JAMA Intern Med. 2013; 8;173(13):1230–​1238. doi: 10.1001/​jamainternmed.2013.6473. 62. Orlich MJ, Fraser GE. Vegetarian diets in the Adventist Health Study 2: A review of initial published findings. Am J Clin Nutr. 2014l;100 Suppl 1(1):353S–​358S. doi: 10.3945/​ajcn.113.071233. 63. Orlich MJ, Singh PN, Sabaté J, Fan J, Sveen L, Bennett H, Knutsen SF, Beeson WL, Jaceldo-​Siegl K, Butler TL, Herring RP, Fraser GE. Vegetarian dietary patterns and the risk of colorectal cancers. JAMA Intern Med. 2015;175(5):767–​776. doi: 10.1001/​ jamainternmed.2015.59. 64. Pettersen BJ, Anousheh R, Fan J, Jaceldo-​Siegl K, Fraser GE. Vegetarian diets and blood pressure among white subjects: results from the Adventist Health Study-​2 (AHS-​2). Public Health Nutr. 2012;15(10):1909–​ 1916. doi: 10.1017/​ S1368980011003454. 65. Tantamango-​Bartley Y, Jaceldo-​Siegl K, Fan J, Fraser G. Vegetarian diets and the incidence of cancer in a low-​risk population. Cancer Epidemiol Biomarkers Prev. 2013;22(2):286–​294. doi: 10.1158/​1055-​9965.EPI-​12-​1060. 66. Tantamango-​Bartley Y, Knutsen SF, Knutsen R, Jacobsen BK, Fan J, Beeson WL, Sabate J, Hadley D, Jaceldo-​Siegl K, Penniecook J, Herring P, Butler T, Bennett H, Fraser G. Are strict vegetarians protected against prostate cancer? Am J Clin Nutr. 2016;103(1):153–​160. doi: 10.3945/​ajcn.114.106450. 67. Tonstad S, Butler T, Yan R, Fraser GE. Type of vegetarian diet, body weight, and prevalence of type 2 diabetes. Diabetes Care. 2009;32(5):791–​796. doi: 10.2337/​ dc08-​1886. 68. Tonstad S, Stewart K, Oda K, Batech M, Herring RP, Fraser GE. Vegetarian diets and incidence of diabetes in the Adventist Health Study-​2. Nutr Metab Cardiovasc Dis. 2013;23(4):292–​299. doi: 10.1016/​j.numecd.2011.07.004. 69. Key TJ, Appleby PN, Spencer EA, Travis RC, Roddam AW, Allen NE. Cancer incidence in vegetarians: Results from the European Prospective Investigation into Cancer and Nutrition (EPIC-​Oxford). Am J Clin Nutr. 2009;89(5):1620S–​1626S. doi: 10.3945/​ ajcn.2009.26736M. 70. Appleby PN, Thorogood M, Mann JI, Key TJ. The Oxford Vegetarian Study: An overview. Am J Clin Nutr. 1999;70(3 Suppl):525S–​531S. doi: 10.1093/​ajcn/​70.3.525s.

35

Optimal Nutrition for Women

35

71. Ley SH, Ardisson Korat AV, Sun Q, et al. Contribution of the nurses’ health studies to uncovering risk factors for type 2 diabetes: Diet, lifestyle, biomarkers, and genetics. Am J Public Health. 2016;106(9):1624–​1630. doi: 10.2105/​AJPH.2016.303314. 72. Ardisson Korat AV, Willett WC, Hu FB. Diet, lifestyle, and genetic risk factors for type 2 diabetes: A review from the Nurses’ Health Study, Nurses’ Health Study 2, and Health Professionals’ Follow-​ up Study. Curr Nutr Rep. 2014;3(4):345–​354. doi: 10.1007/​s13668-​014-​0103-​5. 73. Djoussé L, Gaziano JM, Buring JE, Lee IM. Egg consumption and risk of type 2 diabetes in men and women. Diabetes Care. 2009;32(2):295–​300. doi: 10.2337/​dc08-​1271. 74. Arnett DK, Blumenthal RS, Albert MA, Buroker AB, Goldberger ZD, Hahn EJ, Himmelfarb CD, Khera A, Lloyd-​Jones D, McEvoy JW, Michos ED, Miedema MD, Muñoz D, Smith SC Jr, Virani SS, Williams KA Sr, Yeboah J, Ziaeian B. 2019 ACC/​ AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/​American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;10;140(11):e596–​e646. doi: 10.1161/​ CIR.0000000000000678. 75. Evert AB, Dennison M, Gardner CD, Garvey WT, Lau KHK, MacLeod J, Mitri J, Pereira RF, Rawlings K, Robinson S, Saslow L, Uelmen S, Urbanski PB, Yancy WS Jr. Nutrition therapy for adults with diabetes or prediabetes: A consensus report. Diabetes Care. 2019;42(5):731–​754. doi: 10.2337/​dci19-​0014. 76. Eat a Diet Rich in Whole Grains, Vegetables, Fruits, and Beans. American Institute for Cancer Research. http://​www.aicr.org/​cancer-​prevention/​recommendations/​eat-​a-​ diet-​rich-​in-​whole-​grains-​vegetables-​fruits-​and-​beans/​. Published January 26, 2021. Accessed February 9, 2021. 77. Cison PR Web. American College of Lifestyle Medicine announces dietary lifestyle position statement for treatment and potential reversal of disease. Am J Lifestyle Med, 2018. www.prweb.com/​releases/​american_​college_​of_​lifestyle_​medicine_​ announces_ ​ d ietary_​ l ifestyle_​ p osition_​ s tatement_​ f or_​ t reatment_​ a nd_​ p otential_​ reversal_​of_​disease/​prweb15786205.htm. Published September 25, 2019. Accessed February 27, 2021. 78. Ornish D, Scherwitz LW, Billings JH, Brown SE, Gould KL, Merritt TA, Sparler S, Armstrong WT, Ports TA, Kirkeeide RL, Hogeboom C, Brand RJ. Intensive lifestyle changes for reversal of coronary heart disease. JAMA. 1998;16;280(23):2001–​2007. doi: 10.1001/​jama.280.23.2001. Erratum in: JAMA 1999;281(15):138. 79. Esselstyn CB, Jr, Gendy G, Doyle J, Golubic M, Roizen MF. A way to reverse CAD? J Fam Pract. 2014;63:356–​364b. www.mdedge.com/​familymedicine/​article/​83345/​ cardiology/​way-​reverse-​cad. 80. Orlich MJ, Singh PN, Sabaté J, et al. Vegetarian dietary patterns and mortality in Adventist Health Study 2. JAMA Intern Med. 2013;173(13):1230–​1238. doi: 10.1001/​ jamainternmed.2013.6473. 81. Crowe FL, Appleby PN, Travis RC, Key TJ. Risk of hospitalization or death from ischemic heart disease among British vegetarians and nonvegetarians: results from the EPIC-​Oxford cohort study. Am J Clin Nutr. 2013;97(3):597–​603. doi: 10.3945/​ ajcn.112.044073. 82. Ornish D. Statins and the soul of medicine. Am J Cardiol. 2002;89(11):1286–​1290. doi: 10.1016/​s0002-​9149(02)02327-​5. 83. Tonstad S, Butler T, Yan R, Fraser GE. Type of vegetarian diet, body weight, and prevalence of type 2 diabetes. Diabetes Care. 2009;32(5):791–​796. doi: 10.2337/​ dc08-​1886.

36

36

Kayli Anderson et al. 84. Eichelmann F, Schwingshackl L, Fedirko V, Aleksandrova K. Effect of plant-​based diets on obesity-​related inflammatory profiles: A systematic review and meta-​analysis of intervention trials. Obes Rev. 2016;17(11):1067–​1079. doi: 10.1111/​obr.12439. 85. Barnard ND, Cohen J, Jenkins DJ, Turner-​McGrievy G, Gloede L, Jaster B, Seidl K, Green AA, Talpers S. A low-​fat vegan diet improves glycemic control and cardiovascular risk factors in a randomized clinical trial in individuals with type 2 diabetes. Diabetes Care. 2006;29(8):1777–​1783. doi: 10.2337/​dc06-​0606. 86. Pettersen BJ, Anousheh R, Fan J, Jaceldo-​Siegl K, Fraser GE. Vegetarian diets and blood pressure among white subjects: Results from the Adventist Health Study-​2 (AHS-​2). Public Health Nutr. 2012;15(10):1909–​ 1916. doi: 10.1017/​ S1368980011003454. 87. Wang F, Zheng J, Yang B, Jiang J, Fu Y, Li D. Effects of vegetarian diets on blood lipids: A systematic review and meta-​analysis of randomized controlled trials. J Am Heart Assoc. 2015;4(10): e002408. doi: 10.1161/​JAHA.115.002408. 88. Grodstein F, Levine R, Troy L, Spencer T, Colditz GA, Stampfer MJ. Three-​ year follow-​ up of participants in a commercial weight loss program. Can you keep it off? Arch Intern Med. 1996;156(12):1302–​ 1306. doi: 10.1001/​ archinte.1996.00440110068009. 89. Neumark-​Sztainer D, Wall M, Haines J, Story M, Eisenberg ME. Why does dieting predict weight gain in adolescents? Findings from project EAT-​II: A 5-​year longitudinal study. J Am Diet Assoc. 2007;107(3):448–​455. doi: 10.1016/​j.jada.2006.12.013. 90. Tylka TL, Annunziato RA, Burgard D, Daníelsdóttir S, Shuman E, Davis C, Calogero RM. The weight-​inclusive versus weight-​normative approach to health: evaluating the evidence for prioritizing well-​being over weight loss. J Obes. 2014;2014:983495. doi: 10.1155/​2014/​983495. 91. Hunger JM, Smith JP, Tomiyama AJ. An evidence-​based rationale for adopting weight-​ inclusive health policy. Soc Issues and Policy Rev. 2020;14(1):73–​107. doi: 10.1111/​ sipr.12062. 92. Fikkan JL, Rothblum ED. Is fat a feminist issue? Exploring the gendered nature of weight bias. Sex Roles. 2012;66: 575–​592. doi: 10.1007/​s11199-​011-​0022-​5. 93. Phelan SM, Dovidio JF, Puhl RM, Burgess DJ, Nelson DB, Yeazel MW, Hardeman R, Perry S, van Ryn M. Implicit and explicit weight bias in a national sample of 4,732 medical students: The medical student CHANGES study. Obesity (Silver Spring). 2014;22(4):1201–​1208. doi: 10.1002/​oby.20687. 94. Puhl RM, Heuer CA. The stigma of obesity: A review and update. Obesity (Silver Spring). 2009;17(5):941–​964. doi: 10.1038/​oby.2008.636. 95. Mensinger JL, Tylka TL, Calamari ME. Mechanisms underlying weight status and healthcare avoidance in women: A study of weight stigma, body-​ related shame and guilt, and healthcare stress. Body Image. 2018;25:139–​ 147. doi: 10.1016/​ j.bodyim.2018.03.001. 96. Mensinger JL, Calogero RM, Stranges S, Tylka TL. A weight-​neutral versus weight-​ loss approach for health promotion in women with high BMI: A randomized-​controlled trial. Appetite. 2016;105:364–​374. doi: 10.1016/​j.appet.2016.06.006. 97. Bacon L, Stern JS, Van Loan MD, Keim NL. Size acceptance and intuitive eating improve health for obese, female chronic dieters. J Am Diet Assoc. 2005;105(6):929–​ 936. doi: 10.1016/​j.jada.2005.03.011. 98. Bacon L, Keim NL, Van Loan MD, Derricote M, Gale B, Kazaks A, Stern JS. Evaluating a ‘non-​diet’ wellness intervention for improvement of metabolic fitness, psychological well-​being and eating and activity behaviors. Int J Obes Relat Metab Disord. 2002;26(6):854–​865. doi: 10.1038/​sj.ijo.0802012.

37

Optimal Nutrition for Women

37

99. Tylka TL, Wilcox JA. Are intuitive eating and eating disorder symptomatology opposite poles of the same construct? Jour Couns Psychol. 2006;53(4):474–​485. doi: 10.1037/​0022-​0167.53.4.474. 100. Van Dyke N, Drinkwater EJ. Relationships between intuitive eating and health indicators: Literature review. Public Health Nutr. 2014;17(8):1757–​1766. doi: 10.1017/​S1368980013002139. 101. Smith TS, Hawks SR. Intuitive eating, diet composition, and the meaning of food in healthy weight promotion. Am J Health Educ. 2006;37(3):130–​136. doi: 10.1080/​ 19325037.2006.10598892. 102. Arcelus J, Mitchell AJ, Wales J, Nielsen S. Mortality rates in patients with anorexia nervosa and other eating disorders. A meta-​analysis of 36 studies. Arch Gen Psychiatry. 2011;68(7):724–​731. doi: 10.1001/​archgenpsychiatry.2011.74. 103. Shisslak CM, Crago M, Estes LS. The spectrum of eating disturbances. Int J Eat Disord. 1995 Nov;18(3):209–​ 219. doi: 10.1002/​ 1098-​ 108x(199511)18: 33.0.co;2-​e. 104. Striegel-​Moore RH, Rosselli F, Perrin N, DeBar L, Wilson GT, May A, Kraemer HC. Gender difference in the prevalence of eating disorder symptoms. Int J Eat Disord. 2009;42(5):471–​474. doi: 10.1002/​eat.20625. 105. Greenleaf C, Petrie TA, Carter J, Reel JJ. Female collegiate athletes: Prevalence of eating disorders and disordered eating behaviors. J Am Coll Health. 2009;57(5):489–​ 495. doi: 10.3200/​JACH.57.5.489-​496. 106. National Eating Disorders Association. Risk Factors. www.nationaleatingdis orders.org/​risk-​factors. Published August 3, 2018. Accessed February 5, 2021. 107. Marques L, Alegria M, Becker AE, Chen CN, Fang A, Chosak A, Diniz JB. Comparative prevalence, correlates of impairment, and service utilization for eating disorders across US ethnic groups: Implications for reducing ethnic disparities in health care access for eating disorders. Int J Eat Disord. 2011;44(5):412–​420. doi: 10.1002/​eat.20787. 108. Nagata JM, Garber AK, Tabler JL, Murray SB, Bibbins-​Domingo K. Prevalence and correlates of disordered eating behaviors among young adults with overweight or obesity. J Gen Intern Med. 2018;33(8):1337–​1343. doi: 10.1007/​s11606-​018-​4465-​z. 109. Flament MF, Henderson K, Buchholz A, Obeid N, Nguyen HN, Birmingham M, Goldfield G. Weight status and DSM-​5 diagnoses of eating disorders in adolescents from the community. J Am Acad Child Adolesc Psychiatry. 2015;54(5):403–​411.e2. doi: 10.1016/​j.jaac.2015.01.020. 110. Duncan AE, Ziobrowski HN, Nicol G. The prevalence of past 12-​month and lifetime DSM-​IV eating disorders by BMI category in US men and women. Eur Eat Disord Rev. 2017;(3):165–​171. doi: 10.1002/​erv.2503. 111. Hackert AN, Kniskern MA, Beasley TM. Academy of Nutrition and Dietetics: Revised 2020 Standards of Practice and Standards of Professional Performance for Registered Dietitian Nutritionists (Competent, Proficient, and Expert) in Eating Disorders. J Acad Nutr Diet. 2020;120(11):1902–​1919.e54. doi: 10.1016/​j.jand.2020.07.014. 112. U.S. Cancer Statistics Working Group. U.S. Cancer Statistics Data Visualizations Tool, Based on 2019 Submission Data (1999–​2017): U.S. Department of Health and Human Services, Centers for Disease Control and Prevention and National Cancer Institute. https://​gis.cdc.gov/​Cancer/​USCS/​DataViz.html. Published June 8, 2020. Accessed February 5, 2021. 113. Kim YB. Endometrial Cancer. In: Hoffman BL, Schorge JO, Halvorson LM, Hamid CA, Corton MM, Schaffer JI. eds. Williams Gynecology, 4th

38

38

Kayli Anderson et al. ed. New York: McGraw-​ Hill; 2020. https://​accessmedicine.mhmedical.com/​ content.aspx?bookid=2658§ionid=241073913. Accessed September 26, 2020. 114. Richardson DL. Cervical Cancer. In: Hoffman BL, Schorge JO, Halvorson LM, Hamid CA, Corton MM, Schaffer JI. eds. Williams Gynecology, 4th ed. New York: McGraw-​ Hill; 2020. Accessed September 26, 2020. https://​accessmedicine.mhmedical.com/​ content.aspx?bookid=2658§ionid=241012569. 115. Schorge JO. Epithelial Ovarian Cancer. In: Hoffman BL, Schorge JO, Halvorson LM, Hamid CA, Corton MM, Schaffer JI. eds. Williams Gynecology, 4th ed. New York: McGraw-​ Hill; 2020. https://​accessmedicine.mhmedical.com/​ content.aspx?bookid=2658§ionid=241074196. Accessed September 26, 2020. 116. Menopause and the mature woman. In: Hoffman BL, Schorge JO, Halvorson LM, Hamid CA, Corton MM, Schaffer JI. eds. Williams Gynecology, 4th ed. NewYork: McGraw-​Hill; 2020. https://​accessmedicine.mhmedical.com/​content.aspx? bookid=2658§ionid=241010835. Accessed September 26, 2020. 117. Gagne L, Maizes V. Osteoporosis. In: Rakel D, ed. Integrative Medicine, 4th ed., Philadelphia, PA: Elsevier; 2018: Chapter 36. 118. Gaby, A. Vitamin B12. In: Nutritional Medicine, 2nd ed. Concord: Fritz Perlberg Publishing, 2017: Chapter 20. 119. Heaney RP, Weaver CM. Calcium absorption from kale. Am J Clin Nutr. 1990;51(4):656–​657. doi: 10.1093/​ajcn/​51.4.656. 120. Nutrition Working Group, O’Connor DL, Blake J, Bell R, Bowen A, Callum J, Fenton S, Gray-​Donald K, Rossiter M, Adamo K, Brett K, Khatri N, Robinson N, Tumback L, Cheung A. Canadian consensus on female nutrition: Adolescence, reproduction, menopause, and beyond. J Obstet Gynaecol Can. 2016;38(6):508–​554.e18. doi: 10.1016/​j.jogc.2016.01.001. 121. Bjelakovic G, Gluud LL, Nikolova D, Whitfield K, Wetterslev J, Simonetti RG, Bjelakovic M, Gluud C. Vitamin D supplementation for prevention of mortality in adults. Cochrane Database Syst Rev. 2014;(1):CD007470. doi: 10.1002/​14651858. CD007470.pub3. 122. Holick MF, Binkley NC, Bischoff-​Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: An Endocrine Society clinical practice guideline [published correction appears in J Clin Endocrinol Metab. 2011 Dec;96(12):3908]. J Clin Endocrinol Metab. 2011;96(7):1911–​1930. doi: 10.1210/​jc.2011-​0385. 123. Qi L, van Dam RM, Rexrode K, Hu FB. Heme iron from diet as a risk factor for coronary heart disease in women with type 2 diabetes. Diabetes Care. 2007;30(1):101–​ 106. doi: 10.2337/​dc06-​1686. 124. Inoue-​Choi M, Sinha R, Gierach GL, Ward MH. Red and processed meat, nitrite, and heme iron intakes and postmenopausal breast cancer risk in the NIH-​AARP Diet and Health Study. Int J Cancer. 2016;138(7):1609–​1618. doi: 10.1002/​ijc.29901. 125. Ward MH, Cross AJ, Abnet CC, Sinha R, Markin RS, Weisenburger DD. Heme iron from meat and risk of adenocarcinoma of the esophagus and stomach. Eur J Cancer Prev. 2012;21(2):134–​138. doi: 10.1097/​CEJ.0b013e32834c9b6c. 126. Turnlund JR, King JC, Keyes WR, Gong B, Michel MC. A stable isotope study of zinc absorption in young men: Effects of phytate and alpha-​cellulose. Am J Clin Nutr. 1984;40(5):1071–​1077. doi: 10.1093/​ajcn/​40.5.1071. 127. Lightowler HJ, Davies GJ. Iodine intake and iodine deficiency in vegans as assessed by the duplicate-​portion technique and urinary iodine excretion. Br J Nutr. 1998;80(6):529–​535. doi: 10.1017/​s0007114598001627. 128. National Institutes of Health, Iodine Fact Sheet for Health Professionals. NIH Office of Dietary Supplements. Updated May 1, 2020. https://​ods.od.nih.gov/​factsheets/​ Iodine-​HealthProfessional/​#ref. Accessed July 3, 2020.

39

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129. Gaby, A. Omega-​3 fatty acids. Nutritional Medicine, 2nd ed. Concord: Fritz Perlberg Publishing, 2017: Chapter 66. 130. Centers for Disease Control and Prevention. Infertility FAQ. Content source: Division of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion. www.cdc.gov/​reproductivehealth/​infertility/​index.htm. Updated January 16, 2019. Accessed February 5, 2021. 131. Chavarro JE, Rich-​Edwards JW, Rosner BA, Willett WC. Diet and lifestyle in the prevention of ovulatory disorder infertility. Obstet Gynecol. 2007;110(5):1050–​ 1058. doi: 10.1097/​01.AOG.0000287293.25465.e1. 132. Gaskins AJ, Chavarro JE. Diet and fertility: A review. Am J Obstet Gynecol. 2018;218(4):379–​389. doi: 10.1016/​j.ajog.2017.08.010. 133. Comerford KB, Ayoob KT, Murray RD, Atkinson SA. The role of avocados in maternal diets during the periconceptional period, pregnancy, and lactation. Nutrients. 2016;8(5):313. doi: 10.3390/​nu8050313. 134. Hatch EE, Wesselink AK, Hahn KA, Michiel JJ, Mikkelsen EM, Sorensen HT, Rothman KJ, Wise LA. Intake of sugar-​sweetened beverages and fecundability in a North American preconception cohort. Epidemiology. 2018;29(3):369–​378. doi: 10.1097/​EDE.0000000000000812. 135. Grieger JA, Grzeskowiak LE, Bianco-​ Miotto T, Jankovic-​ Karasoulos T, Moran LJ, Wilson RL, Leemaqz SY, Poston L, McCowan L, Kenny LC, Myers J, Walker JJ, Norman RJ, Dekker GA, Roberts CT. Pre-​pregnancy fast food and fruit intake is associated with time to pregnancy. Hum Reprod. 2018;33(6):1063–​1070. doi: 10.1093/​humrep/​dey079. 136. Chavarro JE, Rich-​Edwards JW, Rosner BA, Willett WC. Protein intake and ovulatory infertility. Am J Obstet Gynecol. 2008;198(2):210.e1–​210.e7. doi: 10.1016/​ j.ajog.2007.06.057. 137. Chavarro JE, Rich-​Edwards JW, Rosner BA, Willett WC. Caffeinated and alcoholic beverage intake in relation to ovulatory disorder infertility. Epidemiology. 2009;20(3):374–​381. doi: 10.1097/​EDE.0b013e31819d68cc. 138. Anderson K, Nisenblat V, Norman R. Lifestyle factors in people seeking infertility treatment –​A review. Aust N Z J Obstet Gynaecol. 2010;50(1):8–​20. doi: 10.1111/​ j.1479-​828X.2009.01119.x. 139. Visioli F, Hagen TM. Antioxidants to enhance fertility: Role of eNOS and potential benefits. Pharmacol Res. 2011;64(5):431–​437. doi: 10.1016/​j.phrs.2011.06.021. 140. Rich-​Edwards JW, Spiegelman D, Garland M, Hertzmark E, Hunter DJ, Colditz GA, Willett WC, Wand H, Manson JE. Physical activity, body mass index, and ovulatory disorder infertility. Epidemiology. 2002;13(2):184–​ 190. doi: 10.1097/​ 00001648-​200203000-​00013. 141. Kiddy DS, Hamilton-​Fairley D, Bush A, Short F, Anyaoku V, Reed MJ, Franks S. Improvement in endocrine and ovarian function during dietary treatment of obese women with polycystic ovary syndrome. Clin Endocrinol (Oxf). 1992;36(1):105–​ 111. doi: 10.1111/​j.1365-​2265.1992.tb02909.x. 142. Schwarzenberg SJ, Georgieff MK. Committee on Nutrition. Advocacy for improving nutrition in the first 1000 days to support childhood development and adult health. Pediatrics. 2018;141(2):e20173716. doi: 10.1542/​peds.2017-​3716. 143. Flaxman SM, Sherman PW. Morning sickness: A mechanism for protecting mother and embryo. Q Rev Biol. 2000;75(2):113–​148. doi: 10.1086/​393377. 144. Einarson TR, Piwko C, Koren G. Prevalence of nausea and vomiting of pregnancy in the USA: A meta analysis. J Popul Ther Clin Pharmacol. 2013;20(2):e163–​e170. https://​pubmed.ncbi.nlm.nih.gov/​23863545/​. Accessed February 5, 2021.

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Kayli Anderson et al. 145. Festin M. Nausea and vomiting in early pregnancy. BMJ Clin Evid. 2014;2014:1405. www.ncbi.nlm.nih.gov/​pmc/​articles/​PMC3959188/​. Published March 19, 2014. Accessed February 5, 2021. 146. Kominiarek MA, Rajan P. Nutrition recommendations in pregnancy and lactation. Med Clin North Am. 2016;100(6):1199–​1215. doi: 10.1016/​j.mcna.2016.06.004. 147. Desrosiers TA, Siega-​ Riz AM, Mosley BS, Meyer RE. National Birth Defects Prevention Study. Low carbohydrate diets may increase risk of neural tube defects. Birth Defects Res. 2018;110(11):901–​909. doi: 10.1002/​bdr2.1198. 148. Wiedeman AM, Barr SI, Green TJ, Xu Z, Innis SM, Kitts DD. Dietary choline intake: current state of knowledge across the life cycle. Nutrients. 2018;16;10(10):1513. doi: 10.3390/​nu10101513. 149. Office of Dietary Supplements -​Vitamin A. NIH Office of Dietary Supplements. https://​ods.od.nih.gov/​factsheets/​VitaminA-​HealthProfessional/​. Published February 14, 2020. Accessed February 5, 2021. 150. Institute of Medicine (US) Subcommittee on Interpretation and Uses of Dietary Reference Intakes. Summary tables: Dietary reference intakes. DRI dietary reference intakes: Applications in dietary assessment. www.ncbi.nlm.nih.gov/​books/​ NBK222881/​. Published January 1, 1970. Accessed February 5, 2021. 151. National Academies of Sciences, Engineering, and Medicine. 2020. Nutrition during Pregnancy and Lactation: Exploring New Evidence: Proceedings of a Workshop—​In Brief. Washington, DC: The National Academies Press. doi: 10.17226/​25831. 152. Hudson T. Menopause. In: Women’s Encyclopedia of Natural Medicine. New York: McGraw-​Hill, 2008. 153. Klein-​ Patel M, Gergen-​ Barnett K, Balk J. Managing menopausal symptoms. In: Rakel D, ed. Integrative Medicine, 4th ed., Elsevier; 2018: Chapter 55. 154. Gaby, A. Menopause. In: Nutritional Medicine, 2nd ed. Concord: Fritz Perlberg Publishing, 2017: Chapter 225. 155. Bailey TG, Cable NT, Aziz N, Dobson R, Sprung VS, Low DA, Jones H. Exercise training reduces the frequency of menopausal hot flushes by improving thermoregulatory control. Menopause. 2016;23(7):708–​ 718. doi: 10.1097/​ GME.0000000000000625. 156. Atalay M, Lappalainen J, Sen CK. Dietary antioxidants for the athlete. Curr Sports Med Rep. 2006 Jun;5(4):182–​186. doi: 10.1097/​01.csmr.0000306504.71105.6e. 157. De Souza MJ, Nattiv A, Joy E, Misra M, Williams NI, Mallinson RJ, Gibbs JC, Olmsted M, Goolsby M, Matheson G. Expert Panel. 2014 Female Athlete Triad Coalition Consensus Statement on Treatment and Return to Play of the Female Athlete Triad: 1st International Conference held in San Francisco, California, May 2012 and 2nd International Conference held in Indianapolis, Indiana, May 2013. Br J Sports Med. 2014;48(4):289. doi: 10.1136/​bjsports-​2013-​093218. 158. Journal of the Academy of Nutrition and Dietetics. Sports Nutrition Care Manual. The Academy of Nutrition and Dietetics’ Nutrition Care Manual® www.nutritioncaremanual.org/​sports-​nutrition-​care. Published September 25, 2020. Accessed December 16, 2020. 159. Position of the American Dietetic Association, Dietitians of Canada, and the American College of Sports Medicine: Nutrition and athletic performance. J Am Diet Assoc. 2009;109(3):509–​527. doi: 10.1016/​j.jada.2009.01.005.

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Physical Activity for Women Ginger Garner, PT, DPT, ATC/​L, DipABLM Living Well InstituteEude MOMia® Integrative Physical Therapy & Lifestyle Medicine Greensboro, NC

Wendy Farnen Price, PT, DPT, MS, DipABLM Healthcore Lifestyle Medicine; Yale University Woodbridge, CT

2.1 Introduction......................................................................................................42 2.2 Children and adolescents..................................................................................44 2.3 Adults...............................................................................................................46 2.3.1 PA Prescription.....................................................................................46 2.3.2 Measuring PA Intensity........................................................................47 2.3.3 Screening PA Participation...................................................................47 2.4 Preconception to Postpartum............................................................................48 2.4.1 PA Guidelines and Contraindications...................................................48 2.4.2 PA Measurement..................................................................................50 2.4.3 Postpartum............................................................................................50 2.4.4 Improving Postpartum PA Screening...................................................51 2.4.5 Future Considerations..........................................................................51 2.5 Older Healthy Women......................................................................................51 2.5.1 Menopause...........................................................................................52 2.6 Conclusion........................................................................................................55

KEY POINTS • Physical activity (PA) has many positive biopsychosocial health benefits for women across the lifespan. However, women are consistently less physically active than men and are often considered at risk for poor health outcomes. • The PA vital sign (PAVS) should be administered at each patient encounter to determine if PA guidelines are being met. • Exercise is only a subcategory of PA. PA prescription should also include occupational, domestic, transportation, as well as leisure time activities. • Any amount of activity counts. There is no lower threshold for benefits from PA. The first edition of the PAGA guidelines states as little as 10-​minute bouts DOI: 10.1201/9781003110682-3

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of PA were beneficial, while the second edition removed the 10-​minute requirement since some PA health benefits are immediate. • Use SMART goals and the FITT principle to create multi-​modal, personalized programming using an interprofessional team approach tailored to goals and interests, plus existing comorbidities.

2.1  INTRODUCTION Regular physical activity (PA) has well-​documented benefits for women of all ages.1,2 Despite the numerous health benefits (Table 2.1), women are consistently less physically active than men and PA participation decreases as women age.3 More than 80% of women do not achieve recommended PA guidelines.1 TABLE 2.1 Health Benefits of Physical Activity1,2 Age Group

Health Benefits

Children and Adolescents

•  Improved bone health •  Improved weight status •  Improved CRF and muscular fitness •  Improved cardiometabolic health •  Improved cognition •  Decreased risk of depression and anxiety4

Adults

•  Lower risk of all-​cause mortality •  Lower risk of CVD and stroke •  Lower risk of hypertension •  Lower risk of type 2 diabetes •  Lower risk of adverse blood lipid profile •  Lower risk of cancers •  Improved cognition •  Improved quality of life •  Decreased risk of anxiety and depression •  Improved sleep •  Decreased obesity •  Improved bone health •  Improved physical function

Older Adults

• Lower risk of falls, fall-​related injuries Dementia, including Alzheimer’s disease

Pregnancy/​Postpartum

Reduced risk of the following: •  Excessive weight gain5 • Preeclampsia6 •  Musculoskeletal pain •  Gestational diabetes • HTN7 •  Preterm birth, lower birth weight, cesarean6 •  Postpartum depression8

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FIGURE 2.1  The physical activity sign. (Created with data from Strath Scott J., Kaminsky Leonard A., Ainsworth Barbara E., et al. Guide to the assessment of physical activity: Clinical and research applications. Circulation. 2013;128(20):2259–​2279.)

Physical inactivity is a leading contributor to the development of noncommunicable diseases (NCDs), and can negatively affect mental health and quality of life.9,10 Given that two in every three deaths among women are caused by NCDs, the promotion of PA should play a fundamental role in mitigating the impact of these diseases in women.11 The use of the physical activity vital sign (PAVS) at each visit is a key strategy for healthcare providers (HCPs) (Figure 2.1)12,13 to screen for inadequate PA, which should prompt PA prescription or referral.14,15 HCPs should work to understand why many women do not achieve PA guidelines, which are often influenced by social determinants of health. Personal, physical, and environmental barriers to PA in women may include lack of time, enjoyment and motivation, mobility, resources and support, and/​or self-​consciousness about body size, shape, and PA ability, pain or injury, and/​or urinary incontinence.16,17,18 HCPs can improve PA adherence by addressing identifiable barriers, tailoring the PA program and making appropriate referrals,16 and by being a role model for activity.19,20 Physically active HCPs are more likely to counsel patients about PA and provide more credible, motivating preventive counseling.20 HCPs should routinely

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address the benefits of incorporating PA into daily life, goal setting, and self-​ monitoring of PA by utilizing motivational interviewing.16,21 Women cleared for independent PA provide an exercise prescription or referral to a qualified fitness professional or community program.14,22 However, those with impairments, comorbid conditions, and/​or physical barriers to PA require a physical therapy referral for personalized evaluation, diagnosis, and intervention.23 PA should not be confused with physical exercise, as physical exercise is a subcategory of PA and typically refers to organized, planned, repetitive, and structured sports or fitness activities. The Centers for Disease Control (CDC) defines PA as “anything that gets your body moving”.24

2.2  CHILDREN AND ADOLESCENTS Regular PA in girls supports growth, learning, and development with numerous biopsychosocial health benefits (Table 2.1).1,2,25 PA can help prevent and treat childhood obesity, which is a major public health concern with increasing prevalence.26 Increased body mass index (BMI) in girls can cause early onset puberty and menstrual irregularities.27 Menstrual disorders such as dysmenorrhea, abnormal uterine bleeding (AUB), and premenstrual syndrome (PMS) that are common among adolescent girls and young women can be improved with PA.27–​30 PA can improve self-​esteem and mental health, to which adolescent girls are vulnerable, with double the incidence of anxiety and depressive disorders when compared to boys.31 Girls who are more physically active and participate in sports have positive health behaviors, such as improved diet, safer sexual practices, decreased substance abuse, and better academic achievement and school attendance.31 Nonetheless, girls are notably less physically active than boys.32 Physical inactivity in adolescents is recognized as a serious and growing public health problem. Although World Health Organization (WHO) guidelines aim to improve activity levels in all children by 10% by 2025, the prevalence of female insufficient PA has shown no improvement since 2001.32 Globally, 85% of girls aged 11–​17 years do not meet the PA guidelines (Table 2.2), and this trend may continue into adulthood, contributing to long-​term poor health outcomes.32 This PA gender gap begins early, starting in preschool, and then increases more rapidly in adolescence, especially among minority and low-​income backgrounds.32,33,34 However, the passage of Title IX in 1972 significantly improved PA and female participation in US athletics over the past 50 years, and has led to more research on how to manage risks and maximize benefits for young female athletes.35 Gender-​based differences in anatomy, physiology, and training also contribute to an elevated risk of concussions, musculoskeletal injuries, and the female athlete triad.36 Female athlete triad is relatively common among young women participating in sports and is a combination of three interrelated conditions that are associated with athletic training: menstrual dysfunction, low energy availability, and decreased bone mineral density.36 Girls also appear to be more prone to spondylolisthesis, anterior cruciate ligament injuries, patellofemoral pain, ankle sprains, and stress fractures.37,38 Based on these differences, females are considered to be at higher risk of poor health

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TABLE 2.2 Key Physical Activity Guidelines for Children, Adolescents, and Adults Age Group

Physical Activity Guidelines

Children and Adolescents

• It is important to provide young people opportunities and encouragement to participate in physical activities that are appropriate for their age, that are enjoyable, and that offer variety. • Children and adolescents aged 6 through 17 years should do 60 minutes (1 hour) or more of moderate-​to-​vigorous physical activity daily: •  Aerobic: Most of the 60 minutes or more per day should be either moderate-​or vigorous-​intensity aerobic physical activity and should include vigorous-​intensity physical activity on at least 3 days a week. •  Muscle strengthening: As part of their 60 minutes or more of daily physical activity, children and adolescents should include muscle-​ strengthening physical activity on at least 3 days a week. •  Bone strengthening: As part of their 60 minutes or more of daily physical activity, children and adolescents should include bone-​ strengthening physical activity on at least 3 days a week.

Adults

• Adults should move more and sit less throughout the day. Some physical activity is better than none. Adults who sit less and do any amount of moderate-​to-​vigorous physical activity gain some health benefits. • For substantial health benefits, adults should do at least 150 minutes (2 hours and 30 minutes) to 300 minutes (5 hours) a week of moderate-​ intensity, or 75 minutes (1 hour and 15 minutes) to 150 minutes (2 hours and 30 minutes) a week of vigorous-​intensity aerobic physical activity, or an equivalent combination of moderate-​and vigorous-​intensity aerobic activity. Preferably, aerobic activity should be spread throughout the week. • Additional health benefits are gained by engaging in physical activity beyond the equivalent of 300 minutes (5 hours) of moderate-​intensity physical activity a week. • Adults should also do muscle-​strengthening activities of moderate or greater intensity and that involve all major muscle groups on two or more days a week, as these activities provide additional health benefits.

Source: Piercy KL, Troiano RP, Ballard RM, et al. The physical activity guidelines for Americans. JAMA. 2018;320(19):2020.

outcomes and certain musculoskeletal injuries, identifying them as a high-​priority group for PA interventions.38 HCPs should include PA assessment, counseling, and prescription at each visit. The menstrual cycle as a vital sign should also be used to provide additional information or clues regarding pathology secondary to excessive PA.39,40 HCPs can help coordinate recommendations and referrals for girls at high risk or special needs, including appropriate utilization of physical therapy and community-​based resources. The HCP should act as a role model for PA, collaborate with parents, and advocate for policies to increase access and opportunities for PA for girls.

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2.3  ADULTS 2.3.1 PA Prescription Adults need to perform two types of PA each week to improve their health: aerobic activity and muscle strengthening.1 The guidelines do not provide gender-​specific guidelines for PA; however, this chapter addresses recommendations specifically for women. There are five different types of PA, which include aerobic, muscle strengthening, bone-​building, balance, and flexibility activities. There are also five components of physical fitness (Figure 2.2). See Table 2.2 for PA guidelines. Engagement in safe PA should consider the following guidelines:1 • Be aware of risks and also understand that PA can be safe for nearly everyone. • Choose PA based on what is appropriate for an individual’s current fitness level and personal health goals. • Gradually increase PA to meet key guidelines or health goals. • Use appropriate gear and equipment to engage in safe PA. • Be under the care of a medical provider if chronic conditions or symptoms are present.

FIGURE 2.2  Measuring physical activity intensity. (Created with data from measuring physical activity intensity | physical activity | CDC. Published September 17, 2020.)

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There are four dimensions to include for PA prescription, often called the FITT principle:1 F –​Frequency: how often PA is performed. I –​Intensity: mild, moderate, or vigorous level activity performance. T –​Time: how long the activity is performed. T –​Type: the type of activity performed. Domains of PA should also be considered since promotion of PA has historically focused on activity that centered around recreational time. However, other non-​ leisure activities also provide health benefits. The American Heart Association (AHA) Guide identifies four domains of PA41: occupational, domestic, transportation, and leisure time. All of the listed domains should be recognized as valuable contributors to overall PA in an individual. Future remote patient monitoring systems and in-​clinic screens should seek to both educate the individual about all domains of PA and include all domains of PA in the total tally of accumulated daily or weekly PA. Not doing so is a barrier to meeting the minimum requirements for PA participation.

2.3.2 Measuring PA Intensity A method proven to be reliable for measuring the intensity of aerobic activity, and easier than using target heart rate via estimated maximum heart rate, is the Talk Test.2 For moderate activity, one should be able to talk but not sing during the activity. For vigorous activity, one should be able to say no more than a few words without pausing for breath (see Figure 2.3 on measuring intensity). An alternate method is using the Borg Rating of Perceived Exertion, which demonstrates a high correlation between a person’s perceived exertion and actual heart rate during the activity.42 The scale runs from 6 to 20, with 6 perceiving no exertion and 20 being maximal effort. A rating of 12–​14 is considered moderate-​level intensity. This is also the method used for those who must take medications like beta-​blockers which control heart rate.

2.3.3 Screening PA Participation Assessment of PA can be highly complex, with expensive measurement tools being inaccessible and unrealistic for most segments of the population. A systematic review concluded that no perfect tool exists for the measurement of PA; however, observed PA was cited as better than self-​reported PA. Because of the cost-​prohibitive nature of objective PA measurement, subjective assessment and observation of PA have arisen as accessible, accurate means of measuring PA.41 The American Heart Association lists diaries/​logs and questionnaires as feasible subjective measures of PA assessment. Questionnaires are low cost, low burden, convenient and easy to administer, applicable to a large number of individuals, allow for single time point assessment, are valid to assess structured PA, can successfully rank PA into high and low categories, and are able to assess different dimensions and domains of PA.41 In a systematic review, the PAVS and the exercise vital sign (EVS)

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FIGURE 2.3  Components of physical fitness. (Created with data from Piercy KL, Troiano RP, Ballard RM, et al. The physical activity guidelines for Americans. JAMA. 2018;320 (19):2020.)

showed good discriminant validity, both of which are two-​item global questionnaires that take less than 30 seconds to administer.41,43

2.4  PRECONCEPTION TO POSTPARTUM PA is associated with minimal risk and promotes healthy conception and pregnancy as well as the prevention of gestational diseases and NCDs.44 Establishing regular PA and healthy habits during preconception is a strong predictor of continued PA during pregnancy.45 See Table 2.1 for PA benefits and Table 2.3 for PA guidelines.

2.4.1 PA Guidelines and Contraindications Fundamental guidelines to PA prescription during pregnancy should consider the following: • Women who were sedentary before pregnancy can still participate in PA but should start with no more than 15 minutes of continuous exercise three times a week,46 and should follow a lower intensity and duration.5 • Women should gradually increase the daily sessions to 30 minutes.46

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TABLE 2.3 Key Physical Activity Guidelines for Pregnancy and Postpartum Age Group

Physical Activity Guidelines

Pregnancy and Postpartum

• Women should do at least 150 minutes (2 hours and 30 minutes) of moderate-​intensity aerobic activity a week during pregnancy and the postpartum period. Preferably, aerobic activity should be spread throughout the week. • Women who habitually engaged in vigorous-​intensity aerobic activity or who were physically active before pregnancy can continue these activities during pregnancy and the postpartum period. • Women who are pregnant should be under the care of a health care provider who can monitor the progress of the pregnancy. Women who are pregnant can consult their health care provider about whether or how to adjust their physical activity during pregnancy and after the baby is born.

Source: Piercy KL, Troiano RP, Ballard RM, et al. the physical activity guidelines for Americans. JAMA. 2018;320(19):2020.

• Women who exercised routinely before pregnancy can maintain an exercise routine without the occurrence of adverse effects.46,47 • Pregnant athletes with healthy pregnancies appear to be able to continue with vigorous-​intensity exercise into the third trimester safely.47 Close supervision is recommended for competitive athletes and should attend to avoiding hyperthermia, maintaining proper hydration, and sustaining adequate caloric intake to prevent weight loss, which may adversely affect fetal growth.47 • Recreational exercises such as swimming or fast walking and exercises for the conditioning of muscle strength are safe and beneficial.46 • The objective of recreational exercise is to maintain and not necessarily increase physical fitness.46 • Prolonged isometric contraction, Valsalva maneuver, and motionless standing are to be avoided.5 • Pregnant women who are obese can participate in PA safely by starting low-​intensity exercise, making dietary changes toward healthy choices, and following the guidelines above. There is evidence to support safe PA in pregnant women with obesity having no adverse outcomes.48 • Avoid the supine position during exercise after 20 weeks of gestation in order to prevent decreased venous return due to aortocaval compression from the gravid uterus, leading to hypotension.49 • Women with obstetric or medical comorbidities should have individualized PA prescription.47 It is plausible then that for the more than 60% of pregnant women who experience low back pain,50 combined with hemodynamic changes that would require skilled monitoring, a best evidence option could be prenatal physical therapy for this population and others with similar conditions. • There is no credible evidence to prescribe bed rest in pregnancy for the prevention of preterm labor, and it should not be routinely recommended.47 McCall

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TABLE 2.4 Activities to Avoid and Include during Pregnancy and Warning Signs

Activities to Participate in6 Activities to Avoid5,46 • Walking • Swimming • Stationary bike • Aerobic, low impact activities such as Yoga or Pilates • Racquet sports • Running • Resistance training

• Horseback riding • Scuba diving • Hot yoga • Hot Pilates • Outdoor cycling • Contact sports • Skiing • Surfing • PA in supine after the first trimester

Warning Signs to Discontinue Exercise While Pregnant47 • Vaginal bleeding • Abdominal pain • Regular painful contractions • Amniotic fluid leakage • Dyspnea before exertion • Dizziness • Headache • Chest pain • Muscle weakness affecting balance • Calf pain or swelling

et al. cite that “Cochrane systematic reviews do not support ‘therapeutic’ bed rest for threatened abortion, hypertension, preeclampsia, preterm birth, multiple gestations, or impaired fetal growth.”51 Further, women who are put on prolonged bed rest or prescribed restricted PA are at risk of venous thromboembolism, bone demineralization, and deconditioning.47 • See Table 2.4 for activities to include and avoid plus warning signs.

2.4.2 PA Measurement Despite the overwhelming evidence that supports PA as beneficial and safe for an expectant mother and her fetus, PA levels reportedly decrease as pregnancy progresses, with PA becoming shorter in duration, frequency, and intensity.52 Therefore, it is of particular importance that HCPs encourage and provide the following variables to improve PA participation:47 • Use motivational counseling such as the five A’s (ask, advise, assess, assist, and arrange). • Screen for barriers to PA. • Individualize activity prescription. • Measure PA intensity with the Talk Test or Borg Scale for moderate-​intensity PA as mentioned in Section 2.3.

2.4.3 Postpartum There is a paucity of research regarding the impacts of PA on postpartum recovery. Six guidelines from five countries (Australia, Canada, Norway, the United Kingdom, and the United States) recommended the following PA activities: aerobic (3/​6), pelvic floor exercise (3/​6), strengthening (2/​6), stretching (2/​6), and walking (2/​6).53

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Currently, the return to PA is largely left up to personal preference, with no guidelines being given for rehabilitation after childbirth. The American College of Obstetrics and Gynecology (ACOG) recommends that PA should resume as early as medically possible, depending on the mode of delivery and the presence of medical complications;47 however, there are no guidelines that specify different recommendations for women with vaginal delivery that require sutures.53 Australia, UK, and Norway provide similar nonspecific recommendations,53 which include initiating: • Pelvic floor exercises in the immediate postpartum period. • Abdominal strengthening exercises for addressing diastasis rectus abdominis and improving pelvic floor function.54,55 • Regular aerobic exercise. • PA in lactating women, which can improve maternal cardiovascular fitness without compromise of milk production, composition, or infant growth.56

2.4.4 Improving Postpartum PA Screening Health professionals should include assessment of postpartum health in all healthcare encounters, including well-​baby visits during the fourth trimester.57 Some of the inventories and suggested methods for doing this include:53 • Use the PA Readiness Medical Examination (PARmed-​X) for pregnancy. • Adapt a postpartum version of the tool to increase adherence and facilitate PA participation. • Start a low-​intensity PA program that includes walking, pelvic floor exercise, and abdominal exercise prior to the six-​week postpartum checkup.

2.4.5 Future Considerations Future research should investigate details on individualized prescription of optimal intensity level for PA and associated behavioral counseling methods in order to maximize benefits for expectant and new mothers and their offspring.47,53,91 In addition, research should seek to improve the evidence base concerning the effects of occupational PA on maternal-​fetal health, the effects of vigorous-​intensity exercise in the first and second trimesters, and the safety of exercise intensities that exceed the 90% maximum heart rate.47 If well-​researched guidelines for PA and rehabilitation exist for other orthopedic conditions, then it is feasible to suggest that guideline creation should be a priority for postpartum women, where the rate of experiencing pelvic floor and abdominal (diastasis rectus abdominis, or in 33% of American cases, Cesarean section) trauma alone is 100%.

2.5  OLDER HEALTHY WOMEN The key guidelines for older healthy women and men are identical (Table 2.1). However, aerobic activity and muscle strengthening are of additional importance with

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TABLE 2.5 Best Fit Activities for Older Healthy Women Moderate-​Intensity Activities

Best Fit Muscle Strengthening Activities

• Walking briskly (2.5 miles per hour or faster) • Recreational swimming • Bicycling slower than 10 miles per hour on level terrain • Tennis (doubles) • Active forms of yoga • Ballroom or line dancing • General yard work and home repair work • Exercise classes like water aerobics

• Yard work • Golf • Weight-​lifting, machines or hand-​held weights, or body weight activities such as Yoga or Pilates that include activities like planks, squats, lunges, etc. • Gardening if it includes digging and lifting • Housework if it includes lifting, stair climbing, and squatting • Tai Chi • Yoga • Pilates • Errands like grocery shopping if it includes lifting and carrying

Source: Piercy KL, Troiano RP, Ballard RM, et al. The physical activity guidelines for Americans. JAMA. 2018;320(19):2020.

respect to women’s health to prevent or address osteoporosis since incidence rates are higher for women. The non-​communicable disease (NCDs) section in supplemental materials will provide an overview of PA prescription in adult and older adult women with chronic or persistent conditions. See Table 2.5 for best fit examples of moderate-​ intensity aerobic physical activities for older women.1

2.5.1 Menopause Menopause, the cessation of regular menstruation, typically occurs between the ages of 49–​52 years, although it may be earlier in cases of gynecologic surgery or cancer treatment.58,59 There is a decreased quality of life reported due to the onset of menopausal symptoms, chronic diseases, and disability that occur during and after menopause.60 PA is commonly recommended to reduce menopausal symptoms and chronic diseases.61 However, most menopausal women do not meet PA guidelines.62 The decline in estrogen and other hormones at menopause often leads to vasomotor, psychological, somatic/​physical, and genitourinary symptoms.63,64 Vasomotor symptoms (VMS) are the most common and disruptive symptom during menopause and the most common reason for which women seek medical attention.65 Obesity and physical inactivity are risk factors for VMS.66 Despite the uncertainty about effectiveness of PA in improving VMS, there is abundant evidence that improving PA has many benefits for physical and psychological health.67,68 Due to fluctuations of hormones during the menopausal transition, women have significant increases in mood swings and risk of new-​onset depression.63,69 Depression, which is twice as common in women as in men, increases 2.5 times

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during menopause.70 Anxiety and depression can also cause a decline in cognitive performance and sleep disturbances even in the absence of hot flashes.63 Urinary incontinence (UI) affects about half of postmenopausal women.71,72 UI is linked to lower levels of PA in women and PA to reduce obesity and pelvic floor muscle strengthening can decrease symptoms.71,72,73 HCPs should also screen for UI symptoms, which negatively impact the quality of life and PA activity and adherence, as well as identify barriers to activity, help set realistic goals, and provide a comprehensive PA program that follows the PA guidelines (Table 2.6).

TABLE 2.6 Key Physical Activity Guidelines for Older Adults and Adults with Chronic Illnesses and/​or Disabilities Age Group

Physical Activity Guidelines

Older Adults

The key guidelines for adults also apply to older adults. In addition, the following key guidelines are just for older adults: • As part of their weekly physical activity, older adults should do multicomponent physical activity that includes balance training as well as aerobic and muscle-​strengthening activities. • Older adults should determine their level of effort for physical activity relative to their level of fitness. • Older adults with chronic conditions should understand whether and how their conditions affect their ability to do regular physical activity safely. • When older adults cannot do 150 minutes of moderate-​intensity aerobic activity a week because of chronic conditions, they should be as physically active as their abilities and conditions allow.

Adults with • Adults with chronic conditions or disabilities, who are able, should do Chronic Health at least 150 minutes (2 hours and 30 minutes) to 300 minutes (5 hours) a Conditions and/​ week of moderate-​intensity, or 75 minutes (1 hour and 15 minutes) to 150 or Disabilities minutes (2 hours and 30 minutes) a week of vigorous-​intensity aerobic physical activity, or an equivalent combination of moderate-​and vigorous-​ intensity aerobic activity. Preferably, aerobic activity should be spread throughout the week. • Adults with chronic conditions or disabilities, who are able, should also do muscle-​strengthening activities of moderate or greater intensity and that involve all major muscle groups on two or more days a week, as these activities provide additional health benefits. • When adults with chronic conditions or disabilities are not able to meet the above key guidelines, they should engage in regular physical activity according to their abilities and should avoid inactivity. • Adults with chronic conditions or symptoms should be under the care of a healthcare provider. People with chronic conditions can consult a healthcare professional or physical activity specialist about the types and amounts of activity appropriate for their abilities and chronic conditions. Source: Piercy KL, Troiano RP, Ballard RM, et al. The physical activity guidelines for Americans. JAMA. 2018;320(19):2020.

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Long-​term effects of estrogen deficiency from menopause include osteoporosis, osteoarthritis, cardiovascular disease (CVD), and changes in body composition.74 The three main causes of illness and disability for postmenopausal women are CVD, breast and colorectal cancer, and osteoporosis-​associated fractures.75 PA is beneficial in postmenopausal women for addressing pathophysiology of menopause-​related health problems.74 Weight gain and changes in body composition during and after menopause are common due to fat redistribution causing central adiposity and decreased lean body mass and muscle loss.74 This is of major concern because of the adverse effects of obesity on women’s health, especially risk of cardiovascular disease, metabolic disorders, and cancers.74,76 Regular PA can help prevent weight gain, improve body composition by increasing lean body mass, reduce body weight and body fat, and promote development of muscle strength and functional capacity.74 The most important benefit of regular exercise in postmenopausal women may be the prevention of heart disease, the number one cause of death in women.77,78 While premenopausal women typically have lower blood pressure than men, after menopause the prevalence of hypertension is higher in women, impacting three-​fourths of post-​menopausal women.79 Hypertension is the most important risk factor contributing to cardiovascular disease.80 Aerobic activity promotes cardiovascular and respiratory fitness and is an effective way for women to modify cardiac risk factors.81 Bone loss accelerates in menopause and estrogen deficiency is the primary factor interfering with normal bone remodeling that can lead to osteoporosis.82 Approximately half of women over the age of 50 years will fracture a bone because of osteoporosis and suffer considerable morbidity and indirect mortality.83 PA is an effective means to stimulate bone osteogenesis in woman with osteoporosis as well as increase bone mass and reduce the fracture risk in postmenopausal women.64,74,84 Aerobic activity, especially walking, provides minimal loading on the skeleton, which limits improving bone mass but is able to limit its progressive loss.64,74,84 Resistance training preferentially increases muscle and bone mass, promotes strength development, and improves functional capacity.64,74,84 Yoga and Pilates can also improve strength, balance, and flexibility. However, certain positions including flexion and rotation may not be safe and need to be modified for people with osteoporosis.84,85 A comprehensive evaluation including muscle strength, range of motion, balance, gait, cardiopulmonary function, comorbidities, bone density, history of previous fractures, and the risk of falling needs to be completed first in order to provide an appropriate PA prescription.84,85 High-​impact activities that are effective in increasing bone mass in young women may not be indicated for some elderly women with osteoporosis.84,85 Menopause is associated with the onset and progression of osteoarthritis (OA) in women and the leading cause of physical disability in the United States.86,87 There is a higher prevalence of OA in women especially in the knee.86,87 Joint aches and pain are a commonly (50–​60%) reported symptom among women during menopause.63 A combination of aerobic and strength PA is indicated to improve pain and function and decrease weight; however, optimal prescription should be individualized.86,87

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The onset of menopause offers a unique opportunity to improve overall health and longevity. For many women, menopause can be a difficult physiological and psychological transition.63,79,88 HCPs can assist by offering more information on menopause transition and via supporting and encouraging regular PA.88 Many patients prefer PA as a first option to treat menopausal symptoms.88 The most common barrier to PA adherence for menopausal women is time.88 The establishment of a daily structure that incorporates PA, anticipation of positive feelings associated with exercise, and accountability to others are the cited factors to best promote PA adherence.88

2.6  CONCLUSION Few policies and little research exist on sex and gender-​based guidelines for PA across the lifespan, especially for NCDs.89,90 However, gender is a known critical social determinant of health. Policies and evidence-​based interventions that address the gender gap in PA would be expected to have a substantial impact on overall population health and to improve women’s health, opportunities, and equality.33,91 For additional reading, see supplementary material.

REFERENCES 1. Piercy KL, Troiano RP, Ballard RM, et al. The physical activity guidelines for Americans. JAMA. 2018;320(19):2020. https://​jamanetwork.com/​journals/​jama/​ fullarticle/​2712935 2. CDC. Benefits of physical activity. Centers for Disease Control and Prevention. Published September 11, 2020. Accessed February 4, 2021. www.cdc.gov/​ physicalactivity/​basics/​pa-​health/​index.htm 3. WHO | Physical Activity. WHO. Published November 26, 2020. Accessed February 23, 2021 www.who.int/​news-​room/​fact-​sheets/​detail/​physical-​activity 4. Hörder H, Johansson L, Guo X, Grimby G, Kern S, Skoog I. Author response: Midlife cardiovascular fitness and dementia: A 44-​year longitudinal population study in women. Neurology. 2018;91(16):763–​763. https://​pubmed.ncbi.nlm.nih.gov/​29540588/​ 5. Evenson KR, Mottola MF, Artal R. Review of recent physical activity guidelines during pregnancy to facilitate advice by health care providers. Obstet Gynecol Surv. 2019;74(8):481–​489. https://​pubmed.ncbi.nlm.nih.gov/​31418450/​ 6. Berghella V, Saccone G. Exercise in pregnancy! Am J Obstet Gynecol. 2017;216(4):335–​ 337. www.ajog.org/​article/​S0002-​9378(17)30130-​8/​fulltext 7. Magro-​Malosso ER, Saccone G, Di Mascio D, Di Tommaso M, Berghella V. Exercise during pregnancy and risk of preterm birth in overweight and obese women: A systematic review and meta-​analysis of randomized controlled trials. Acta Obstet Gynecol Scand. 2017;96(3):263–​273. https://​obgyn.onlinelibrary.wiley.com/​doi/​abs/​10.1111/​ aogs.13087 8. Shakeel N, Richardsen KR, Martinsen EW, Eberhard-​Gran M, Slinning K, Jenum AK. Physical activity in pregnancy and postpartum depressive symptoms in a multiethnic cohort. J Affect Disord. 2018;236:93–​100. https://​pubmed.ncbi.nlm.nih.gov/​ 29723768/​ 9. WHO. Global action plan on physical activity 2018–​2030: More active people for a healthier world. June 2018. https://​apps.who.int/​iris/​bitstream/​handle/​10665/​272722/​ 9789241514187-​eng.pdf

56

56

Ginger Garner and Wendy Farnen Price 10. Lee J, Dunlop D, Ehrlich-​Jones L, et al. The public health impact of risk factors for physical inactivity in adults with rheumatoid arthritis. Arthritis Care Res. 2012;64(4):488–​493. https://​onlinelibrary.wiley.com/​doi/​abs/​10.1002/​acr.21582 11. Bonita R, Beaglehole R. Women and NCDs: Overcoming the neglect. Glob Health Action. 2014;7. www.tandfonline.com/​doi/​full/​10.3402/​gha.v7.23742 12. Golightly YM. Physical activity as a vital sign: A systematic review. Prev Chronic Dis. 2017;14. www.cdc.gov/​pcd/​issues/​2017/​17_​0030.htm. 13. Bowen PG, Mankowski RT, Harper SA, Buford TW. Exercise is medicine as a vital sign: Challenges and opportunities. Transl J Am Coll Sports Med. 2019;4(1):1–​7. https://​pubmed.ncbi.nlm.nih.gov/​30828640/​ 14. Sallis R. Exercise is medicine: A call to action for physicians to assess and prescribe exercise. Phys Sportsmed. 2015;43(1):22–​26. www.tandfonline.com/​doi/​full/​10.1080/​ 00913847.2015.1001938 15. Tuso P. Strategies to increase physical activity. Perm J. 2015;19(4):84–​88. http://​ www.thepermanentejournal.org/​issues/​2015/​fall/​5942-​physical-​activity.html 16. Moreno JP, Johnston CA. Barriers to physical activity in women. Am J Lifestyle Med. 2014;8(3):164–​166. http://​journals.sagepub.com/​doi/​10.1177/​1559827614521954 17. Hall KS, McAuley E. Individual, social environmental and physical environmental barriers to achieving 10 000 steps per day among older women. Health Educ Res. 2010;25(3):478–​488. https://​academic.oup.com/​her/​article/​25/​3/​478/​654736. 18. CDC. Overcoming barriers to physical activity. Centers for Disease Control and Prevention. Published September 17, 2020. Accessed November 16, 2020. www.cdc.gov/​physicalactivity/​basics/​adding-​pa/​barriers.html 19. Rogers LQ, Gutin B, Humphries MC, et al. A physician fitness program: Enhancing the physician as an “exercise” role model for patients. Teach Learn Med. 2005;17(1):27–​ 35. www.tandfonline.com/​doi/​abs/​10.1207/​s15328015tlm1701_​6 20. Lobelo F, de Quevedo IG. The evidence in support of physicians and health care providers as physical activity role models. Am J Lifestyle Med. 2014;10(1):36–​52. https://​journals.sagepub.com/​doi/​10.1177/​1559827613520120. 21. Falahee ML, Benkert R, George NM, Hartlieb KB, Cederna J. Motivational interviewing to increase physical activity in underserved women. J Nurse Pract. 2016;12(10):704–​ 709. www.sciencedirect.com/​science/​article/​abs/​pii/​S1555415516306262 22. Exercise is medicine. Published November 16, 2020. Accessed November 16, 2020. www.exerciseismedicine.org/​support_​page.php/​provider-​action-​guide/​ 23. Avoid chronic disease with regular physical activity. American Physical Therapy Association. Published November 14, 2018. Accessed November 16, 2020. www.choosept.com/​resources/​detail/​avoid-​chronic-​disease-​with-regular-​physicalactivi 24. CDC. Move more; sit less. Centers for Disease Control and Prevention. Published October 7, 2020. Accessed November 16, 2020. www.cdc.gov/​physicalactivity/​basics/​ adults/​index.htm 25. Kohl HW III, Cook HD, Environment C on PA and PE in the S, Board F and N, Medicine I of. Physical Activity and Physical Education: Relationship to Growth, Development, and Health. National Academies Press (US); 2013. Accessed November 16, 2020. www.ncbi.nlm.nih.gov/​books/​NBK201497/​ 26. CDC. Childhood overweight and obesity | overweight & obesity. Published February 7, 2019. Accessed November 24, 2020. www.cdc.gov/​obesity/​childhood/​index.html 27. ACOG Committee Opinion No. 651: Menstruation in girls and adolescents: Using the menstrual cycle as a vital sign. Obstet Gynecol. 2015 Dec;126(6):e143–​e146. https://​ journals.lww.com/​greenjournal/​Fulltext/​2015/​12000/​Committee_​Opinion_​No_​_​651_​ _​Menstruation_​in_​Girls.59.aspx

57

Physical Activity for Women

57

28. Daley, A.J. Exercise and Primary Dysmenorrhoea. Sports Med 38, 659–​670 (2008). https://​link.springer.com/​article/​10.2165%2F00007256-​200838080-​00004 29. Yaşa C, Güngör Uğurlucan F. Approach to abnormal uterine bleeding in adolescents. J Clin Res Pediatr Endocrinol. 2020;12(Suppl 1):1–​6. https://​pubmed.ncbi.nlm.nih.gov/​ 32041387/​ 30. Rupa VK, Veena KS, Subitha L, Hemanth Kumar VR, Bupathy AB. Menstrual abnormalities in school going girls –​Are they related to dietary and exercise pattern? J Clin Diagn Res JCDR. 2013;7(11):2537–​2540. https://​pubmed.ncbi.nlm.nih.gov/​ 24392394 31. Hashim MS, Obaideen AA, Jahrami HA, et al. Premenstrual syndrome is associated with dietary and lifestyle behaviors among university students: A cross-​sectional study from Sharjah, UAE. Nutrients. 2019;11(8). https://​pubmed.ncbi.nlm.nih.gov/​ 31426498/​ 32. Staurowsky EJ, Watanabe N, Cooper J, Cooky C, Lough N, Paule-​Koba A, … Snyder M. (2020). Chasing Equity: The Triumphs, Challenges, and Opportunities in Sports for Girls and Women. New York, NY: Women’s Sports Foundation. Retrieved from www.womenssportsfoundation.org/​wp-​content/​uploads/​2020/​01/​Chasing-​Equity-​ Full-​Report-​Web.pdf.org/​sites/​default/​files/​Girls.pdf 33. Guthold R, Stevens GA, Riley LM, Bull FC. Global trends in insufficient physical activity among adolescents: A pooled analysis of 298 population-​ based surveys with 1.6 million participants. Lancet Child Adolesc Health. 2020;4(1):23–​35. www.thelancet.com/​journals/​lanchi/​article/​PIIS2352-​4642(19)30323-​2/​fulltext 34. Health TLP. Time to tackle the physical activity gender gap. Lancet Public Health. 2019;4(8):e360. https://​pubmed.ncbi.nlm.nih.gov/​31345750/​ 35. Edwards ES, Sackett SC. Psychosocial variables related to why women are less active than men and related health implications. Clin Med Insights Womens Health. 2016;9(Suppl 1):47–​56. https://​journals.sagepub.com/​doi/​10.4137/​CMWH. S34668. 36. History of Title IX. Women’s Sports Foundation. Accessed September 25, 2020. www.womenssportsfoundation.org/​advocacy/​history-​of-​title-​ix/​ 37. Nazem TG, Ackerman KE. The female athlete triad. Sports Health. 2012;4(4):302–​ 311. http://​journals.sagepub.com/​doi/​10.1177/​1941738112439685 38. McClure SK, Adams JE, Dahm DL. Common musculoskeletal disorders in women. Mayo Clin Proc. 2005;80(6):796–​802. doi:10.4065/​80.6.796. www. mayoclinicproceedings.org/​article/​S0025-​6196(11)61534-​6/​abstract 39. Sommerfield LM, Harrison CB, Whatman CS, Maulder PS. A prospective study of sport injuries in youth females. Phys Ther Sport. 2020;44:24–​32. www.sciencedirect.com/​ science/​article/​abs/​pii/​S1466853X1930392X 40. Meczekalski B, Katulski K, Czyzyk A, Podfigurna-​ Stopa A, Maciejewska-​ Jeske M. Functional hypothalamic amenorrhea and its influence on women's health. J Endocrinol Invest. 2014;37(11):1049–​1056. doi:10.1007/​s40618-​014-​0169-​341. 41. Strath Scott J., Kaminsky Leonard A., Ainsworth Barbara E., et al. Guide to the assessment of physical activity: Clinical and research applications. Circulation. 2013;128(20):2259–​ 2279. www.ahajournals.org/​doi/​10.1161/​01.cir.0000435708.67487.da 42. Measuring physical activity intensity | physical activity | CDC. Published September 17, 2020. Accessed November 20, 2020. www.cdc.gov/​physicalactivity/​basics/​ measuring/​index.html 43. Golightly YM. Physical activity as a vital sign: A systematic review. Prev Chronic Dis. 2017;14. www.cdc.gov/​pcd/​issues/​2017/​17_​0030.htm 44. Hill B, Skouteris H, Teede HJ, et al. Health in preconception, pregnancy and postpartum global alliance: International network preconception research priorities for the

58

58

Ginger Garner and Wendy Farnen Price prevention of maternal obesity and related pregnancy and long-​term complications. J Clin Med. 2019;8(12). www.mdpi.com/​2077-​0383/​8/​12/​2119 45. Harrison CL, Brown WJ, Hayman M, Moran LJ, Redman LM. the role of physical activity in preconception, pregnancy and postpartum health. Semin Reprod Med. 2016;34(2):e28–​e37. https://​pubmed.ncbi.nlm.nih.gov/​27169984/​ 46. Oliveira C, Imakawa TDS, Moisés ECD. Physical activity during pregnancy: Recommendations and assessment tools. Rev Bras Ginecol E Obstet Rev Fed Bras Soc Ginecol E Obstet. 2017;39(8):424–​432. https://​pubmed.ncbi.nlm.nih.gov/​2878 3859/​ 47. Physical activity and exercise during pregnancy and the postpartum period: ACOG Committee opinion, Number 804. Obstet Gynecol. 2020;135(4):e178. https://​ journals.lww.com/​ g reenjournal/​ F ulltext/​ 2 020/ ​ 0 4000/ ​ P hysical_ ​ A ctivity_ ​ a nd_​ Exercise_​During_​Pregnancy.61.aspx 48. Flannery C, Fredrix M, Olander EK, McAuliffe FM, Byrne M, Kearney PM. Effectiveness of physical activity interventions for overweight and obesity during pregnancy: A systematic review of the content of behaviour change interventions. Int J Behav Nutr Phys Act. 2019;16(1):97. https://​ijbnpa.biomedcentral.com/​articles/​ 10.1186/​s12966-​019-​0859-​5. 49. Mottola MF, Davenport MH, Ruchat S-​M, et al. 2019 Canadian guideline for physical activity throughout pregnancy. Br J Sports Med. 2018;52(21):1339–​1346. https://​ bjsm.bmj.com/​content/​52/​21/​1339 50. Wang S-​M, Dezinno P, Maranets I, Berman MR, Caldwell-​Andrews AA, Kain ZN. Low back pain during pregnancy: Prevalence, risk factors, and outcomes. Obstet Gynecol. 2004;104(1):65–​70. https://​pubmed.ncbi.nlm.nih.gov/​15229002/​ 51. McCall C, Grimes D, Lyerly A. “Therapeutic” bed rest in pregnancy: Unethical and unsupported by data. Obstet Gynecol. 2013;121(6):1305–​1308. https://​ pubmed.ncbi.nlm.nih.gov/​23812466/​ 52. Forczek W, Curyło M, Forczek B. Physical activity assessment during gestation and its outcomes: A review. Obstet Gynecol Surv. 2017;72(7):425–​444. https://​ pubmed.ncbi.nlm.nih.gov/​28715061/​ 53. Evenson KR, Mottola MF, Owe KM, Rousham EK, Brown WJ. Summary of international guidelines for physical activity after pregnancy. Obstet Gynecol Surv. 2014;69(7):407–​414. https://​pubmed.ncbi.nlm.nih.gov/​25112589/​ 54. Mota P, Pascoal AG, Carita AI, Bø K. The immediate effects on inter-​rectus distance of abdominal crunch and drawing-​in exercises during pregnancy and the postpartum period. J Orthop Sports Phys Ther. 2015;45(10):781–​788. www.jospt.org/​doi/​abs/​ 10.2519/​jospt.2015.5459 55. Sancho MF, Pascoal AG, Mota P, Bø K. Abdominal exercises affect inter-​ rectus distance in postpartum women: A two-​ dimensional ultrasound study. Physiotherapy. 2015;101(3):286–​291. www.physiotherapyjournal.com/​article/​S0031-​ 9406(15)03778-​5/​abstract 56. Cary GB, Quinn TJ. Exercise and lactation: Are they compatible? Can J Appl Physiol Rev Can Physiol Appl. 2001;26(1):55–​75. https://​pubmed.ncbi.nlm.nih.gov/​ 11173670/​ 57. Sword W, Watt S. Learning needs of postpartum women: Does socioeconomic status matter? Birth Berkeley Calif. 2005;32(2):86–​92. https://​pubmed.ncbi.nlm.nih.gov/​ 15918864/​ 58. Schoenaker DAJM, Jackson CA, Rowlands JV, Mishra GD. Socioeconomic position, lifestyle factors and age at natural menopause: A systematic review and meta-​analyses

59

Physical Activity for Women

59

of studies across six continents. Int J Epidemiol. 2014;43(5):1542–​1562. https://​ academic.oup.com/​ije/​article/​43/​5/​1542/​695928 59. The menopause years. Accessed November 22, 2020. www.acog.org/​Womens Health/​ FAQs/​The Menopause Years 60. Mohammadalizadeh Charandabi S, Rezaei N, Hakimi S, et al. Quality of life of postmenopausal women and their spouses: A community-​ based study. Iran Red Crescent Med J. 2015;17(3). https://​sites.kowsarpub.com/​ircmj/​articles/​16447.html 61. Dąbrowska-​Galas M, Dąbrowska J, Ptaszkowski K, Plinta R. High physical activity level may reduce menopausal symptoms. Medicina (Mex). 2019;55(8). www.mdpi.com/​ 1010-​660X/​55/​8/​466 62. Pettee Gabriel K, Mason JM, Sternfeld B. Recent evidence exploring the associations between physical activity and menopausal symptoms in midlife women: Perceived risks and possible health benefits. Womens Midlife Health. 2015;1(1):1. https://​ womensmidlifehealthjournal.biomedcentral.com/ ​ a rticles/ ​ 1 0.1186/s40695015-​0004-​9 63. Santoro N, Epperson CN, Mathews SB. Menopausal symptoms and their management. Endocrinol Metab Clin North Am. 2015;44(3):497–​515. https://​ pubmed.ncbi.nlm.nih.gov/​26316239/​ 64. Grindler NM, Santoro NF. Menopause and exercise. Menopause. 2015;22(12):1351–​ 1358. https://​pubmed.ncbi.nlm.nih.gov/​26382311/​ 65. Avis NE, Crawford SL, Green R. Vasomotor symptoms across the menopause transition: Differences among women. Obstet Gynecol Clin North Am. 2018;45(4):629–​640. https://​pubmed.ncbi.nlm.nih.gov/​30401547/​ 66. Koo S, Ahn Y, Lim J-​Y, Cho J, Park H-​Y. Obesity associates with vasomotor symptoms in postmenopause but with physical symptoms in perimenopause: A cross-​sectional study. BMC Womens Health. 2017;17. https://​bmcwomenshealth.biomedcentral.com/​ articles/​10.1186/​s12905-​017-​0487-​7 67. Atapattu P. Vasomotor symptoms: What is the impact of physical exercise? J South Asian Fed Menopause Soc. 2015;3:15–​19. www.researchgate.net/​publication/​ 312666989_​Vasomotor_​Symptoms_​What_​is_​the_​Impact_​of_​Physical_​Exercise 68. Daley A, Stokes-​ Lampard H, Thomas A, MacArthur C. Exercise for vasomotor menopausal symptoms. Cochrane Database Syst Rev. 2014;11:CD006108. www.cochranelibrary.com/​cdsr/​doi/​10.1002/​14651858.CD006108.pub4/​abstract 69. Bromberger JT, Kravitz HM. Mood and menopause: Findings from the study of women’s health across the nation (SWAN) over ten years. Obstet Gynecol Clin North Am. 2011;38(3):609–​625. https://​pubmed.ncbi.nlm.nih.gov/​21961723/​ 70. Clayton AH, Ninan PT. Depression or menopause? Presentation and management of major depressive disorder in perimenopausal and postmenopausal women. Prim Care Companion J Clin Psychiatry. 2010;12(1). https://​pubmed.ncbi.nlm.nih.gov/​ 20582297/​ 71. Kołodyńska G, Zalewski M, Rożek-​ Piechura K. Urinary incontinence in postmenopausal women –​causes, symptoms, treatment. Przegla̜d Menopauzalny Menopause Rev. 2019;18(1):46–​50. https://​pubmed.ncbi.nlm.nih.gov/​31114458/​ 72. Markland AD, Richter HE, Fwu C-​W, Eggers P, Kusek JW. Prevalence and trends of urinary incontinence in adults in the United States, 2001 to 2008. J Urol. 2011;186(2):589–​593. https://​pubmed.ncbi.nlm.nih.gov/​21684555/​ 73. Involuntary urinary incontinence can discourage sufferers from exercise. ScienceDaily. Published February 27, 2017.Accessed November 22, 2020. www.sciencedaily.com/​ releases/​2017/​02/​170227082742.htm

60

60

Ginger Garner and Wendy Farnen Price 74. Atapattu PM, Fern D, Wasalathanthri S, Silva AD. Menopause and exercise: Linking pathophysiology to effects. Arch Med. 2015;7(1). www.archivesof medicine.com/​m edicine/​m enopause-​a nd-​exercise-​l inking-​p athophysiology-to-​ effects.php?aid=7062 75. Largest women’s health prevention study ever. womenshealth.gov. Published August 16, 2017. Accessed November 22, 2020. www.womenshealth.gov/​30-​achievements/​25 76. Greendale GA, Sternfeld B, Huang M, et al. Changes in body composition and weight during the menopause transition. JCI Insight. 4(5). https://​insight.jci.org/​articles/​view/​ 124865 77. Buttar HS, Li T, Ravi N. Prevention of cardiovascular diseases: Role of exercise, dietary interventions, obesity and smoking cessation. Exp Clin Cardiol. 2005;10(4):229–​249. https://​pubmed.ncbi.nlm.nih.gov/​19641674/​ 78. CDC. Women and heart disease. Centers for Disease Control and Prevention. Published January 31, 2020. Accessed November 23, 2020. www.cdc.gov/​heartdisease/​ women.htm 79. Lima R, Wofford M, Reckelhoff JF. Hypertension in postmenopausal women. Curr Hypertens Rep. 2012;14(3):254–​260. https://​link.springer.com/​article/​10.1007/​ s11906-​012-​0260-​0 80. CDC. Heart disease facts | cdc.gov. Centers for Disease Control and Prevention. Published September 8, 2020. Accessed November 13, 2020. https://​www.cdc.gov/​ heartdisease/​facts.htm 81. Pinckard K, Baskin KK, Stanford KI. Effects of exercise to improve cardiovascular health. Front Cardiovasc Med. 2019;6. www.frontiersin.org/​articles/​10.3389/​ fcvm.2019.00069/​full 82. Tella SH, Gallagher JC. Prevention and treatment of postmenopausal osteoporosis. J Steroid Biochem Mol Biol. 2014;142:155–​170. www.ncbi.nlm.nih.gov/​pmc/​articles/​ PMC4187361/​ 83. Nazrun AS, Tzar MN, Mokhtar SA, Mohamed IN. A systematic review of the outcomes of osteoporotic fracture patients after hospital discharge: Morbidity, subsequent fractures, and mortality. Ther Clin Risk Manag. 2014;10:937–​948. www.dovepress.com/ ​ a - ​ s ystematic- ​ r eview- ​ o f- ​ t he- ​ o utcomes- ​ o fnbsposteoporotic-​ fracture-​patien-​peer-​reviewed-​article-​TCRM 84. Benedetti MG, Furlini G, Zati A, Letizia Mauro G. The effectiveness of physical exercise on bone density in osteoporotic patients. BioMed Res Int. 2018;2018. www.hindawi.com/​journals/​bmri/​2018/​4840531/​ 85. Mishra N, Mishra VN, Devanshi. Exercise beyond menopause: Dos and don’ts. J -​ Life Health. 2011;2(2):51–​56. www.jmidlifehealth.org/​article.asp?issn=0976-​ 7800;year=2011;volume=2;issue=2;spage=51;epage=56;aulast=Mishra 86. Mahajan A, Patni R. Menopause and osteoarthritis: Any association? J -​Life Health. 2018;9(4):171–​172. https://​pubmed.ncbi.nlm.nih.gov/​30692810/​ 87. Stevens-​ Lapsley JE, Kohrt WM. Osteoarthritis in women: Effects of estrogen, obesity and physical activity. Women’s Health. 2010;6(4):601–​615. http://​ journals.sagepub.com/​doi/​10.2217/​WHE.10.38 88. Thomas A, Daley AJ. Women’s views about physical activity as a treatment for vasomotor menopausal symptoms: A qualitative study. BMC Womens Health. 2020;20(1):203. https://​bmcwomenshealth.biomedcentral.com/​articles/​10.1186/​ s12905-020-​01063-​w

61

Physical Activity for Women

61

89. WHO | NCD and women. WHO. Published November 16, 2020. Accessed November 16, 2020. www.who.int/​global-​coordination-​mechanism/​ncd-​themes/​NCD-​and-​women/​en/​ 90. Francesca B, Monica A, Valeria C. Gender-​ based approaches for the prevention and control of noncommunicable diseases. Stroke. 2018;49(12):2810–​2811. www.ahajournals.org/​doi/​10.1161/​STROKEAHA.118.023633 91. Beagley J. The other 49.6% -​why gender parity is vital for women’s health. NCD Alliance. Published March 8, 2016. Accessed November 15, 2020. https://​ ncdalliance.org/​n ews- ​ events/ ​ b log/ ​ t he- ​o ther- ​4 96- ​w hy- ​ g ender- ​ p arity- ​ i s- ​v italfor-​womens-​health

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Sleep and Women’s Health Cindy Geyer, MD Ultrawellness Center Lenox, MA

3.1 Introduction......................................................................................................64 3.2 Overview of Sleep Physiology and Circadian Biology....................................64 3.2.1 Sleep Need and Circadian Processes....................................................64 3.2.2 Sleep Stages..........................................................................................65 3.2.3 Obstructive Sleep Apnea and Upper Airway Resistance in Women..............................................................................................65 3.3 Relationship Between Sleep and Health Outcomes.........................................66 3.3.1 Sleep, Weight, and Cardiometabolic Risk............................................66 3.3.2 Sleep, Inflammation, and Immunity.....................................................67 3.3.3 Sleep and Mood....................................................................................67 3.3.4 Sleep, Sex Hormones, and Gender.......................................................68 3.4 Sleep and Other Lifestyle Medicine Pillars......................................................68 3.4.1 Diet and Sleep......................................................................................68 3.4.2 Exercise and Sleep................................................................................69 3.5 Sleep and Life Stages in Women......................................................................69 3.5.1 Adolescents and Teenagers..................................................................69 3.5.2 Menstrual Cycles and Sleep.................................................................72 3.5.3 Pregnancy and Sleep............................................................................72 3.5.4 Mothers of Young Children..................................................................73 3.5.5 Sleep and the Menopause Transition....................................................73 3.6 Conclusions......................................................................................................74

KEY POINTS • Quality, quantity, and timing of sleep impact health outcomes in a bidirectional relationship. • Hormonal fluctuations, life stages, caregiving responsibilities, and gender-​ related factors can negatively impact sleep in women. • Both insomnia and restless leg syndrome are more common in women. • There is a bidirectional relationship between sleep and diet: improving diet quality may improve sleep and ensuring adequate restorative sleep may support people’s ability to choose more nutritious food. DOI: 10.1201/9781003110682-4

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• Sleep apnea may present differently in women and frequently goes undiagnosed. Because of its negative impact on cardiometabolic health and pregnancy outcomes, early recognition, referral and treatment for sleep apnea may improve women’s health as well as the health of their children.

3.1  INTRODUCTION There has been an important paradigm shift regarding sleep: in the past it was often viewed as “wasted time,” and growing evidence now underscores how sleep quantity, quality, and timing directly impact every aspect of our physiology, health, and well-​ being. Women face unique challenges regarding sleep which can be related to biologic differences and/​or gender factors, including behaviors, expectations, attitudes and expressions that are socially, culturally and personally defined and exist along a continuum.1 For example: • Fluctuating hormones during puberty, menstrual cycles, pregnancy, and the menopause transition can impact sleep quality.2,3,4 • Both insomnia and restless leg syndrome (RLS, or Willis Ekbom disease) are more prevalent in women.5,6 • Caregiving demands (infants, children, and aging parents), often higher for women, can negatively impact sleep.7 • Women are more likely to experience intimate partner violence and sexual harassment in the workplace, both of which can adversely impact sleep quality, including insomnia and nightmares.8,9 • Obstructive sleep apnea (OSA) is often overlooked in women. Contributing factors include clinician stereotypes as well as differences in the phenotype and clinical presentation of sleep apnea in women.10 This chapter will outline normal sleep physiology and circadian biology, describe the bidirectional relationship between sleep and women’s health outcomes, review the impact of sex hormones and gender on sleep, and outline practical lifestyle strategies to address sleep concerns throughout a woman’s lifespan.

3.2  OVERVIEW OF SLEEP PHYSIOLOGY AND CIRCADIAN BIOLOGY 3.2.1 Sleep Need and Circadian Processes Sleep is influenced by a homeostatic process, sleep need, and a circadian process that influences alertness and sleep urge.11 The suprachiasmatic nucleus (SCN, or “master clock”) in the brain is impacted both by one’s genetic chronotype and by external factors (“zeitgebers” or “time givers”), especially light exposure. The SCN influences other “clocks” in the brain, organs and cells to coordinate biology and behavior on approximately a 24-​hour cycle. The SCN influences temperature regulation in the hypothalamus, as well as the hypothalamic/​pituitary/​adrenal (HPA) axis in part through neuronal projections. Cortisol, insulin, and growth hormone are examples of

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hormones that are entrained in a diurnal pattern and variably influenced by light and sleep activity.12 Peripheral clocks are independently influenced by other zeitgebers such as exercise (skeletal muscle and lung clocks) and food intake (liver, kidney, heart, and pancreas clocks).13 The complex mechanisms of communication that coordinate the central, peripheral and cellular clocks are not completely understood. However, mounting evidence links inconsistent and fluctuating timing of sleep/​wake cycles, irregular eating schedules, and dysregulated circadian rhythms with elevated risks of insulin resistance, overweight, and obesity.14

3.2.2 Sleep Stages Sleep is divided into non-​rapid eye movement (non-​REM) and REM sleep stages. Non-​REM sleep is further divided into stages 1, 2, and 3. Normal sleep is comprised of 4–​6 cycles through the different stages of sleep. Stage 1, the “dozing off” period, usually lasts for 1–​5 minutes. Stage 2, or light sleep, makes up about 50% of total sleep time and is characterized by a slowing of brain activity; reduction in body temperature, breathing, and heart rate; and relaxation of muscles. Stage 3 is the deepest sleep, normally 20% of total sleep time, characterized by further muscle relaxation and slowing of heart rate and breathing. Stage 3 is more prevalent in the first half of the night, reduces homeostatic sleep drive, and is involved in memory consolidation, insight and creativity.15 Slow-​wave sleep in stage 3 affects fluid dynamics in the cerebrospinal fluid, increasing flow through the glymphatic system that regulates removal of amyloid-​beta and tau.16 Each sleep cycle usually concludes with time in REM, with increasing time in REM the second half of the night. During REM, brain activity picks up while muscles lose their tone (except the eyes and diaphragm). REM plays a role in memory consolidation and motor function.

3.2.3 Obstructive Sleep Apnea and Upper Airway Resistance in Women Sleep apnea, often viewed as a condition predominantly impacting overweight men, may be undiagnosed in women. Screening questionnaires such as the STOP Bang, designed for men, are less sensitive for women,17 while women with sleep apnea report lower scores on the Epworth Sleepiness Scale. Women with OSA are more likely than men to present with daytime symptoms such as fatigue, depression, and fibromyalgia as opposed to nocturnal gasping, choking, or increased urination.10 Women are more likely to deny or underestimate snoring, potentially lowering both their own and their clinicians’ awareness of the possibility of OSA.18 The most common phenotypic expression of sleep disordered breathing (SDB) in women is upper airway resistance syndrome (UARS), characterized by prolonged upper airway obstruction or increased respiratory resistance coupled with respiratory event-​ related arousals (RERAs, detectable by electroencephalogram [EEG] monitoring) without significant hypopnea or desaturation. UARS may be missed with home studies that rely on oxygen desaturation or airflow limitations, although peripheral artery tonometry may be more sensitive.19,20 UARS is associated with a significantly increased risk of hypertension, and patients experience daytime fatigue equal to that seen in patients with more severe OSA and a higher apnea hypopnea

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index (AHI).21,22 Despite improvement in UARS with positive airway pressure (PAP) therapy, insurance will not cover the cost of treatment in the absence of an elevated AHI. Because of the muscle paralysis during REM sleep, OSA may be isolated to or significantly worsened during REM sleep. This pattern, also more common in women, is not without risk.23 REM-​isolated OSA is correlated with hypertension, atherosclerosis, and adverse cardiovascular outcomes.24,25 As many as a third of women with polycystic ovarian syndrome (PCOS) have OSA, and prevalence increases with increasing age and higher weight.26,27 The relationship between PCOS and OSA is likely bidirectional. Elevated testosterone may contribute to the development of apnea, and levels correlate with AHI independent of weight in women with PCOS.28 In turn, sleep apnea contributes to oxidative stress, inflammation, insulin resistance, and sympathetic activation, which negatively impact ovarian function.29 It is important for Lifestyle Medicine practitioners to have a high index of suspicion for possible OSA or UARS in women with fatigue, depression, fibromyalgia, PCOS, hypertension or cardiometabolic risk factors. Referral for a full attended overnight polysomnogram (PSG) may be indicated even with a negative home study. Weight loss in women who are overweight may help reduce respiratory events.30 Evaluation of the upper airway by an otolaryngologist, increasing the potency of the upper airway by using intranasal silicone dilators,31 treating existing nasal congestion with nasal saline irrigation or intranasal steroids, and positional therapy are options to consider. A mandibular advancement device has been shown to reduce RERAs, improve sleep quality, and benefit daytime focus and depression.32,33

3.3  RELATIONSHIP BETWEEN SLEEP AND HEALTH OUTCOMES 3.3.1 Sleep, Weight, and Cardiometabolic Risk There is evidence of a bidirectional relationship between sleep disruption (such as SDB, short sleep times, and disrupted circadian rhythms) and weight gain and cardiometabolic risk. Sleep apnea increases chronic systemic inflammation, an important driver of both insulin resistance and cardiovascular risk.34 This association is stronger in women35 and in people reporting subjective social isolation.36 Under conditions of sleep deprivation, executive functioning in the brain is downregulated, coupled with an increase in emotional and impulsive decision-​making,37,38 higher levels of the “hunger hormone” ghrelin, lower levels of the “satiety” hormone leptin, and higher cortisol, insulin, and glucose.39 This combination contributes to a preference for energy-​dense foods and higher overall calorie intake. Small studies in healthy non-​overweight adults have shown increased intake of total calories, saturated fat, and late night eating after several days of sleep deprivation.40 Repeated patterns of recovery sleep during the weekend followed by sleep deprivation during the week did not reverse the resulting decrease in whole body, hepatic and muscle insulin sensitivity and increase in body weight.41 Resulting weight gain can then increase the risk of sleep apnea or worsen existing apnea, perpetuating the cycle.

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3.3.2 Sleep, Inflammation, and Immunity There is also crosstalk between sleep and immune function. The inflammatory response seen in acute bacterial or viral illness can both increase sleep duration and intensity, and also disrupt sleep. Increase in sleep in turn improves immunologic response to infection.42 Good quality and adequate quantity of sleep have been associated with reduced risk of infection43 and improved response to vaccinations.44,45 Autoimmune disorders, which are more prevalent in women, are associated with higher risk of OSA. Multiple sclerosis, psoriasis, and rheumatoid arthritis are associated with higher risk of restless leg syndrome.46 The inflammation and pain common in autoimmune conditions can independently disrupt sleep quality. In a prospective study in Taiwan, non-​apnea sleep disorders increased the risk of future development of numerous autoimmune conditions.47 Another prospective study in patients with rheumatoid arthritis found that one night of partial sleep deprivation exacerbated fatigue, depression, and pain.48 In animal models, melatonin has been shown to modulate some of the effects of sleep on autoimmunity: mechanisms include the impact of melatonin on reducing inflammatory cytokines such as TNF alpha, IL beta, IL-​6, and NK Kappa-​B; regulation of nitric oxide; and modulation of TH1/​TH2 balance.49 Sleep disruption may be a stronger predictor of pain than pain is of sleep disruption, and this association is stronger for women than men.50,51,52 A 10-​year prospective study of Norwegian women found that poor subjective quality of sleep increased the likelihood of a subsequent diagnosis of fibromyalgia (odds ratio of 5.41 for older women).53 Sleep disturbance was associated with greater knee pain severity and more painful sites in both men and women, with and without radiographic evidence of knee osteoarthritis.54

3.3.3 Sleep and Mood Understanding the overlapping relationship between sleep and mood is particularly important for women’s health: both insomnia and depression/​anxiety are more prevalent in women. Insomnia and poor-​quality sleep are common symptoms of depression, present in >90% of people with major depression.55 Evening chronotype and poor sleep quality correlated with depression severity in patients hospitalized with depression, and persistent insomnia predicts relapse.56 It is less clear whether difficulty sleeping is a symptom or contributing cause of mood disorders. In adults, the presence of insomnia predicted future risk of depression and may be a prodromal symptom.57 A study of adults in the Netherlands found that the presence of chronic insomnia (defined as difficulty initiating or maintaining sleep) at either time frame was a marker of current depression or anxiety. The presence of insomnia also predicted future risk of developing anxiety, but not depression. The authors theorized that the presence of insomnia may be a trait marker for susceptibility to anxiety and recommended that people with insomnia should be screened for anxiety and depression.58 Guided online cognitive behavioral therapy for insomnia (CBT-​I) combined with a sleep diary in patients with both depression and insomnia resulted in significant reductions in depressive symptoms, insomnia severity, anxiety, and perseverative thinking. Daytime function was also improved. Benefits persisted at 3-​month and

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6-​month follow-​ups.59 A large meta-​analysis confirmed the benefits of CBT-​I in increasing remission of insomnia; improving sleep efficiency, sleep onset latency, and sleep quality; and improving psychiatric comorbidities and quality of life.60

3.3.4 Sleep, Sex Hormones, and Gender Sex and gender differences in sleep emerge in puberty, suggesting a possible role for sex hormones. After menarche, women are more likely to report insomnia than men, which coincides with (but does not completely explain) higher rates of depression. Sleep patterns are relatively stable across the menstrual cycle in healthy women, with a slight decrease in REM in the luteal phase and an increase in sleep spindles. Subjective sleep quality is lowest in the week before menses, potentially influenced by higher body temperature and lower amplitude of the diurnal fluctuations in cortisol and melatonin.61 Adult women are more likely than men to have a morning chronotype, be more active in the day and less energetic at night.62 Traditional gender roles as opposed to hormones may be partly responsible, as this pattern is more similar to that of young children and, in fact, is more prevalent in women with children than those without.63 These gender differences in chronotype also diminish with age.64 While animal models show an interaction between circadian biology, ovulation, and fertility,65 there is little prospective data in humans. Evidence that circadian disruption may impact sex hormones includes the observation that women performing shift work have a twofold higher risk of breast cancer,66 shorter menstrual cycles, more menstrual disruption, reduced fertility, and higher rates of miscarriage.67 PSG studies demonstrate that women spend more time sleeping and have more slow wave sleep than men. However, they generally take a longer time to fall asleep, have longer REM latency, and report lower quality sleep despite higher objective total sleep time and deep sleep.68 Both estradiol and progesterone activate pharyngeal dilator muscles and stimulate respiratory centers, yet the impact may be greater with estradiol. PSG studies in menstruating women with OSA have shown higher AHIs in the luteal phase, with its higher levels of both estradiol and progesterone, than in the follicular phase, when estradiol is relatively unopposed by progesterone.69 Estradiol modulates vagal and sympathetic control of heart rate, with lower heart rates and higher heart rate variability (HRV, a marker of vagal activity) seen when estradiol levels are higher. In contrast, progesterone reduces HRV and vagal tone,70 which may contribute to the higher rates of sleep disruption in the luteal phase for women with premenstrual syndrome (PMS), premenstrual dysphoric disorder (PMDD), and in the menopause transition. Women who developed insomnia in the menopause transition were found to have elevated heart rates and lower HRV than controls, and this was worsened in the luteal phase.71 Oral contraceptives have been shown to increase REM and light sleep while reducing slow-​wave sleep.72

3.4  SLEEP AND OTHER LIFESTYLE MEDICINE PILLARS 3.4.1 Diet and Sleep Consumption of a diet higher in fat and lower in fiber is associated with higher risk of sleep apnea, daytime sleepiness, and reduced sleep quality, even in people

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with no prior history of sleep concerns.73,74 Diets with a higher glycemic index and glycemic load are associated with insomnia in postmenopausal women.75 Higher consumption of fruits, vegetables, and legumes (part of DASH76 and Mediterranean dietary patterns77) has been associated with better sleep quality, improved sleep efficiency, and fewer sleep disturbances in various populations, including older adults, adolescents, and women between the ages of 20–​75 years. Higher intake of fruits and vegetables in pregnancy is associated with improved sleep quality as measured by the Pittsburgh Sleep Quality Index (PSQI).78 While causality cannot be concluded from these studies, proposed mechanisms of benefit include food sources of isoflavones and tryptophan such as seeds, nuts, and beans,79 and benefits on increasing gut microbial diversity.80 Higher microbial diversity is associated with increased sleep efficiency and total sleep time, as well as decreased wake after sleep onset.81,82 The interplay between diet, sleep, biological factors, and chronic disease/​health outcomes is summarized in Figure 3.1.83

3.4.2 Exercise and Sleep A review of the research on exercise and sleep found that regular activity is associated with improvement in sleep quality and duration, although data is mixed in adolescents and young adults.84 Possible confounding factors included the timing of aerobic activity, which increases sympathetic tone and could negatively impact sleep if performed later in the day. No negative effect on sleep was observed in the timing of resistance training. The benefits of exercise may be greatest for those with insomnia, with improvements in PSQI and insomnia severity index scores, although selection bias was high.85 In older adults, the evidence for effects of exercise on sleep quality and quantity is more robust and consistent, especially in those with coexisting medical conditions, and was seen regardless of exercise type or intensity. Because of the sympathetic effects of aerobic activity and the fact that physical activity is also a zeitgeber for the SCN and peripheral clocks, timing aerobic activity earlier in the day may be the most beneficial. Stretching or mind body movement practices such as yoga or tai qi may be beneficial in the evenings as part of a wind-​down routine for rest and relaxation.86,87

3.5  SLEEP AND LIFE STAGES IN WOMEN 3.5.1 Adolescents and Teenagers There is a phase delay in circadian rhythm with puberty, and this evening-​type circadian preference emerges earlier in girls due to earlier onset of puberty. Earlier school start times and increased use of screens and social media exacerbate circadian rhythm misalignment and contribute to sleep deprivation.88 Most adolescents sleep less than the recommended 9 hours per night. Reduced sleep time and “social jet lag” (going to bed and getting up later on the weekends) increases the risk of depression in girls but not in boys.89 Girls report more difficulties falling asleep, waking up in the middle of the night, and waking up tired. Lower intake of fruits and vegetables and use of alcohol are associated with more sleep problems in girls compared to boys.90,91

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Additional chronic disease/ health outcomes for women include PCOS, gestational diabetes, hypertensive disorders of pregnancy, and fibromyalgia.

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(Reprinted with permission from Josiemer Mattei, [email protected], Diet and sleep physiology: Public health and clinical implications, Frontiers in Neurology 2017;8:2.)

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FIGURE 3.1  Conceptual framework for the interconnections between dietary factors, sleep, and disease.

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There are also sleep health disparities, not necessarily gender specific, that need to be taken into consideration for children with lower socioeconomic status.92 Contributing factors include household and neighborhood variables such as overcrowding, noise, and concerns about safety.93 Insomnia disorder, which is defined as difficulty in falling asleep, staying asleep, and/​or early morning awakening with inability to fall back to sleep and persisting at least 3 months, often emerges in adolescence and is twice as prevalent in girls compared to boys.94 Higher school pressure and perceived stress experienced by girls may play a role. Insomnia is associated with inflammation, increased cortisol activity, and depression, and it is an independent risk factor for substance use and suicide.95 The consequences of inadequate sleep in adolescents are significant: in addition to depression and fatigue, there are negative impacts on attention, focus, school performance, likelihood of graduation, and increased risk of automobile accidents. Recognizing this, numerous professional organizations have recommended that school start times should be no earlier than 8:30 am for adolescents and teens.96,97 Conversations and education about the role of sleep in improving energy, mood, and school performance can be performed at check-​ups. When parents set bedtimes, adolescents have longer, better sleep and improved daytime functioning.98 Suggestions for realigning circadian rhythms include limiting light exposure at night with reasonable limits on screen use (stopping screens 30–​60 minutes before bedtime, keeping them out of the bedroom). Reinforcing and reminding older adolescents of the aftereffects of staying up late (tiredness and irritability) may help them internalize their awareness of the importance of consistent and adequate sleep.99 Encouraging a relaxation practice in the evening such as meditation, yoga, reading, or journaling may be helpful. Melatonin may be considered in adolescents with insomnia or an evening chronotype, with regular follow-​ up. There is a lack of consistency in dosing guidelines: the Canadian Pediatric Society recommends 5 mg of melatonin 30–​60 minutes before bed.100 An encouraging long-​term follow-​up study in prepubertal children who started melatonin for chronic sleep onset insomnia not responsive to sleep hygiene measures found that after 7–​10 years, 75% had normal sleep without medications. The other 25% who continued melatonin had improved sleep quality and no significant adverse effects.101 Since melatonin is regulated as a dietary supplement, finding a good-​quality brand is essential. CBT-​ I in children and adolescents has been shown to significantly improve sleep onset latency and sleep efficiency as measured by sleep logs and actigraphy. Protocols are usually six sessions –​delivered individually or in groups, in person, by phone, or through Internet. Multiple modalities are included, such as relaxation, sleep hygiene, cognitive techniques, sleep education, stimulus control, and sleep restriction.102 A randomized controlled trial of CBT-​I for adolescents with coexisting mood, attention, or behavioral concerns (delivered via Internet or in person groups) improved insomnia symptoms, affect, anxiety, somatic symptoms, and attention at 2 months. Improvements persisted at 1 year follow-​up.103,104

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3.5.2 Menstrual Cycles and Sleep Dysmenorrhea is common in adolescence and is associated with longer sleep latency and efficiency, while women with insomnia rated their dysmenorrhea as more severe.105 From a lifestyle perspective, smoking cessation, reducing sugar intake, increasing magnesium-​rich foods, stretching, and/​or aerobic activity may address both: reducing pain and improving sleep quality.106,107 In girls and women with PMS or PMDD, there is a reduction in melatonin production and responsiveness in the luteal phase. While melatonin supplementation has not been clearly shown to benefit symptoms, bright light therapy may improve mood, tension, and stress.108 Women with coexisting PCOS and sleep apnea have worse metabolic profiles than women who do not have apnea.109 While it is less clear if treating sleep apnea improves ovulation and fertility, treatment is associated with improved cardiometabolic parameters, mood, and quality of life.110

3.5.3 Pregnancy and Sleep The dynamic physiologic changes of pregnancy can affect sleep quality and quantity, and also increase the risk for sleep disorders. In the first trimester, increased nighttime urination, breast tenderness, and nausea can interfere with sleep. In the second trimester, increasing musculoskeletal discomfort and uterine contractions may interfere with sleep quality. In the third trimester, increasing nocturia, leg cramps, uterine contractions, heartburn and sleep position can affect sleep.111,112 A meta-​analysis of studies involving >11,000 women in pregnancy found that 46% experienced poor sleep quality, and sleep quality worsened from the second to the third trimester.113 Poor-​quality sleep was associated with depression and anxiety in pregnancy114 and with increased suicidal ideation in late pregnancy independent of depression.115 Changes in folate and iron metabolism have been postulated to contribute to the increasing prevalence of RLS in pregnancy, affecting as many as 36% of women in the third trimester.116,117 Sleep-​disordered breathing may develop or worsen with advancing pregnancy, potentially exacerbated by nasal congestion and increasing body habitus. Sleep apnea (defined as AHI > 5 by home testing) was associated with a significantly increased risk of preeclampsia, hypertensive disorders of pregnancy, and gestational diabetes in a dose–​response relationship.118 Increasing age, body mass index or BMI (as opposed to pregnancy-​associated weight gain), and presence of frequent snoring were strong predictors of sleep-​disordered breathing in all three trimesters of pregnancy.119 Obstetricians should strongly consider screening for OSA in any pregnant woman with symptoms of snoring, elevated blood pressure or glucose, or pre-​pregnancy history of hypertension. In addition to physiologic changes, excitement or worries about upcoming labor, motherhood, or other concerns can negatively impact sleep and worsen insomnia. Experiencing intimate partner violence in the year before pregnancy was associated with a twofold increase in the risk of stress-​related sleep disturbance and reduced sleep quality in pregnancy.120 A history of childhood abuse was also associated with higher risk.121

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It is crucial to identify and manage sleep disorders appropriately in pregnant women for supporting a healthy pregnancy and a healthy mother. For RLS, folate and iron-​rich foods as well as supplementation with iron as needed to maintain a serum ferritin >75 mg/​dL may be beneficial. Vitamin D may also be helpful:122 a case control study found the odds ratio for RLS was 3.1 for those with a vitamin D level 50 nmol/​L.123 Vitamin D supplementation after 12 weeks gestation has been found to be well-​tolerated in doses as high as 4,000 IU daily.124 Other modalities which may be beneficial include exercise, yoga, massage, and sequential compression.125 Eating smaller, more frequent meals; avoiding reflux triggers such as caffeine, carbonated beverages, and fatty foods; and sleeping with a wedge pillow may help reduce nighttime reflux symptoms. In addition to regular exercise, CBT-​I is the most effective and safest modality to address insomnia in pregnancy.126 Online and telephone-​delivered sessions can be efficacious.127 If sleep quality remains low, timely referral to a sleep specialist with expertise in the management of sleep disorders in pregnancy is recommended in light of the negative impact on pregnancy outcomes and maternal health and mood.

3.5.4 Mothers of Young Children Mothers of young children face additional challenges with sleep. While directionality is not clear, mothers with lower sleep quality also reported lower physical activity, lower intake of fruits and vegetables, more emotional or disinhibited eating and fewer family meals. In addition, they had a lower sense of parenting self-​efficacy, more depression and stress, and higher BMIs.128 In the Prevention of Overweight in Infancy trial in New Zealand, a program focused on infant sleep education interventions starting 3 weeks before birth followed by three additional parent education contacts over 6 months, was associated with a 50% reduced risk of childhood obesity at age 3.5 and 5 years. The emphasis was on developing appropriate sleep habits as measured by the ability of infants to regulate sleep (fall asleep when tired, without being fed or rocked to sleep).129 Implementing a regular bedtime routine was associated with improved sleep in infants and toddlers. Mothers in the treatment group were less likely to rate their children’s sleep as problematic and were more likely to see improvement in their own mood.130

3.5.5 Sleep and the Menopause Transition The menopause transition is associated with fluctuating hormones starting several years before a woman’s last menstrual period. A high percentage of women in the menopause transition reported poor-​quality sleep and nocturnal awakenings, which worsen as they transition to menopause (40–​56% compared to 31% in premenopausal women).131 Lower estradiol levels correlated with both difficulty in falling asleep and difficulty in staying asleep, while higher FSH levels were found to correlate with predicting difficulty in staying asleep. The frequency and severity of vasomotor symptoms correlate with sleep disturbances, and both are severe with surgical menopause.132

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Objective PSG measures of sleep are not always consistent with subjective reports of reduced sleep quality. However, using in home PSG measurements, the SWAN study found a strong correlation between both reduced sleep efficiency and higher AHI scores and metabolic syndrome, independent of other risk factors.133 The prevalence of OSA increases in the menopause transition, some of which is independent of age and weight. In the Sleep in Midlife Women Study, home PSGs administered every 6 months found a 21% higher AHI in perimenopausal women and a 31% higher AHI in postmenopausal women. For every year since entering the menopause transition, there was a 4% increase in AHI.134 Lower estradiol correlated with higher prevalence of OSA and higher AHI scores for women in peri-​or post-​ menopause with depression.135 OSA rates were also higher in women undergoing surgical menopause compared to natural menopause, and this was more pronounced in women not taking hormone therapy (HT).136 Studies on the independent effects of HT on sleep and sleep apnea for women in the menopause transition have been mixed, partially related to discrepancies between subjective assessments and PSG measured variables.137 In the presence of vasomotor symptoms, HT was associated with improvements in sleep quality, and benefits mirrored the reduction in vasomotor symptoms.138,139 Vasomotor symptoms have been associated with higher sleep apnea risk scores140 and higher cardiovascular risk,141 suggesting shared mechanisms. Since vasomotor symptoms are one of the most common concerns for which women seek care, inquiring about symptoms and risks of sleep apnea at those visits is important, with referral for screening as indicated. The benefits of weight loss, incorporating more diverse plant-​based foods, regular exercise, and breath-​based movement in improving sleep quality have already been reviewed. Education that these same factors may improve vasomotor symptoms was highly motivating for women to lose weight with a behaviorally focused lifestyle program,142 providing an excellent opportunity to engage women in healthy lifestyle changes. Reduction or elimination of alcohol may benefit both vasomotor symptoms and sleep quality. CBT-​I is effective for insomnia in women in menopause, and telephone-​delivered CBT-​I has been shown to improve both chronic insomnia and vasomotor symptoms.143,144

3.6  CONCLUSIONS Sleep is a fundamental pillar of health in Lifestyle Medicine that interacts with all the other pillars in a bidirectional relationship. Women have unique challenges with sleep that vary with life stages –​there is also a bidirectional interaction between sleep and health outcomes. In 2017, the Society of Women’s Health Research published a detailed guide on women and sleep that is an excellent resource for both healthcare providers and patients. It includes practical recommendations to improve the diagnosis, treatment, and management of sleep and circadian rhythm sleep-​wake disorders.145 For Lifestyle Medicine practitioners, heightened understanding of the prevalence and presentation of sleep concerns for women; educating their patients about the benefits of diet, exercise, realigning circadian rhythms, and addressing stress to improve sleep quality and quantity; and knowing how to identify sleep disorders

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and when to refer to a sleep specialist may help improve the physical and emotional well-​being of women throughout their lives. For additional reading see supplementary material.

REFERENCES 1. Mallampalli MP, Carter CL. Exploring sex and gender differences in sleep health: A society for women’s health research report. J Women’s Health (Larchmt). 2014;23(7):553–​562. DOI: http://​doi.org/​10.1289/​ehp.6714 2. Baker FC, Lee KA. Menstrual cycle effects on sleep. Sleep Med Clin. 2018;13(3):283–​ 294. DOI: http://​doi.org/​10.1016/​j.jsmc.2018.04.002 3. Sedov ID, Cameron EE, Madigan S, Tomfohr-​Madsen LM. Sleep quality during pregnancy: A meta-​analysis. Sleep Med Rev. 2018; 38:168–​176. DOI: http://​doi.org/​ 10.1016/​j.smrv.2017.06.005 4. Baker FC, Lampio L, Saaresranta T, Polo-​Kantola P. Sleep and sleep disorders in the menopausal transition. Sleep Med Clin. 2018;13(3):443–​456. DOI: http://​doi.org/​ 10.1016/​j.jsmc.2018.04.011 5. Roth T. Insomnia: Definition, prevalence, etiology, and consequences. J Clin Sleep Med. 2007;3(5Suppl): S7–​S10. 6. Seeman MV. Why are women prone to restless legs syndrome? Int J Environ Res Public Health. 2020;17(1):368. DOI: http://​doi.org/​10.3390/​ijerph17010368 7. Caregiver Statistics: Demographics. Caregiver.org. www.caregiver.org/​caregiver-​ statistics-​demographics. Published 2016. Accessed November 22, 2020. 8. Thurston RC, Chang Y, Matthews KA, von Känel R, Koenen K. Association of sexual harassment and sexual assault with midlife women’s mental and physical health. JAMA Intern Med. 2019;179(1):48–​ 53. DOI: http://​doi.org/​10.1001/​ jamainternmed.2018.4886 9. Gallgos AM, Trabold N, Cerulli C, Pigeon WR. Sleep and interpersonal violence: A systematic review. Trauma Violence Abuse. Published online 2019:1524838019852633. DOI: http://​doi.org/​10.1177/​1524838019852633 10. Wimms A, Woehrle H, Ketheeswaran S, Ramanan D, Armitstead J. Obstructive sleep apnea in women: Specific issues and interventions. Biomed Res Int. 2016; 2016:1764837. DOI: http://​doi.org/​10.1155/​2016/​1764837 11. Foley L. Sleep drive and your body clock. Sleepfoundation.org. Published September 25, 2020. Accessed December 1, 2020. www.sleepfoundation.org/​circadian-​rhythm/​ sleep-​drive-​and-​your-​body-​clock 12. Smith PC, Mong JA. Neuroendocrine control of sleep. Curr Top Behav Neurosci. 2019; 43:353–​378. DOI: http://​doi.org/​10.1007/​7854_​2019_​107 13. Astiz M, Heyde I, Oster H. Mechanisms of communication in the mammalian circadian timing system. Int J Mol Sci. 2019;20(2):343. DOI: http://​doi.org/​10.3390/​ ijms20020343 14. Potter GDM, Skene DJ, Arendt J, Cade JE, Grant PJ, Hardie LJ. Circadian rhythm and sleep disruption: Causes, metabolic consequences, and countermeasures. Endocr Rev. 2016;37(6):584–​608. DOI: http://​doi.org/​10.1210/​er.2016-​1083 15. Zielinski MR, McKenna JT, McCarley RW. Functions and mechanisms of sleep. AIMS Neurosci. 2016;3(1):67–​104. DOI: http://​doi.org/​10.3934/​Neuroscience.2016.1.67 16. Hablitz LM, Vinitsky HS, Sun Q, et al. Increased glymphatic influx is correlated with high EEG delta power and low heart rate in mice under anesthesia. Sci Adv.2019;5(2): eaav5447. DOI: http://​doi.org/​0.1126/​sciadv.aav5447

76

76

Cindy Geyer 17. Orbea CAP, Lloyd RM, Faubion SS, Miller VM, Mara KC, Kapoor E. Predictive ability and reliability of the STOP-​BANG questionnaire in screening for obstructive sleep apnea in midlife women. Maturitas. 2020;135:1 DOI: http://​doi.org/​10.1016/​ j.maturitas.2020.02.004 18. Westreich R, Gozlan-​Talmor A, Geva-​Robinson S, et al. The presence of snoring as well as its intensity is underreported by women. J Clin Sleep Med. 2019;15(3):471–​ 476. DOI: http://​doi.org/​10.5664/​jcsm.7678 19. Yalamanchali S, Farajian V, Hamilton C, Pott TR, Samuelson CG, Friedman M. Diagnosis of obstructive sleep apnea by peripheral arterial tonometry: meta-​ analysis: Meta-​analysis. JAMA Otolaryngol Head Neck Surg. 2013;139(12):1343–​ 1350. DOI: http://​doi.org/​10.1001/​jamaoto.2013.5338 20. Choi JH, Lee B, Lee JY, Kim HJ. Validating the Watch-​PAT for diagnosing obstructive sleep apnea in adolescents. J Clin Sleep Med. 2018;14(10):1741–​1747. DOI: http://​ doi.org/​10.5664/​jcsm.7386 21. Anttalainen U, Polo O, Vahlberg T, Saaresranta T. Women with partial upper airway obstruction are not less sleepy than those with obstructive sleep apnea. Sleep Breath. 2013;17(2):873–​876. DOI: http://​doi.org/​10.1007/​s11325-​012-​0735-​x 22. Anttalainen U, Tenhunen M, Rimpilä V, et al. Prolonged partial upper airway obstruction during sleep -​An underdiagnosed phenotype of sleep-​disordered breathing. Eur Clin Respir J. 2016;3(1):31806. DOI: http://​doi.org/​10.3402/​ecrj.v3.31806 23. Bahammam RA, Al-​ Qahtani KM, Aleissi SA, Olaish AH, Almeneessier AS, Bahammam AS. The associations of gender, menopause, age, and asthma with REM-​ predominant obstructive sleep apnea: A prospective observational study. Nat Sci Sleep. 2020;12:721–​735. DOI: http://​doi.org/​10.2147/​NSS.S275051 24. Varga AW, Mokhlesi B. REM obstructive sleep apnea: Risk for adverse health outcomes and novel treatments. Sleep Breath. 2019;23(2):413–​423. DOI: http://​doi. org/​10.1007/​s11325-​018-​1727-​2 25. Ljunggren M, Lindberg E, Franklin KA, et al. Obstructive sleep apnea during rapid eye movement sleep is associated with early signs of atherosclerosis in women. Sleep. 2018;41(7). DOI: http://​doi.org/​0.1093/​sleep/​zsy099 26. Helvaci N, Karabulut E, Demir AU, Yildiz BO. Polycystic ovary syndrome and the risk of obstructive sleep apnea: A meta-​analysis and review of the literature. Endocr Connect. 2017;6(7):437–​445. DOI: http://​doi.org/​10.1530/​EC-​17-​0129 27. Kahal H, Kyrou I, Uthman OA, et al. The prevalence of obstructive sleep apnoea in women with polycystic ovary syndrome: A systematic review and meta-​analysis. Sleep Breath. 2020;24(1):339–​350. DOI: http://​doi.org/​10.1007/​s11325-​019-​01835-​1 28. Yang H-​P, Kang J-​H, Su H-​Y, Tzeng C-​R, Liu W-​M, Huang S-​Y. Apnea-​hypopnea index in nonobese women with polycystic ovary syndrome. Int J Gynaecol Obstet. 2009;105(3):226–​229. DOI: http://​doi.org/​10.1016/​j.ijgo.2009.02.004 29. Khashchenko E, Vysokikh M, Uvarova E, et al. Activation of systemic inflammation and oxidative stress in adolescent girls with polycystic ovary syndrome in combination with metabolic disorders and excessive body weight. J Clin Med. 2020;9(5):1399. DOI: http://​doi.org/​10.3390/​jcm9051399 30. Carneiro-​Barrera A, Díaz-​Román A, Guillén-​Riquelme A, Buela-​Casal G. Weight loss and lifestyle interventions for obstructive sleep apnoea in adults: Systematic review and meta-​analysis. Obes Rev. 2019;20(5):750–​762. DOI: http://​doi.org/​10.1111/​obr.12824 31. Camacho M, Malu OO, Kram YA, et al. Nasal dilators (Breathe Right Strips and NoZovent) for snoring and OSA: A systematic review and meta-​analysis. Pulm Med. 2016; 2016:4841310. DOI: http://​doi.org/​10.1155/​2016/​4841310

77

Sleep and Women’s Health

77

32. Serra-​Torres S, Bellot-​Arcís C, Montiel-​Company JM, Marco-​Algarra J, Almerich-​ Silla JM. Effectiveness of mandibular advancement appliances in treating obstructive sleep apnea syndrome: A systematic review: Oral appliances for sleep apnea. Laryngoscope. 2016;126(2):507–​514. DOI: http://​doi.org/​10.1002/​lary.25505 33. Godoy LBM, Palombini L, Poyares D, et al. Long-​ term oral appliance therapy improves daytime function and mood in upper airway resistance syndrome patients. Sleep. 2017;40(12). DOI: http://​doi.org/​10.1093/​sleep/​zsx175 34. Irwin MR, Olmstead R, Carroll JE. Sleep disturbance, sleep duration, and inflammation: A systematic review and meta-​analysis of cohort studies and experimental sleep deprivation. Biol Psychiatry. 2016;80(1):40–​52. DOI: http://​doi.org/​10.1016/​ j.biopsych.2015.05.014 35. Prather AA, Epel ES, Cohen BE, Neylan TC, Whooley MA. Gender differences in the prospective associations of self-​reported sleep quality with biomarkers of systemic inflammation and coagulation: Findings from the Heart and Soul Study. J Psychiatr Res. 2013;47(9):1228–​1235. DOI: http://​doi.org/​10.1016/​j.jpsychires.2013.05.004 36. Cho HJ, Seeman TE, Kiefe CI, Lauderdale DS, Irwin MR. Sleep disturbance and longitudinal risk of inflammation: Moderating influences of social integration and social isolation in the Coronary Artery Risk Development in Young Adults (CARDIA) study. Brain Behav Immun. 2015; 46:319–​ 326. DOI: http://​doi.org/​10.1016/​ j.bbi.2015.02.023 37. Greer SM, Goldstein AN, Walker MP. The impact of sleep deprivation on food desire in the human brain. Nat Commun. 2013;4(1):2259. DOI: http://​doi.org/​10.1038/​ ncomms3259 38. Salfi F, Lauriola M, Tempesta D, et al. Effects of total and partial sleep deprivation on reflection impulsivity and risk-​taking in deliberative decision-​making. Nat Sci Sleep. 2020; 12:309–​324. DOI: http://​doi.org/​10.2147/​NSS.S250586 39. Hirotsu C, Tufik S, Andersen ML. Interactions between sleep, stress, and metabolism: From physiological to pathological conditions. Sleep Sci. 2015;8(3):143–​152. DOI: http://​doi.org/​10.1016/​j.slsci.2015.09.002 40. Spaeth AM, Goel N, Dinges DF. Caloric and macronutrient intake and meal timing responses to repeated sleep restriction exposures separated by varying intervening recovery nights in healthy adults. Nutrients. 2020;12(9):2694. DOI: http://​doi.org/​ 10.3390/​nu12092694 41. Depner CM, Melanson EL, Eckel RH, et al. Ad libitum weekend recovery sleep fails to prevent metabolic dysregulation during a repeating pattern of insufficient sleep and weekend recovery sleep. Curr Biol. 2019;29(6):957–​967.e4. DOI: http://​doi.org/​ 10.1016/​j.cub.2019.01.069 42. Besedovsky L, Lange T, Haack M. The sleep-​immune crosstalk in health and disease. Physiol Rev. 2019;99(3):1325–​ 1380. DOI: http://​doi.org/​10.1152/​physrev. 00010.2018 43. Prather AA, Janicki-​Deverts D, Hall MH, Cohen S. Behaviorally assessed sleep and susceptibility to the common cold. Sleep. 2015;38(9):1353–​1359. DOI: http://​doi.org/​ 10.5665/​sleep.4968 44. Taylor DJ, Kelly K, Kohut ML, Song K-​S. Is insomnia a risk factor for decreased influenza vaccine response? Behav Sleep Med. 2017;15(4):270–​287. DOI: http://​doi.org/​ 10.1080/​15402002.2015.1126596 45. Lange T, Dimitrov S, Bollinger T, Diekelmann S, Born J. Sleep after vaccination boosts immunological memory. J Immunol. 2011;187(1):283–​290. DOI: http://​doi. org/​10.4049/​jimmunol.1100015

78

78

Cindy Geyer 46. Zielinski MR, Systrom DM, Rose NR. Fatigue, sleep, and autoimmune and related disorders. Front Immunol. 2019; 10:1827. DOI: http://​doi.org/​0.3389/​fimmu. 2019.01827 47. Hsiao Y-​H, Chen Y-​T, Tseng C-​M, et al. Sleep disorders and increased risk of autoimmune diseases in individuals without sleep apnea. Sleep. 2015;38(4):581–​586. DOI: http://​doi.org/​10.5665/​sleep.4574 48. Irwin M, Olmstead R, Carillo C, et al. Sleep loss exacerbates fatigue, depression and pain in rheumatoid arthritis. Sleep.2012;35(4):537–​543. DOI: http://​doi.org/​10.5665/​ sleep.1742 49. Lin G-​J, Huang S-​H, Chen S-​J, Wang C-​H, Chang D-​M, Sytwu H-​K. Modulation by melatonin of the pathogenesis of inflammatory autoimmune diseases. Int J Mol Sci. 2013;14(6):11742–​11766. DOI: http://​doi.org/​10.3390/​ijms140611742 50. Finan PH, Goodin BR, Smith MT. The association of sleep and pain: An update and a path forward. J Pain. 2013;14(12):1539–​1552. DOI: http://​doi.org/​10.1016/​ j.jpain.2013.08.007 51. Koffel E, Kroenke K, Bair MJ, Leverty D, Polusny MA, Krebs EE. The bidirectional relationship between sleep complaints and pain: Analysis of data from a randomized trial. Health Psychol. 2016;35(1):41–​49. DOI: http://​doi.org/​10.1037/​hea0000245 52. Frohnhofen H. Pain and sleep: A bidirectional relationship. Z Gerontol Geriatr. 2018;51(8):871–​874. DOI: http://​doi.org/​10.1007/​s00391-​018-​01461-​8 53. Mork PJ, Nilsen TIL. Sleep problems and risk of fibromyalgia: Longitudinal data on an adult female population in Norway. Arthritis Rheum. 2012;64(1):281–​284. DOI: http://​doi.org/​0.1002/​art.33346 54. Pan F, Tian J, Cicuttini F, Jones G. Sleep disturbance and its association with pain severity and multisite pain: A prospective 10.7-​year study. Pain Ther. 2020;9(2):751–​ 763. DOI: http://​doi.org/​10.1007/​s40122-​020-​00208-​x 55. Geoffroy PA, Hoertel N, Etain B, et al. Insomnia and hypersomnia in major depressive episode: Prevalence, sociodemographic characteristics and psychiatric comorbidity in a population-​based study. J Affect Disord. 2018; 226:132–​141 DOI: http://​doi.org/​ 10.1016/​j.jad.2017.09.032 56. Müller MJ, Kundermann B, Cabanel N. Eveningness and poor sleep quality independently contribute to self-​reported depression severity in psychiatric inpatients with affective disorder. Nord J Psychiatry. 2016;70(5):329–​334. DOI: http://​doi.org/​ 10.3109/​08039488.2015.1112832 57. Fang H, Tu S, Sheng J, Shao A. Depression in sleep disturbance: A review on a bidirectional relationship, mechanisms and treatment. J Cell Mol Med.2019;23(4):2324–​ 2332. DOI: http://​doi.org/​10.1111/​jcmm.14170 58. Neckelmann D, Mykletun A, Dahl AA. Chronic insomnia as a risk factor for developing anxiety and depression. Sleep. 2007;30(7):873–​880. DOI: http://​doi.org/​ 10.1093/​sleep/​30.7.873 59. van der Zweerde T, van Straten A, Effting M, Kyle SD, Lancee J. Does online insomnia treatment reduce depressive symptoms? A randomized controlled trial in individuals with both insomnia and depressive symptoms. Psychol Med. 2019;49(3):501–​509. DOI: http://​doi.org/​10.1017/​S0033291718001149 60. Wu JQ, Appleman ER, Salazar RD, Ong JC. Cognitive behavioral therapy for insomnia comorbid with psychiatric and medical conditions: A meta-​analysis. JAMA Intern Med. 2015;175(9):1461–​1472. DOI: http://​doi.org/​10.1001/​jamainternmed.2015.3006 61. Baker FC, Driver HS. Circadian rhythms, sleep, and the menstrual cycle. Sleep Med. 2007;8(6):613–​622. DOI: http://​doi.org/​10.1016/​j.sleep.2006.09.011

79

Sleep and Women’s Health

79

62. Anderson ST, FitzGerald GA. Sexual dimorphism in body clocks. Science. 2020;369(6508):1164–​1165. DOI: http://​doi.org/​10.1126/​science.abd4964 63. Leonhard C, Randler C. In sync with the family: Children and partners influence the sleep-​wake circadian rhythm and social habits of women. Chronobiol Int. 2009;26(3):510–​525. DOI: http://​doi.org/​10.1080/​07420520902821101 64. Randler C, Engelke J. Gender differences in chronotype diminish with age: A meta-​analysis based on morningness/​chronotype questionnaires. Chronobiol Int. 2019;36(7):888–​905. DOI: http://​doi.org/​10.1080/​07420528.2019.1585867 65. Sciarra F, Franceschini E, Campolo F, et al. Disruption of circadian rhythms: A crucial factor in the etiology of infertility. Int J Mol Sci. 2020;21(11):3943. DOI: http://​doi. org/​10.3390/​ijms21113943 66. Szkiela M, Kusideł E, Makowiec-​Dąbrowska T, Kaleta D. Night shift work -​A risk factor for breast cancer. Int J Environ Res Public Health. 2020;17(2):659. DOI: http://​ doi.org/​10.3390/​ijerph17020659 67. Gamble KL, Resuehr D, Johnson CH. Shift work and circadian dysregulation of reproduction. Front Endocrinol (Lausanne). 2013; 4:92. DOI: http://​doi.org/​10.3389/​ fendo.2013.00092 68. Silva A, Andersen ML, De Mello MT, Bittencourt LRA, Peruzzo D, Tufik S. Gender and age differences in polysomnography findings and sleep complaints of patients referred to a sleep laboratory. Braz J Med Biol Res. 2008;41(12):1067–​1075. DOI: http://​doi. org/​10.1590/​s0100-​879x2008001200005 69. Spector AR, Loriaux D, Alexandru D, Auerbach SH. The influence of the menstrual phases on polysomnography. Cureus. 2016;8(11): e871. DOI: http://​doi.org/​10.7759/​ cureus.871 70. de Zambotti M, Trinder J, Colrain IM, Baker FC. Menstrual cycle-​related variation in autonomic nervous system functioning in women in the early menopausal transition with and without insomnia disorder. Psychoneuroendocrinology. 2017; 75:44–​51. DOI: http://​doi.org/​10.1016/​j.psyneuen.2016.10.009 71. Schmalenberger KM, Eisenlohr-​Moul TA, Jarczok MN, et al. Menstrual cycle changes in vagally-​mediated heart rate variability are associated with progesterone: Evidence from two within-​ person studies. J Clin Med. 2020;9(3):617. DOI: http://​doi.org/​ 10.3390/​jcm9030617 72. Baker FC, Mitchell D, Driver HS. Oral contraceptives alter sleep and raise body temperature in young women. Pluggers Arch. 2001;442(5):729–​737. DOI: http://​doi.org/​ 10.1007/​s004240100582 73. St-​Onge M-​P, Roberts A, Shechter A, Choudhury AR. Fiber and saturated fat are associated with sleep arousals and slow wave sleep. J Clin Sleep Med. 2016;12(1):19–​ 24. DOI: http://​doi.org/​10.5664/​jcsm.5384 74. Frank S, Gonzalez K, Lee-​Ang L, Young MC, Tamez M, Mattei J. Diet and sleep physiology: Public health and clinical implications. Front Neurol. 2017;8:393. DOI: http://​ doi.org/​10.3389/​fneur.2017.00393 75. Gangwisch JE, Hale L, St-​Onge M-​P, et al. High glycemic index and glycemic load diets as risk factors for insomnia: Analyses from the Women’s Health Initiative. Am J Clin Nutr. 2020;111(2):429–​439. DOI: http://​doi.org/​10.1093/​ajcn/​nqz275 76. Liang H, Beydoun HA, Hossain S, et al. Dietary approaches to stop hypertension (DASH) score and its association with sleep quality in a national survey of middle-​ aged and older men and women. Nutrients. 2020;12(5):1510. DOI: http://​doi.org/​ 10.3390/​nu12051510

80

80

Cindy Geyer 77. Zuraikat FM, Makarem N, St-​ Onge M-​ P, Xi H, Akkapeddi A, Aggarwal B. A Mediterranean dietary pattern predicts better sleep quality in US women from the American heart association go red for women strategically focused research network. Nutrients. 2020;12(9). DOI: http://​doi.org/​10.3390/​nu12092830 78. van Lee L, Chia A-​R, Loy SL, et al. Sleep and dietary patterns in pregnancy: Findings from the GUSTO cohort. Int J Environ Res Public Health. 2017;14(11). DOI: http://​ doi.org/​10.3390/​ijerph14111409 79. St-​Onge M-​P, Crawford A, Aggarwal B. Plant-​based diets: Reducing cardiovascular risk by improving sleep quality? Curr Sleep Med Rep. 2018;4(1):74–​78. 80. St-​Onge M-​P, Zuraikat FM. Reciprocal roles of sleep and diet in cardiovascular health: A review of recent evidence and a potential mechanism. Curr Atheroscler Rep. 2019;21(3):11. DOI: http://​doi.org/​10.1007/​s11883-​019-​0772-​z 81. Smith RP, Easson C, Lyle SM, et al. Gut microbiome diversity is associated with sleep physiology in humans. PLoS One. 2019;14(10): e0222394. DOI: http://​doi.org/​ 10.1371/​journal.pone.0222394 82. Li Y, Hao Y, Fan F, Zhang B. The role of microbiome in insomnia, circadian disturbance and depression. Front Psychiatry. 2018; 9:669. DOI: http://​doi.org/​10.3389/​ fpsyt.2018.00669 83. Frank S, Gonzalez K, Lee-​Ang L, Young MC, Tamez M, Mattei J. Diet and sleep physiology: Public health and clinical implications. Front Neurol. 2017;8:393. DOI: http://​ doi.org/​0.3389/​fneur.2017.00393 84. Dolezal BA, Neufeld EV, Boland DM, Martin JL, Cooper CB. Interrelationship between sleep and exercise: A systematic review. Adv Prev Med. 2017; 2017:1364387. DOI: http://​doi.org/​10.1155/​2017/​1364387 85. Banno M, Harada Y, Taniguchi M, et al. Exercise can improve sleep quality: A systematic review and meta-​analysis. PeerJ. 2018;6(e5172): e5172. DOI: http://​doi.org/​ 10.7717/​peerj.5172 86. Siddarth D, Siddarth P, Lavretsky H. An observational study of the health benefits of yoga or tai chi compared with aerobic exercise in community-​dwelling middle-​aged and older adults. Am J Geriatr Psychiatry. 2014;22(3):272–​273. DOI: http://​doi.org/​ 10.1016/​j.jagp.2013.01.065 87. D’Aurea CVR, Poyares D, Passos GS, et al. Effects of resistance exercise training and stretching on chronic insomnia. Rev Bras Psiquiatr. 2019;41(1):51–​57. DOI: http://​ doi.org/​0.1590/​1516-​4446-​2018-​0030 88. Owens J, Adolescent Sleep Working Group, Committee on Adolescence. Insufficient sleep in adolescents and young adults: An update on causes and consequences. Pediatrics. 2014;134(3):e921–​e932. DOI: http://​doi.org/​10.1542/​peds.2014-​1696 89. Mathew GM, Hale L, Chang A-​M. Sex moderates relationships among school night sleep duration, social jetlag, and depressive symptoms in adolescents. J Biol Rhythms. 2019;34(2):205–​217. DOI: http://​doi.org/​10.1177/​0748730419828102 90. de Matos MG, Marques A, Peralta M, et al. Sleep in adolescence: Sex matters? Sleep Sci. 2019;12(3):138–​146. DOI: http://​doi.org/​10.5935/​1984-​0063.20190075 91. Miguez MJ, Bueno D, Perez C. Disparities in sleep health among adolescents: The role of sex, age, and migration. Sleep Disord. 2020; 2020:5316364. DOI: http://​doi.org/​ 10.1155/​2020/​5316364 92. Marco CA, Wolfson AR, Sparling M, Azuaje A. Family socioeconomic status and sleep patterns of young adolescents. Behav Sleep Med. 2011;10(1):70–​80. DOI: http://​ doi.org/​10.1080/​15402002.2012.636298 93. Bagley EJ, Kelly RJ, Buckhalt JA, El-​Sheikh M. What keeps low-​SES children from sleeping well: The role of presleep worries and sleep environment. Sleep Med. 2015;16(4):496–​502. DOI: http://​doi.org/​10.1016/​j.sleep.2014.10.008

81

Sleep and Women’s Health

81

94. de Zambotti M, Goldstone A, Colrain IM, Baker FC. Insomnia disorder in adolescence: Diagnosis, impact, and treatment. Sleep Med Rev. 2018; 39 :12–​ 24. DOI: http://​doi.org/​10.1016/​j.smrv.2017.06.009 95. Lin H-​T, Lai C-​H, Perng H-​J, et al. Insomnia as an independent predictor of suicide attempts: A nationwide population-​ based retrospective cohort study. BMC Psychiatry. 2018;18(1):117. DOI: http://​doi.org/​10.1186/​s12888-​018-​1702-​2 96. Watson NF, Martin JL, Wise MS, et al. Delaying middle school and high school start times promotes student health and performance: An American Academy of Sleep Medicine position statement. J Clin Sleep Med. 2017;13(04):623–​625. DOI: http://​ doi.org/​10.5664/​jcsm.6558 97. Start School Later. Startschoollater.net. Accessed December 2, 2020. www.startschoollater.net 98. Short MA, Gradisar M, Wright H, Lack LC, Dohnt H, Carskadon MA. Time for bed: Parent-​set bedtimes associated with improved sleep and daytime functioning in adolescents. Sleep. 2011;34(6):797–​800. DOI: http://​doi.org/​10.5665/​SLEEP.1052 99. Hale L, Kirschen GW, LeBourgeois MK, et al. Youth screen media habits and sleep. Child Adolesc Psychiatr Clin N Am. 2018;27(2):229–​ 245. DOI: http://​doi.org/​ 10.1016/​j.chc.2017.11.014 100. Janjua I, Goldman RD. Sleep-​related melatonin use in healthy children. Can Fam Physician. 2016;62(4):315–​317. 101. Zwart TC, Smits MG, Egberts TCG, Rademaker CMA, van Geijlswijk IM. Long-​ term melatonin therapy for adolescents and young adults with chronic sleep onset insomnia and late melatonin onset: Evaluation of sleep quality, chronotype, and lifestyle factors compared to age-​related randomly selected population cohorts. Healthcare (Basel). 2018;6(1). DOI: http://​doi.org/​10.3390/​healthcare6010023 102. Ma Z-​R, Shi L-​J, Deng M-​H. Efficacy of cognitive behavioral therapy in children and adolescents with insomnia: A systematic review and meta-​analysis. Braz J Med Biol Res. 2018;51(6):e7070. DOI: http://​doi.org/​10.1590/​1414-​431x20187070 103. de Bruin EJ, Bögels SM, Oort FJ, Meijer AM. Efficacy of cognitive behavioral therapy for insomnia in adolescents: A randomized controlled trial with internet therapy, group therapy and a waiting list condition. Sleep. 2015;38(12):1913–​1926. DOI: http://​doi.org/​10.1590/​1414-​431x20187070 104. de Bruin EJ, Bögels SM, Oort FJ, Meijer AM. Improvement of adolescent psychopathology after insomnia treatment: Results from a randomized controlled trial over one year. J Child Psychol Psychiatry. 2018;59(5):509–​522. DOI: http://​doi.org/​ 10.1111/​jcpp.12834 105. Sahin S, Ozdemir K, Unsal A, Arslan R. Review of frequency of dysmenorrhea and some associated factors and evaluation of the relationship between dysmenorrhea and sleep quality in university students. Gynecol Obstet Invest. 2014;78(3):179–​185. DOI: http://​doi.org/​10.1159/​000363743 106. Bavil DA, Dolatian M, Mahmoodi Z, Baghban AA. Comparison of lifestyles of young women with and without primary dysmenorrhea. Electron Physician. 2016;8(3):2107–​2114. DOI: http://​doi.org/​10.19082/​2107 107. Vaziri F, Hoseini A, Kamali F, Abdali K, Hadianfard M, Sayadi M. Comparing the effects of aerobic and stretching exercises on the intensity of primary dysmenorrhea in the students of universities of Bushehr. J Family Reprod Health. 2015;9(1):23–​28. 108. Jehan S, Auguste E, Hussain M, et al. Sleep and premenstrual syndrome. J Sleep Med Disord. 2016;3(5). 109. Sam S, Ehrmann DA. Pathogenesis and consequences of disordered sleep in PCOS. Clin Med Insights Reprod Health. 2019; 13:1179558119871269. DOI: http://​doi.org/​ 10.1177/​1179558119871269

82

82

Cindy Geyer 110. Tasali E, Chapotot F, Leproult R, Whitmore H, Ehrmann DA. Treatment of obstructive sleep apnea improves cardiometabolic function in young obese women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2011;96(2):365–​374. DOI: http://​ doi.org/​0.1210/​jc.2010-​1187 111. Pengo MF, Won CH, Bourjeily G. Sleep in women across the life span. Chest. 2018;154(1):196–​206. DOI: http://​doi.org/​10.1016/​j.chest.2018.04.005 112. Silvestri R, Aricò I. Sleep disorders in pregnancy. Sleep Sci. 2019;12(3):232–​239. DOI: http://​doi.org/​10.5935/​1984-​0063.20190098 113. Sedov ID, Cameron EE, Madigan S, Tomfohr-​Madsen LM. Sleep quality during pregnancy: A meta-​analysis. Sleep Med Rev. 2018; 38:168–​176. DOI: http://​doi.org/​ 10.1016/​j.smrv.2017.06.005 114. Yu Y, Li M, Pu L, et al. Sleep was associated with depression and anxiety status during pregnancy: A prospective longitudinal study. Arch Womens Ment Health. 2017;20(5):695–​701. DOI: http://​doi.org/​10.1007/​s00737-​017-​0754-​5 115. Gelaye B, Addae G, Neway B, et al. Poor sleep quality, antepartum depression and suicidal ideation among pregnant women. J Affect Disord. 2017; 209:195–​200. DOI: http://​doi.org/​10.1016/​j.jad.2016.11.020 116. Dunietz GL, Lisabeth LD, Shedden K, et al. Restless legs syndrome and sleep-​wake disturbances in pregnancy. J Clin Sleep Med. 2017;13(7):863–​870. DOI: http://​doi. org/​10.5664/​jcsm.6654 117. Darvishi N, Daneshkhah A, Khaledi-​Paveh B, et al. The prevalence of restless legs syndrome/​Willis-​Ekbom disease (RLS/​WED) in the third trimester of pregnancy: A systematic review. BMC Neurol. 2020;20(1):132. DOI: http://​doi.org/​ 10.1186/​s12883-​020-​01709-​0 118. Facco FL, Parker CB, Reddy UM, et al. Association between sleep-​disordered breathing and hypertensive disorders of pregnancy and gestational diabetes mellitus. Obstet Gynecol. 2017;129(1):31–​ 41. DOI: http://​doi.org/​10.1097/​ AOG.0000000000001805 119. Louis JM, Koch MA, Reddy UM, et al. Predictors of sleep-​disordered breathing in pregnancy. Am J Obstet Gynecol. 2018;218(5):521.e1–​521.e12. DOI: http://​doi.org/​ 10.1016/​j.ajog.2018.01.031 120. Sanchez SE, Islam S, Zhong Q-​Y, Gelaye B, Williams MA. Intimate partner violence is associated with stress-​related sleep disturbance and poor sleep quality during early pregnancy. PLoS One. 2016;11(3):e0152199. DOI: http://​doi.org/​10.1371/​journal. pone.0152199 121. Gelaye B, Kajeepeta S, Zhong Q-​Y, et al. Childhood abuse is associated with stress-​related sleep disturbance and poor sleep quality in pregnancy. Sleep Med. 2015;16(10):1274–​1280. DOI: http://​doi.org/​10.1016/​j.sleep.2015.07.004 122. Wali S, Shukr A, Boudal A, Alsaiari A, Krayem A. The effect of vitamin D supplements on the severity of restless legs syndrome. Sleep Breath. 2015;19(2):579–​ 583. DOI: http://​doi.org/​10.1007/​s11325-​014-​1049-​y 123. Mithal A, Kalra S. Vitamin D supplementation in pregnancy. Indian J Endocrinol Metab. 2014;18(5):593–​596. DOI: http://​doi.org/​10.4103/​2230-​8210.139204 124. Dawodu A, Saadi HF, Bekdache G, Javed Y, Altaye M, Hollis BW. Randomized controlled trial (RCT) of vitamin D supplementation in pregnancy in a population with endemic vitamin D deficiency. J Clin Endocrinol Metab. 2013;98(6):2337–​2346. DOI: http://​doi.org/​10.1210/​jc.2013-​1154 125. Jahani KM, Kolla BP, Moore KM, Mansukhani MP. Management of restless legs syndrome in pregnancy and lactation. J Prim Care Community Health. 2020;11:2150132720905950. DOI: http://​doi.org/​10.1177/​2150132720905950

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126. Manber R, Bei B, Simpson N, et al. Cognitive behavioral therapy for prenatal insomnia: A randomized controlled trial. Obstet Gynecol. 2019;133(5):911–​919. DOI: http://​doi.org/​10.1097/​AOG.0000000000003216 127. Felder JN, Epel ES, Neuhaus J, Krystal AD, Prather AA. Efficacy of digital cognitive behavioral therapy for the treatment of insomnia symptoms among pregnant women: A randomized clinical trial. JAMA Psychiatry. 2020;77(5):484–​492. DOI: http://​doi.org/​10.1001/​jamapsychiatry.2019.4491 128. Eck KM, Santiago E, Martin-​Biggers J, Byrd-​Bredbenner C. Maternal sleep quality is associated with personal and parenting weight-​related behaviors. Int J Environ Res Public Health. 2020;17(15). DOI: http://​doi.org/​10.3390/​ijerph17155312 129. Taylor RW, Gray AR, Heath A-​LM, et al. Sleep, nutrition, and physical activity interventions to prevent obesity in infancy: Follow-​ up of the Prevention of Overweight in Infancy (POI) randomized controlled trial at ages 3.5 and 5 y. Am J Clin Nutr. 2018;108(2):228–​236. DOI: https://​doi.org/​10.1093/​ajcn/​nqy090 130. Mindell JA, Telofski LS, Wiegand B, Kurtz ES. A nightly bedtime routine: Impact on sleep in young children and maternal mood. Sleep. 2009;32(5):599–​606. DOI: http://​ doi.org/​10.1093/​sleep/​32.5.599 131. Kravitz HM, Joffe H. Sleep during the perimenopause: A SWAN story. Obstet Gynecol Clin North Am. 2011;38(3):567–​ 586. DOI: http://​doi.org/​10.1016/​ j.ogc.2011.06.002 132. Baker FC, de Zambotti M, Colrain IM, Bei B. Sleep problems during the menopausal transition: Prevalence, impact, and management challenges. Nat Sci Sleep. 2018; 10:73–​95. DOI: http://​doi.org/​10.2147/​NSS.S125807 133. Hall MH, Okun ML, Sowers M, et al. Sleep is associated with the metabolic syndrome in a multi-​ethnic cohort of midlife women: The SWAN Sleep Study. Sleep. 2012;35(6):783–​790. DOI: http://​doi.org/​10.5665/​sleep.1874 134. Mirer AG, Young T, Palta M, Benca RM, Rasmuson A, Peppard PE. Sleep-​disordered breathing and the menopausal transition among participants in the Sleep in Midlife Women Study. Menopause. 2017;24(2):157–​ 162. DOI: http://​doi.org/​10.1097/​ GME.0000000000000744 135. Galvan T, Camuso J, Sullivan K, et al. Association of estradiol with sleep apnea in depressed perimenopausal and postmenopausal women: A preliminary study. Menopause. 2017;24(1):112–​ 117. DOI: http://​doi.org/​10.1097/​GME.0000000000 000737 136. Huang T, Lin BM, Redline S, Curhan GC, Hu FB, Tworoger SS. Type of menopause, age at menopause, and risk of developing obstructive sleep apnea in postmenopausal women. Am J Epidemiol. 2018;187(7):1370–​1379. DOI: http://​doi.org/​10.1093/​aje/​ kwy011 137. Tal JZ, Suh SA, Dowdle CL, Nowakowski S. Treatment of insomnia, insomnia symptoms, and obstructive sleep apnea during and after menopause: Therapeutic approaches. Curr Psychiatry Rev. 2015;11(1):63–​83. DOI: http://​doi.org/​10.2174/​ 1573400510666140929194848 138. Cintron D, Lahr BD, Bailey KR, et al. Effects of oral versus transdermal menopausal hormone treatments on self-​reported sleep domains and their association with vasomotor symptoms in recently menopausal women enrolled in the Kronos Early Estrogen Prevention Study (KEEPS). Menopause. 2018;25(2):145–​153. DOI: http://​ doi.org/​10.1097/​GME.0000000000000971 139. Mirkin S, Graham S, Revicki DA, Bender RH, Bernick B, Constantine GD. Relationship between vasomotor symptom improvements and quality of life and sleep outcomes in menopausal women treated with oral, combined 17β-​estradiol/​

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Cindy Geyer progesterone. Menopause. 2019;26(6):637–​ 642. DOI: http://​doi.org/​10.1097/​ GME.0000000000001294 140. Gao CC, Kapoor E, Lipford MC, et al. Association of vasomotor symptoms and sleep apnea risk in midlife women. Menopause. 2018;25(4):391–​398. DOI: http://​ doi.org/​10.1097/​GME.0000000000001020 141. Muka T, Oliver-​Williams C, Colpani V, et al. Association of vasomotor and other menopausal symptoms with risk of cardiovascular disease: A systematic review and meta-​analysis. PLoS One. 2016;11(6):e0157417. DOI: http://​doi.org/​10.1371/​ journal.pone.0157417 142. Thurston RC, Ewing LJ, Low CA, Christie AJ, Levine MD. Behavioral weight loss for the management of menopausal hot flashes: A pilot study. Menopause. 2015;22(1):59–​65. DOI: http://​doi.org/​10.1097/​GME.0000000000000274 143. Drake CL, Kalmbach DA, Arnedt JT, et al. Treating chronic insomnia in postmenopausal women: A randomized clinical trial comparing cognitive-​behavioral therapy for insomnia, sleep restriction therapy, and sleep hygiene education. Sleep. 2019;42(2). DOI: http://​doi.org/​10.1093/​sleep/​zsy217 144. McCurry SM, Guthrie KA, Morin CM, et al. Telephone-​based cognitive behavioral therapy for insomnia in perimenopausal and postmenopausal women with vasomotor symptoms: A MsFLASH randomized clinical trial. JAMA Intern Med. 2016;176(7):913–​920. DOI: http://​doi.org/​10.1001/​jamainternmed.2016.1795 145. Women and sleep: A guide for better health. Swhr.org. Published November 30, 2017. Accessed December 4, 2020. https://​swhr.org/​swhr_​resource/​women-​andsleep-​a-​guide-​for-​better-​health

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Emotional Wellness and Stress Resilience Gia Merlo, MD, MBA, DipABLM New York University

Ariyaneh Nikbin

Albert Einstein College of Medicine New Youk, NY

Hanjun Ryu, BS Rice University Houston, TX 4.1 4.2 4.3 4.4 4.5 4.6 4.7 4.8

Introduction......................................................................................................86 Emotional Wellness Definition and Stress.......................................................86 Stress Response................................................................................................86 Relaxation Response........................................................................................87 General Adaptation Syndrome (Gas) Model of Stress.....................................88 Consequences of Chronic Stress......................................................................89 Gender Is a Risk Factor for Stress....................................................................89 Stress Appraisal................................................................................................91 4.8.1 A Growth Mindset and Self-​Compassion Can Promote Resilience against Stress......................................................................91 4.9 Positive and Adaptive Aspects of Stress: Coping.............................................92 4.9.1 Positive Cognitive Restructuring..........................................................94 4.9.2 Gratitude...............................................................................................94 4.9.3 Mindfulness and Meditation.................................................................94 4.9.4 Clinician Burnout.................................................................................95

KEY POINTS • Stress describes an individual’s response to a stressor and involves both physiological and psychological components. In particular, chronic stress can dysregulate hormonal systems important in maintaining homeostasis, predispose individuals to medical and psychiatric illness, and produce long-​lasting epigenetic changes.

DOI: 10.1201/9781003110682-5

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• Women are especially susceptible to the deleterious effects of stress during times of significant hormonal change, such as puberty, childbirth, and menopause. • Effective coping strategies and stress management techniques attempt to counter the stress response and elicit the relaxation response, restoring our bodies to homeostasis. • Clinician burnout describes the emotional exhaustion and reduced sense of accomplishment from work that clinicians may experience when working in the healthcare environment. Combating the rise in clinician burnout requires changes in both organizational and personal levels.

4.1  INTRODUCTION When physical and mental stress becomes overwhelming and prolonged, the risk for both medical and psychiatric illnesses increases. There are limitations to the pharmacological approach for treating psychiatric illness, as many major classes of psychiatric drugs create neurotransmitter imbalances, physical and psychological dependence, and undesirable side effects. While medications are necessary or helpful in many cases, there are also non-​drug lifestyle strategies and mental health techniques that can help to manage stress. This chapter explores the concept of stress and how it relates to wellness, and provides practical strategies, both physiological and psychological, to manage stress and optimize long-​term emotional wellness and happiness.

4.2  EMOTIONAL WELLNESS DEFINITION AND STRESS Emotional wellness is “an awareness, understanding, and acceptance of our feelings, and our ability to manage effectively through challenges and change.”1 Challenges and change are inevitable in our daily lives and the lives of our patients, which can result in stress. For women, stress also becomes more pronounced during periods of significant transitions during the lifespan, such as puberty, childbirth, and menopause.2,3,4 Prolonged stress can precipitate or exacerbate both medical and psychiatric illnesses.5,6 Stress is the most time-​consuming topic that primary care physicians discuss with their patients who have chronic illness.7 In fact, it is estimated that 60–​ 90% of primary care physician visits involve stress-​related complaints or an illness augmented by stress.8,9 Therefore, to achieve optimal health and wellness, effective counselling of patients on effective stress management techniques appears an important skill to develop.

4.3  STRESS RESPONSE Stress is a “condition or feeling experienced when a person perceives that demands exceed the personal and social resources the individual is able to mobilize.”10,11 It is important to remember that any change can induce a stress response. Even events that are commonly thought of as positive, such as marriage or childbirth, can increase stress level, as an individual may question whether or not they have the adequate resources to adapt to the change.3

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As defined by Hans Selye, there are two types of stress: eustress and distress.12 Eustress refers to positive stress that motivates individuals to invest more effort on improving performance.11,12 Distress, however, is associated with anxiety and decreased performance, and can have numerous detrimental consequences on medical and mental health.11,12 The stress response in humans evolved as a mechanism for survival.13 The brain has evolved two phases for the stress response: the more rapid-​acting sympathetic-​ adrenal-​ medullary (SAM) pathway and the more delayed but longer-​ acting hypothalamic-​pituitary-​adrenal (HPA) pathway.14 The brain constantly scans the environment for danger. If an immediate threat or stressor is detected, the amygdala of the limbic system becomes activated.15,16 The amygdala then signals the hypothalamus to elicit the “fight or flight” response.17 In the SAM pathway, the hypothalamus relays signals through autonomic nerves to the adrenal medulla.14,18 The chromaffin cells of the adrenal medulla then secrete epinephrine and norepinephrine into the systemic circulation, activating the sympathetic nervous system.14 The body prepares to respond to the danger by enhancing alertness, increasing heart rate and blood pressure, elevating plasma blood glucose, diverting blood flow from the digestive system to skeletal muscles, and activating blood clotting in preparation for tissue damage.19,20,21 If the stressor becomes resolved or is no longer present, the sympathetic nervous system becomes downregulated. The parasympathetic nervous system is then mobilized and promotes recovery and healing of the body through the relaxation response.20 However, if the brain still detects that a threat is present, the HPA axis of the stress response predominates. The paraventricular nucleus of the hypothalamus releases corticotropin-​ releasing hormone (CRH), which causes the release of adrenocorticotropic hormone (ACTH) from the corticotroph cells of the anterior pituitary.14 ACTH then acts on the adrenal cortex, where cortisol synthesis and release is induced.14 The cortisol then ensures that the body has adequate energy to respond to chronic stress by increasing production of glucose in the liver and decreasing glucose uptake in peripheral tissues.22,23 Cortisol then provides negative feedback to receptors in the hypothalamus and anterior pituitary, which inhibits further release of cortisol.24,25

4.4  RELAXATION RESPONSE The relaxation response works in opposition to the stress response to promote recovery and healing of the body.20,26 The relaxation response is based on the parasympathetic pathway.27,28 During the relaxation response, circulating levels of epinephrine, norepinephrine, and cortisol are downregulated, while acetylcholine and nitric oxide levels are upregulated.20 Heart rate, blood pressure, and oxygen consumption decrease and gastrointestinal activity resumes.20,29 The parasympathetic pathway also regulates the inflammatory reflex, which is a physiologic mechanism through which the vagus nerve inhibits pro-​inflammatory cytokine production and has an important role in metabolic regulation.30 Through the relaxation response, the body is returned to homeostasis after a stress response. Many modern-​day therapies,

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FIGURE 4.1  Stress response system.

such as mindfulness and meditation, attempt to elicit the relaxation response while decreasing the stress response.20,27,28

4.5  GENERAL ADAPTATION SYNDROME (GAS) MODEL OF STRESS The GAS model was proposed by Hans Selye in the 1940s to describe the body’s responses in an attempt to restore homeostasis in the face of a prolonged stressor.31 There are three stages of the model. The first stage is the alarm reaction, which occurs when we first perceive a stressor and the “fight or flight” response of the sympathetic nervous system is mobilized.31,32 The second stage is resistance, during which the body remains activated at a higher energy level to maintain physiologic function in the face of the stressor.31 However, since the resistance stage is energetically demanding, it cannot last long before the third and final stage of exhaustion (or recovery through the relaxation response) sets in.20,31 If the stressor is prolonged or the individual does not effectively adapt to the stress, the exhaustion stage depletes the body’s resources and renders the individual susceptible to disease.31,33

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4.6  CONSEQUENCES OF CHRONIC STRESS Because the chronic stress response is centered on the HPA axis, stress exhaustion may cause significant damage to this important system of neuroendocrine activity.34 Prolonged stress may cause epigenetic changes in the expression of glucocorticoids through altering methylation patterns in glucocorticoid receptor gene NR3C1.35 Dysregulation of normal glucocorticoid feedback is associated with numerous systemic effects, including increased serum blood sugar levels, accumulation of fat in visceral areas, breakdown of muscle and bone, atrophy of neurons in the hippocampus and prefrontal cortex, increased blood clotting, atherosclerosis, and infertility.36,37,38,39,40 In chronic stress, the inflammatory reflex of the vagus nerve is disrupted; the body is left in a state of excessive pro-​inflammatory cytokine production, which increases the risk of developing obesity, insulin resistance and type II diabetes mellitus, cardiovascular disease, and other debilitating conditions.30 Chronic stress can also produce epigenetic changes associated with mood and anxiety disorders, such as through the downregulation of the serotonin transporter gene SLC6A4.41 Thus, the stress response involves complex interactions between neurochemical, genetic, epigenetic, and environmental components. The stress response was initially an adaptive response that evolved in times when physical damage and deficiencies were the predominant stressors.42 However, many modern-​day stressors involve social and mental threats that are often prolonged.42 As exhaustion from various stressors compounds, chronic mental illness, medical illness, or burnout may arise.

4.7  GENDER IS A RISK FACTOR FOR STRESS It is particularly important to consider stress within the context of women’s health across the lifespan, as stress is heightened at times of significant hormonal change, such as puberty, childbirth, and menopause.2,3,4 Before the onset of puberty, men and women appear similar in their physiological responses to stress and prevalence of mood disorders.43,44,45,46 During puberty, anatomical and physiologic changes between men and women become pronounced, as each gender expresses different levels of sex steroid hormones.47 In the hypothalamic-​pituitary-​gonadal (HPG) axis of women, the hypothalamus secretes GnRH in a pulsatile manner, which stimulates the gonadotroph cells of the anterior pituitary to release follicle-​stimulating hormone (FSH) and luteinizing hormone (LH).48 The FSH and LH then act on the female ovaries to release sex hormones estrogen and progesterone.48 However, the predominant sex hormone in men is testosterone released from the testes.49 The interplay between the HPA and HPG axis can explain stress response differences between men and women. Testosterone in men is believed to inhibit stress reactivity through the HPA axis, while estrogen in women enhances HPA axis reactivity.50,51 Thus, the HPA axis of women becomes more sensitized, with enhanced glucocorticoid secretion in response to various stressors.43 After puberty and during the transition into adulthood, women become twice as likely as men to develop stress-​ related disorders, such as depression, anxiety, and post-​traumatic stress disorder.52 The HPA axis dysregulation is also believed to explain symptoms in premenstrual

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syndrome (PMS) and premenstrual dysphoric disorder (PMDD).53,54 However, in functional hypothalamic amenorrhea, an overactive HPA axis in women who suffer from chronic stress can downregulate the HPG axis through interference with the pulsatile secretion of GnRH; subsequently, chronic stress can delay puberty, suppress menses, or reduce fertility in these women.55 Throughout pregnancy, the HPA axis undergoes significant change with the rise of cortisol, which is essential for normal brain development in the fetus.56 By the third trimester, serum cortisol levels increase to three times that of non-​pregnant levels.57 Although the HPA axis is normally under negative regulation, it enters a positive feedback loop during pregnancy.57 Increased maternal cortisol levels induce the placenta to release more CRH.57 The CRH then stimulates the maternal pituitary gland to release ACTH, which then stimulates the maternal adrenal gland to further increase cortisol.57 The enzyme 11-​beta-​hydroxysteroid dehydrogenase type 2 (HSD11B2), which converts active cortisol into inactive cortisone, partially protects the fetus from the pro-​apoptotic and growth-​inhibiting effects of high cortisol.58,59 Under normal conditions, 80–​90% of cortisol becomes inactivated by the placenta through HSD11B2.57,60 Psychosocial stressors, infection, and inflammation experienced by the mother during pregnancy can weaken the barrier so that excess cortisol reaches the fetus.57 Overexposure to cortisol has negative health effects on the offspring. High maternal cortisol levels during pregnancy are associated with greater risk of early miscarriage, shorter gestation at delivery, and lower birth weight of offspring.61,62 Fetal glucocorticoid overexposure is also related to greater anxiety levels, more mood disturbances, lower intelligence quotient levels, and greater susceptibility to cardiometabolic diseases that later develop in these children.62,63,64 During the postpartum period, maternal plasma cortisol levels fall and the HPA axis gradually returns to its pre-​pregnant state.57 Following the delivery of the newborn, there is a sharp decrease in placental CRH levels.57 The HPA axis is relatively hyporesponsive to up to 12 weeks postpartum.57,65 However, anxiety disorder, post-​ traumatic stress disorder, and/​or postpartum depression have been observed among 13% of women who recently had a child.66 This may be due to the HPA axis remaining dysregulated during the postpartum period, with impaired glucocorticoid negative feedback regulation of the stress response.67 Menopause involves significant changes in the HPG axis in women with decreased release of sex steroid hormones and subsequent dysregulation of the HPA axis.68,69 Subsequently, cortisol levels in perimenopausal and postmenopausal women increase.70,71 During the transition to menopause period, there is a significant increase in the development of psychiatric disorders, especially depression, anxiety disorder, sleep disorder, and bipolar disorder.72,73 Mid-​life and elderly women also face numerous psychosocial stressors, such as marital issues, career responsibilities, and changes in caregiving responsibilities that also partially explain the increase in depression and anxiety disorders.73 Studies have found that women are more likely than men to devote time for caregiving responsibilities.74,75 These studies have also found that women experience greater mental and physical strain, greater caregiver burden, and higher levels of distress while providing

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care.74,75 When compared to women without caregiving responsibilities, women with caregiving responsibilities are more likely to rate their own health as fair or poor, more likely to suffer from one or more chronic illnesses, and are less likely to have received needed medical care in the past year.76

4.8  STRESS APPRAISAL How can we help ourselves and our patients deal with distress, and mitigate the negative effects on physical and mental health? Stress may be inevitable, but we do have some control over our response to the stressor. When confronted with a stressor, we undergo two forms of cognitive appraisal, as described by Richard Lazarus’ transactional model of stress77: primary appraisal and secondary appraisal. Primary appraisal assesses if an event is stressful or harmful to our well-​being.77 Secondary appraisal gauges if we have the resources to effectively deal with the stressor.77 According to this model, our stress response is not directly a reaction to the stressor, but instead to our cognitive appraisal and perception of the stressor.77 Thus, through reframing our perception of a stressor in a more positive light, we can attenuate and more effectively manage our stress.

4.8.1 A Growth Mindset and Self-​Compassion Can Promote Resilience against Stress There are two processes that can allow for more positive cognitive restructuring in response to a stressor: a growth mindset and self-​compassion. A growth mindset, as defined by Carol Dweck, is the view that an individual’s skills and traits are fluid and develop with time and practice.78 In contrast, a fixed mindset assumes that one’s skills and traits are static and innate.78 Those with a fixed mindset demonstrate reduced confidence when confronted with a stressor, and are more likely to view failure as representation of a lack of ability. However, those who practice a growth mindset are motivated by challenge and view failures as opportunities to expand one’s abilities.78 As a result, those with a growth mindset are more effectively and confidently able to manage difficult life events by reappraising stressors in a more positive light. Self-​compassion entails: [B]‌eing kind and understanding toward oneself in instances of pain or failure rather than being harshly self-​critical; perceiving one’s experiences as part of the larger human experience rather than seeing them as isolating; and holding painful thoughts and feelings in mindful awareness rather than over-​identifying with them.79

Individuals who are self-​compassionate are less likely to catastrophize difficult life events, are better able to mitigate the stress response, and are better prepared to cope with a given stressor.80 Self-​compassion is related to the concept of resilience, which is a dynamic process that reflects an individual’s ability to positively adapt to adversity.81 Resilience is founded on mitigating the stress response, promoting the relaxation response, and

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fostering a growth mindset.82,83 Being diagnosed with a medical condition can be extremely stressful for our patients, but resilience can protect against the negative effects of stress on an individual’s health and wellness. For example, a study found that more resilient women report higher quality of life during a gynecological cancer diagnosis. These women were more likely to express positive emotions, reappraise the experience in a positive light, and find a sense of peace and meaning in their lives.84 Resilience may also protect women from depression and anxiety symptoms and allow them to more effectively manage their health.85

4.9  POSITIVE AND ADAPTIVE ASPECTS OF STRESS: COPING Lazarus and Folkman provided the widely accepted definition of coping as “thoughts and behaviors that people use to manage the internal and external demands of situations that are appraised as stressful.”77 Coping is a multidimensional process that can vary based on the individual, situation, and environment. Lazarus and Folkman divided coping strategies into two major types: problem-​ based coping and emotion-​focused coping.77 Problem-​based coping focuses on specific actions to confront the stressor and alter the source of stress, such as active coping (taking steps to eliminate or alleviate the stressor), planning (thinking about how to deal with the stressor), suppression of competing activities (putting other distracting projects aside to focus on dealing with the stressor), restraint coping (waiting for the right moment to act on the stressor), and seeking of instrumental social support (seeking advice, assistance, or information from others).77,85 Emotion-​ focused coping focuses on regulating the emotions that the stress may trigger, such as through seeking of emotional social support (seeking moral support, sympathy, or understanding from others), positive reinterpretation (reframing the stressor in a positive light), acceptance of the problem, denial, and turning to religion for support.77,85 Evidence suggests that problem-​based coping strategies are associated with a greater sense of personal control and reduced depression and anxiety.86 This relationship may be related to a growth mindset, as those who believe that stressors can be addressed and altered are likely to engage in problem-​based coping. While some data has found that emotion-​focused coping is associated with increased anxiety and depression, the data is conflicting.77,86,87,88,89,90 For example, when the source of stress is outside an individual’s locus of control, emotion-​based coping strategies such as mindfulness and meditation can be effective for dealing with the stressor.77,89 However, it is important to avoid the use of maladaptive coping strategies, which relieve stress symptoms temporarily but maintain or exacerbate the stressor. Maladaptive coping is associated with increased symptoms of anxiety and depression long term.91 Several maladaptive coping methods include behavioral disengagement, denial, self-​blame, and substance use.92 While many stressors are inevitable and out of our control and the control of our patients, we are able to develop effective coping strategies that can manage stress and challenging situations. The rest of the chapter discusses three of the coping and stress

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management strategies that we ourselves can practice and counsel our patients on. A more comprehensive list of stress management techniques is presented in Table 4.1. Remember that the most appropriate and effective coping strategies depend on the individual and the situation.

TABLE 4.1 Common Stress Management Techniques Technique

Concept

Positive cognitive restructuring

Through reflecting on past events to which an individual has had negative feelings toward, an individual is able to evaluate beliefs, modify behaviors, and shape responses to future events. For a more detailed explanation, refer to the chapter subsection.

Gratitude

Expressing more consistent appreciation for one’s life improves resilience and allows for a more positive response to stressors. For a more detailed explanation, refer to the chapter subsection.

Mindfulness and meditation

Mindfulness and meditation involves focusing one’s awareness on the present moment and attempt to elicit the relaxation response. For a more detailed explanation, refer to the chapter subsection.

Building social support systems

Higher levels of social support may improve resilience to stress, facilitate the use of adaptive coping techniques, and buffer against the full impact of mental and medical illness.108

Exercise

Exercise can be used as primary and secondary prevention for numerous medical and psychiatric conditions. Through one mechanism, physical exercise enhances the conversion of kynurenine into kynurenic acid. The reduction of kynurenine protects the brain from stress-​induced changes associated with depression.109,110

Progressive muscle relaxation (PMR)

PMR aims to reduce the sympathetic stress response and stimulate the parasympathetic relaxation response by decreasing muscular tension. Through PMR, an individual tenses and then relaxes specific muscles, while concentrating on the differences between the tense and relaxed states.109,111

Deep or diaphragmatic breathing

Diaphragmatic breathing involves contraction of the diaphragm, expansion of the abdomen, and deepening of inhalation and exhalation in order to decrease respiratory rate and maximize oxygen saturation.112 Deep breathing also works to enhance the relaxation response while reducing the stress response.109 This method has potential for reducing the emotional and physiological consequences of stress in healthy adults.112

Bright light therapy

Bright light therapy can improve emotional regulation in individuals with depressive disorders and alleviate stress and fear conditioning in individuals with anxiety disorders.113 Bright light therapy was also shown to be effective in reducing elevated cortisol levels and improving mood.109,114

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4.9.1 Positive Cognitive Restructuring Positive cognitive restructuring is one of the most effective coping mechanisms because it addresses the negative feelings that contribute to stress. In doing so, we may approach future stressful situations with a more positive outlook. One method incorporating positive cognitive restructuring is the ABC model from cognitive behavioral therapy.93 The ABC technique aims to help one to analyze past events to which they have had an emotional response. At its core, it requires the recognition of a cause-​and-​effect relationship between an event and one’s feelings. The “A” in the model refers to the activating event, which refers to any event that may have led to negative feelings. The “B” refers to our beliefs which may influence or may be influenced by the activating event. Lastly, the “C” represents the emotional or behavioral consequences that we face due to how our beliefs interact with the activating event. The ABC technique focuses on the cognitive space between B and C, pushing us to identify and reflect on our beliefs, recognize that they may be unhealthy and irrational, and modify them in order to reshape the negative consequences. Furthermore, by doing so, we may be able to proactively shape their response to future stressors.

4.9.2 Gratitude Gratitude is a related proactive coping mechanism that allows us to reframe our stressors. Gratitude represents a life orientation to the positive in the world, and may allow for increased social support and wellness.94 Gratitude can also reduce symptoms of burnout and improve resilience.95,96 An easy way to practice gratitude in our daily lives is to keep a gratitude journal. Each day, by writing down three to five things you are grateful for, and by reflecting on why you are grateful, you may be able to reframe your negative thought patterns and refocus mental energy towards positive thinking. A seminal study by Robert Emmons and colleagues found that people who kept gratitude lists were more likely to make progress in personal goals, be more optimistic, exercise more regularly, and feel better about their lives as a whole.97

4.9.3 Mindfulness and Meditation Meditation originated as a religious tool to deepen spiritual understanding and has been practiced for thousands of years. While many still practice meditation with a religious purpose, it is also commonly used as a tool for relaxation and stress reduction and is increasing in practice in the United States.98 Meditation has been associated with improved depression, anxiety, and pain symptoms.99 Meditation may decrease the stress response through eliciting the relaxation response to lower heart rate, blood pressure, and oxygen consumption.82,100 Functional magnetic resonance imaging studies indicate that meditation also acts on the brain, activating neural structures involved in attention, such as the frontal and parietal cortex, as well as structures involved in autonomic control, such as the pregenual anterior cingulate, amygdala, midbrain, and hypothalamus.101

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However, many are wary to meditate due to misconceptions about the practice.102 Some may believe that meditation takes too long, or that one must be spiritual to meditate, or that meditation is difficult. Although becoming proficient in meditation requires practice like any other skill, it can be as simple as closing your eyes and focusing on your breathing for a minute. There is not a single, correct way to practice meditation, and taking just a few minutes out of your day to meditate in a way that works for you may help tremendously for coping with stress. Mindfulness may be more attractive as an option for those who may be wary of the spiritual connotations of meditation. Mindfulness refers to the practice of maintaining a state of awareness of one’s thoughts, emotions, or experiences. Many of the same techniques used in meditation are used to develop mindfulness, such as mindfulness meditation, body awareness, and exploration of thoughts. Mindfulness-​Based Stress Reduction (MBSR) is a popular mindfulness program developed by Jon Kabat-​ Zinn to help people to be aware of and respond consciously to external stressors.103 Mindfulness is associated with improved psychological well-​ being and reduced perceived stress.104,105 Like meditation, mindfulness also has effects on the brain, such as through changes in gray matter concentration regions involved in learning, memory, and emotional regulation.105,106 Crucially, MBSR has been shown to increase self-​compassion in healthcare professionals, allowing us to develop a growth mindset that is inherently more resilient to stress.107

4.9.4 Clinician Burnout While this chapter focuses on the effects of stress on patients, clinicians are also vulnerable to the negative effects of prolonged stress through clinician burnout. Clinician burnout is characterized by emotional exhaustion, depersonalization, and a reduced sense of personal accomplishment from work.115 As emotional exhaustion is exacerbated, clinicians may feel like they are no longer able to give of themselves to their patients.115 Burnout not only leads to increased physician dissatisfaction, turnover rates, likelihood for substance use, depression and suicide rates, and risk for medical illness, but also results in higher rates of medical error, reduced patient satisfaction, and negative patient outcomes. Clinician burnout has been shown to be primarily a systemic issue that has become more prevalent over time. Changes to the healthcare landscape in how care is delivered, documented, and reimbursed have led to decreased autonomy, increased clerical workload, and decreased trust in the system. For example, the widespread adoption of electronic health records (EHRs), and its resulting interference with physician–​ patient interactions and increased clerical burden, has been a frequently cited factor for the increase in burnout. An imbalance of job demands and the resources available to deal with them, compounded with administrative pressures and reimbursement models that incentivize seeing as many patients as possible, may be another factor. Medscape’s National Physician Burnout & Suicide Report 2020 found that female physicians were more likely to report burnout compared to their male counterparts, and this finding has been consistently observed over the past several years.116 The clinician burnout phenomenon is especially prominent in obstetrician –​gynecologists

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(OB/​GYN), as 46% of OB/​GYN physicians reported burnout in the 2020 survey.116 A study published in Clinical Obstetrics and Gynecology estimated that there will be OB/​GYN physician shortages of 17% by 2030, 24% by 2040, and 31% by 2050.117 The high rate of burnout, increasing female population in the United States, and increased access to healthcare that has heightened the demand for healthcare services have made OB/​GYN especially susceptible to the impending physician shortage. The physician burnout phenomenon is a public health concern, and a problem that needs to be addressed, for the well-​ being of physicians and their patients alike. A systems approach to address physician burnout that focuses on improving the structure, organization, and culture of healthcare has been suggested by the National Academy of Medicine’s Action Collaborative on Clinician Well-​Being and Resilience.118 Initiatives by healthcare institutions and policymakers to address burnout are also beginning to arise. Among these are the American Medical Association’s Practice Transformation Initiative and STEPS Forward Program, and formation of wellness committees in medical schools and residency programs across the country.119 A concerted effort by all stakeholders to modify the systems of healthcare will be required to address the roots of the problem. Nevertheless, we are not powerless as individuals. As medical professionals, we also have a mandate to take care of ourselves, just as we aim to take care of our patients. There are steps we can take to abate and adapt to the stresses of the medical profession and protect ourselves from burnout. Adaptation is a normal response that follows a newfound stimulus, and all physicians adapt to the stressors of the healthcare environment in one way or another. Crucially, though, adaptation can be either positive or negative, and when we engage in maladaptive responses to occupational stress, we may be putting ourselves at risk of burnout. By developing an understanding that stress is normal and not any fault of our own, and by training for adaptive and healthy coping responses, we may be able to develop resilience against burnout at the individual level. Additionally, by learning how to adaptively cope with the stressors inherent in our jobs as clinicians, we will be better able to help our patients mitigate their own stress, deliver better quality of care, and improve our patients’ outcomes.

REFERENCES 1. Lerner M. Invest in your greatest asset … people. The National Center for Emotional Wellness. www.nationalcenterforemotionalwellness.org. Published 2019. Accessed September 19, 2020. 2. Romeo RD. The teenage brain: The stress response and the adolescent brain. Curr Dir Psychol Sci. 2013;22(2):140–​145. doi:10.1177/​0963721413475445 3. Holmes TH, Rahe RH. The social readjustment rating scale. J Psychosom Res. 1967;11(2):213–​218. doi:10.1016/​0022-​3999(67)90010-​4 4. Falconi AM, Gold EB, Janssen I. The longitudinal relation of stress during the menopausal transition to fibrinogen concentrations: Results from the study of women’s health across the nation. Menopause. 2016;23(5):518–​527. doi:10.1097/​GME.00000 00000000579 5. Salleh MR. Life event, stress and illness. Malays J Med Sci. 2008;15(4):9–​18.

97

Emotional Wellness and Stress Resilience

97

6. Liu Y-​Z, Wang Y-​X, Jiang C-​L. Inflammation: The common pathway of stress-​related diseases. Front Hum Neurosci. 2017;11. doi:10.3389/​fnhum.2017.00316 7. Russell NK, Roter DL. Health promotion counseling of chronic-​disease patients during primary care visits. Am J Public Health. 1993;83(7):979–​982. doi:10.2105/​ ajph.83.7.979 8. Nerurkar A, Bitton A, Davis RB, Phillips RS, Yeh G. When physicians counsel about stress: Results of a national study. JAMA Intern Med. 2013;173(1):76–​77. doi:10.1001/​ 2013.jamainternmed.480 9. Avey H, Matheny KB, Robbins A, Jacobson TA. Health care providers’ training, perceptions, and practices regarding stress and health outcomes. J Natl Med Assoc. 2003;95(9):833–​845. 10. What is stress? The American Institute of Stress. Accessed October 14, 2020. www.stress.org/​dev/​daily-​life 11. Lazarus RS. Psychological Stress and the Coping Process. New York:McGraw-​ Hill; 1966. 12. Selye H. Stress without distress. Psychopathology of Human Adaptation. 1976:137–​ 146. doi:10.1007/​978-​1-​4684-​2238-​2_​9 13. Cannon WB. Bodily Changes in Pain, Hunger, Fear and Rage. D. Appleton and Company; 1915. 14. Godoy LD, Rossignoli MT, Delfino-​Pereira P, Garcia-​Cairasco N, de Lima Umeoka EH. A comprehensive overview on stress neurobiology: Basic concepts and clinical implications. Front Behav Neurosci. 2018;12. doi:10.3389/​fnbeh.2018.00127 15. Petrovich GD, Canteras NS, Swanson LW. Combinatorial amygdalar inputs to hippocampal domains and hypothalamic behavior systems. Brain Research Reviews. 2001;38(1–​2):247–​289. doi:10.1016/​S0165-​0173(01)00080-​7 16. Sapolsky R. Taming Stress. Scientific American. 2003;289(3):86–​95. 17. Lewis KP, Barton RA. Amygdala size and hypothalamus size predict social play frequency in nonhuman primates: A comparative analysis using independent contrasts. J Comp Psychol. 20060320;120(1):31. doi:10.1037/​0735-​7036.120.1.31 18. McCorry LK. Physiology of the autonomic nervous system. Am J Pharm Educ. 2007;71(4):78. doi:10.5688/​aj710478 19. Ulrich-​Lai YM, Herman JP. Neural regulation of endocrine and autonomic stress responses. Nat Rev Neurosci. 2009;10:397–​409. doi:10.1038/​nrn2647 20. Dusek JA, Benson H. Mind-​body medicine. Minn Med. 2009;92(5):47–​50. 21. Preckel D, von Känel R. Regulation of hemostasis by the sympathetic nervous system: Any contribution to coronary artery disease? Heartdrug. 2004;4:123–​130. doi:10.1159/​000078415 22. Hannibal KE, Bishop MD. Chronic stress, cortisol dysfunction, and pain: A psychoneuroendocrine rationale for stress management in pain rehabilitation. Phys Ther. 2014;94(12):1816–​1825. doi:10.2522/​ptj.20130597 23. Kuo T, McQueen A, Chen T-​C, Wang J-​C. Regulation of glucose homeostasis by glucocorticoids. Adv Exp Med Biol. 2015;872:99–​126. doi:10.1007/​978-​1-​49392895-​8_​5 24. Gupta S, Aslakson E, Gurbaxani BM, Vernon SD. Inclusion of the glucocorticoid receptor in a hypothalamic pituitary adrenal axis model reveals bistability. Theor Biol Med Model. 2007;4:8. doi:10.1186/​1742-​4682-​4-​8 25. Gjerstad JK, Lightman SL, Spiga F. Role of glucocorticoid negative feedback in the regulation of HPA axis pulsatility. Stress. 2018;21(5):403–​ 416. doi:10.1080/​ 10253890.2018.1470238

98

98

Gia Merlo, Ariyaneh Nikbin, and Hanjun Ryu 26. Wallace R, Benson H, Wilson A. A wakeful hypometabolic physiologic state. Am J Physiol. 1971;221(3):795–​799. 27. Jerath R, Barnes VA, Crawford MW. Mind-​body response and neurophysiological changes during stress and meditation: Central role of homeostasis. J Biol Regul Homeost Agents. 2014;28(4):545–​554. 28. Tang Y-​Y, Ma Y, Fan Y, et al. Central and autonomic nervous system interaction is altered by short-​ term meditation. PNAS. 2009;106(22):8865–​ 8870. doi:10.1073/​ pnas.0904031106 29. Browning KN, Travagli RA. Central nervous system control of gastrointestinal motility and secretion and modulation of gastrointestinal functions. Compr Physiol. 2014;4(4):1339–​1368. doi:10.1002/​cphy.c130055 30. Pavlov VA, Tracey KJ. The vagus nerve and the inflammatory reflex—​ linking immunity and metabolism. Nat Rev Endocrinol. 2012;8(12):743–​754. doi:10.1038/​ nrendo.2012.189 31. Selye H. The general adaptation model and the diseases of adaptation. J Clin Endocrinol Metab. 1946;6(2):117–​230. doi:10.1210/​jcem-​6-​2-​117 32. Goldstein DS. Adrenal responses to stress. Cell Mol Neurobiol. 2010;30(8):1433–​ 1440. doi:10.1007/​s10571-​010-​9606-​9 33. Selye H. Stress and the general adaptation syndrome. Br Med J. Published online 1950:1383–​1392. doi:10.1136/​bmj.1.4667.1383 34. Dunlavey CJ. Introduction to the hypothalamic-​ pituitary-​ adrenal axis: Healthy and dysregulated stress responses, developmental stress and neurodegeneration. J Undergrad Neurosci Educ. 2018;16(2):R59–​R60. 35. Parade SH, Ridout KK, Seifer R, et al. Methylation of the glucocorticoid receptor gene promoter in preschoolers: Links with internalizing behavior problems. Child Dev. 2016;87(1):86–​97. doi:10.1111/​cdev.12484 36. Brindley DN, McCann BS, Niaura R, Stoney CM, Suarez EC. Stress and lipoprotein metabolism: Modulators and mechanisms. Metabolism. 1993;42(9 Suppl 1):3–​15. doi:10.1016/​0026-​0495(93)90255-​m 37. Aschbacher K, Kornfeld S, Picard M, et al. Chronic stress increases vulnerability to diet-​ related abdominal fat, oxidative stress, and metabolic risk. Psychoneuroendocrinology. 2014;46:14–​22. doi:10.1016/​j.psyneuen.2014.04.003 38. Mcewen BS. Protection and damage from acute and chronic stress: Allostasis and allostatic overload and relevance to the pathophysiology of psychiatric disorders. Ann NY Acad. 2004;1032(1):1–​7. doi:10.1196/​annals.1314.001 39. Sominsky L, Hodgson DM, McLaughlin EA, Smith R, Wall HM, Spencer SJ. Linking stress and infertility: A novel role for ghrelin. Endocr Rev. 2017;38(5):432–​467. doi:10.1210/​er.2016-​1133 40. Rooney KL, Domar AD. The relationship between stress and infertility. Dialogues Clin Neurosci. 2018;20(1):41–​47. doi:10.31887/​DCNS.2018.20.1/​klrooney 41. Lee JS, Jaini PA, Papa F. An epigenetic perspective on lifestyle medicine for depression: Implications for primary care practice. Am J Lifestyle Med. Published online September 2020:1559827620954779. doi:10.1177/​1559827620954779 42. Nesse RM, Young EA. Evolutionary origins and functions of the stress response. In: Fink J (ed) Encyclopedia of Stress. Vol 2. Academic Press; 2007, pp. 79–​84. 43. Bale TL, Epperson CN. Sex differences and stress across the lifespan. Nat Neurosci. 2015;18:1413–​1420. doi:10.1038/​nn.4112 44. Romeo RD. Pubertal maturation and programming of hypothalamic–​ pituitary–​ adrenal reactivity. Front Neuroendocrinol. 2010;31(2):232–​240. doi:10.1016/​j.yfrne. 2010.02.004

99

Emotional Wellness and Stress Resilience

99

45. Romeo RD, McEwen BS. Stress and the adolescent brain. Ann N Y Acad Sci. 2006;1094:202–​214. doi:10.1196/​annals.1376.022 46. Kessler RC. Epidemiology of women and depression. J Affect Disorders. 2003;74(1):5–​ 13. doi:10.1016/​S0165-​0327(02)00426-​3 47. Frank GR. Role of estrogen and androgen in pubertal skeletal physiology. Med Pediatr Oncol. 2003;41:217–​221. doi:10.1002/​mpo.10340 48. Herbison AE. Control of puberty onset and fertility by gonadotropin-​ releasing hormone neurons. Nat Rev Endocrinol. 2016;12(8):452–​466. doi:10.1038/​nrendo. 2016.70 49. Arora P, Topiwala S. Testosterone | Hormone Health Network. Hormone Health Network. Published April 2020. Accessed October 25, 2020. www.hormone.org/​your-​ health-​and-​hormones/​glands-​and-​hormones-​a-​to-​z/​hormones/​testosterone 50. Herman JP, McKlveen JM, Ghosal S, et al. Regulation of the hypothalamic-​pituitary-​ adrenocortical stress response. Compr Physiol. 2016;6(2):603–​621. doi:10.1002/​cphy. c150015 51. Viau V, Meaney MJ. The inhibitory effect of testosterone on hypothalamic-​pituitary-​ adrenal responses to stress is mediated by the medial preoptic area. J Neurosci. 1996;16(5):1866–​1876. doi:10.1523/​JNEUROSCI.16-​05-​01866.1996 52. Olff M. Sex and gender differences in post-​traumatic stress disorder: An update. Eur J Psychotraumatol. 2017;8(Sup 4). doi:10.1080/​20008198.2017.1351204 53. Rabin DS, Schmidt PJ, Campbell G, et al. Hypothalamic-​pituitary-​adrenal function in patients with the premenstrual syndrome. J Clin Endocrinol Metab. 1990;71(5):1158–​ 1162. doi:10.1210/​jcem-​71-​5-​1158 54. Huang Y, Zhou R, Wu M, Wang Q, Zhao Y. Premenstrual syndrome is associated with blunted cortisol reactivity to the TSST. Stress. 2015;18(2):160–​168. doi:10.3109/​ 10253890.2014.999234 55. Gordon CM. Functional hypothalamic amenorrhea. New Engl J Med. 2010;363(4):365–​ 371. doi:10.1056/​NEJMcp0912024 56. Kapoor A, Dunn E, Kostaki A, Andrews MH, Matthews SG. Fetal programming of hypothalamo-​pituitary-​adrenal function: Prenatal stress and glucocorticoids. J Physiol. 2006;572(Pt 1):31–​44. doi:10.1113/​jphysiol.2006.105254 57. Duthie L, Reynolds RM. Changes in the maternal hypothalamic-​pituitary-​adrenal axis in pregnancy and postpartum: Influences on maternal and fetal outcomes. Neuroendocrinology. 2013;98:106–​115. doi:10.1159/​000354702 58. HSD11B2 hydroxysteroid 11-​ beta dehydrogenase 2 [Homo sapiens (human)] -​Gene -​NCBI. NCBI. Published August 18, 2020. Accessed October 3, 2020. www.ncbi.nlm.nih.gov/​gene/​3291 59. Benediktsson R, Calder AA, Edwards CR, Seckl JR. Placental 11 beta-​hydroxysteroid dehydrogenase: A key regulator of fetal glucocorticoid exposure. Clin Endocrinol (Oxf). 1997;46(2):161–​166. doi:10.1046/​j.1365-​2265.1997.1230939.x 60. Gitau R, Fisk NM, Glover V. Human fetal and maternal corticotrophin releasing hormone responses to acute stress. Archives of Disease in Childhood -​Fetal and Neonatal Edition. 2004;89:F29–​F32. doi:10.1136/​fn.89.1.F29 61. Nepomnaschy PA, Welch KB, McConnell DS, Low BS, Strassmann BI, England BG. Cortisol levels and very early pregnancy loss in humans | PNAS. PNAS. 2006;103(10):3938–​3942. doi:10.1073/​pnas.0511183103 62. Isaksson J, Lindblad F, Valladares E, Högberg U. High maternal cortisol levels during pregnancy are associated with more psychiatric symptoms in offspring at age of nine –​ A prospective study from Nicaragua. J Psychiatr. Res. 2015;71:97–​102. doi:10.1016/​ j.jpsychires.2015.09.016

100

100

Gia Merlo, Ariyaneh Nikbin, and Hanjun Ryu

63. Buss C, Davis EP, Shahbaba B, Pruessner JC, Head K, Sandman CA. Maternal cortisol over the course of pregnancy and subsequent child amygdala and hippocampus volumes and affective problems. PNAS. 2012;109(20):E1312–​E1319. doi:10.1073/​ pnas.1201295109 64. LeWinn KZ, Stroud LR, Molnar BE, Ware JH, Koenen KC, Buka SL. Elevated maternal cortisol levels during pregnancy are associated with reduced childhood IQ. Int J Epidemiol. 2009;38(6):1700–​1710. doi:10.1093/​ije/​dyp200 65. Magiakou MA, Mastorakos G, Rabin D, Dubbert B, Gold PW, Chrousos GP. Hypothalamic corticotropin-​releasing hormone suppression during the postpartum period: Implications for the increase in psychiatric manifestations at this time. J Clin Endocrinol Metab. 1996;81(5):1912–​1917. doi:10.1210/​jcem.81.5.8626857 66. Razurel C, Bruchon-​ Schweitzer M, Dupanloup A, Irion O, Epiney M. Stressful events, social support and coping strategies of primiparous women during the postpartum period: A qualitative study. Midwifery. 2011;27(2):237–​242. doi:10.1016/​ j.midw.2009.06.005 67. Cox EQ, Stuebe A, Pearson B, Grewen K, Rubinow D, Meltzer-​Brody S. Oxytocin and HPA stress axis reactivity in postpartum women. Psychoneuroendocrinology. 2015;55:164–​172. doi:10.1016/​j.psyneuen.2015.02.009 68. Atwood CS, Meethal SV, Liu T, et al. Dysregulation of the hypothalamic-​pituitary-​ gonadal axis with menopause and andropause promotes neurodegenerative senescence. J Neuropathol Exp Neurol. 2005;64(2):93–​103. doi:10.1093/​jnen/​64.2.93 69. Gordon JL, Girdler SS, Meltzer-​Brody SE, et al. Ovarian hormone fluctuation, neurosteroids and HPA axis dysregulation in perimenopausal depression: A novel heuristic model. Am J Psychiatry. 2015;172(3):227–​236. doi:10.1176/​appi. ajp.2014.14070918 70. Woods NF, Mitchell ES, Smith-​DiJulio K. Cortisol levels during the menopausal transition and early postmenopause: Observations from the Seattle Midlife Women’s Health Study. Menopause. 2009;16(4):708–​718. doi:10.1097/​gme.0b013e318198d6b2 71. Woods NF, Carr MC, Tao EY, Taylor HJ, Mitchell ES. Increased urinary cortisol levels during the menopausal transition. Menopause. 2006;13(2):212–​ 221. doi:10.1097/​ 01.gme.0000198490.57242.2e 72. Bale TL, Epperson CN. Sex differences and stress across the lifespan. Nat Neurosci. 2015;18:1413–​1420. doi:10.1038/​nn.4112 73. Hu L-​Y, Shen C-​C, Hung J-​H, et al. Risk of psychiatric disorders following symptomatic menopausal transition. Medicine. 2016;95(6). doi:10.1097/​ MD.000 0000000002800 74. Sharma N, Chakrabarti S, Grover S. Gender differences in caregiving among family -​caregivers of people with mental illnesses. World J Psychiatry. 2016;6(1):7–​17. doi:10.5498/​wjp.v6.i1.7 75. Yee JL, Schulz R. Gender differences in psychiatric morbidity among family caregivers: A review and analysis. The Gerontologist. 2000;40(2):147–​164. doi:10.1093/​geront/​40.2.147 76. Collins KS, Schoen C, Joseph S, et al. Informal Caregiving. The Commonwealth Fund. Published May 1, 1999. Accessed October 3, 2020. www.commonwealthfund.org/​ publications/​other-​publication/​1999/​may/​informal-​caregiving 77. Lazarus RS, Folkman S. Stress, Appraisal, and Coping. New York: Springer Publishing Company; 1984. 78. Dweck CS. Mindset: The New Psychology of Success. Reprint, Updated Edition. New York: Ballantine Books; 2007.

101

Emotional Wellness and Stress Resilience

101

79. Neff KD. The development and validation of a scale to measure self-​compassion. Self and Identity. 2008;2:223–​250. doi:10.1080/​15298860309027 80. Allen AB, Leary MR. Self-​compassion, stress, and coping. Soc Personal Psychol Compass. 2010;4(2):107–​118. doi:10.1111/​j.1751-​9004.2009.00246.x 81. Alizadeh S, Khanahmadi S, Vedadhir A, Barjasteh S. The relationship between resilience with self-​compassion, social support and sense of belonging in women with breast cancer. Asian Pac J Cancer Prev. 2018;19(9):2469–​2474. doi:10.22034/​ APJCP.2018.19.9.2469 82. Rippe JM, Loiselle E, Mehta D, Proszynski J. Behavioral approaches to manage stress. In: Lifestyle Medicine. 3rd ed. CRC Press Taylor & Francis Group; 2019. 83. Park ER, Traeger L, Vranceanu A-​M, et al. The development of a patient-​centered program based on the relaxation response: The Relaxation Response Resiliency Program (3RP). Psychosomatics. 2013;54(2):165–​174. doi:10.1016/​j.psym.2012.09.001 84. Manne S, Myers-​Virtue S, Kashy D, et al. Resilience, positive coping, and quality of life among women newly diagnosed with gynecological cancers. Cancer Nurs. 2015;38(5):375–​382. doi:10.1097/​NCC.0000000000000215 85. Carver CS, Weintraub JK, Scheier MF. Assessing coping strategies: A theoretically based approach. J Pers Soc Psychol. 1989;56(2):267–​283. 86. Penley JA, Tomaka J, Wiebe JS. The association of coping to physical and psychological health outcomes: A meta-​analytic review. J Behav Med. 2002;25:551–​603. doi:10.1023/​A:1020641400589 87. Guardino CM, Schetter CD. Coping during pregnancy: A systematic review and recommendations. Health Psychol Rev. 2014;8(1):70–​ 94. doi:10.1080/​ 17437199.2012.752659 88. Giurgescu C, Penckofer S, Maurer MC, Bryant FB. Impact of uncertainty, social support, and prenatal coping on the psychological well-​being of high-​risk pregnant women. Nurs Res. 2006;55(5):356–​365. doi:10.1097/​00006199-​200609000-​00008 89. Yali AM, Lobel M. Coping and distress in pregnancy: An investigation of medically high risk women. J Psychosom Obstet Gynaecol. 1999;20(1):39–​52. doi:10.3109/​ 01674829909075575 90. Lobel M, DeVincent CJ, Kaminer A, Meyer BA. The impact of prenatal maternal stress and optimistic disposition on birth outcomes in medically high-​risk women. Health Psychol. 2000;19(6):544–​553. doi:10.1037//​0278-​6133.19.6.544 91. Thompson RJ, Mata J, Jaeggi SM, Buschkuehl M, Jonides J, Gotlib IH. Maladaptive coping, adaptive coping, and depressive symptoms: Variations across age and depressive state. Behav Res Thery. 2010;48(6):459–​466. doi:10.1016/​j.brat.2010.01.007 92. Carver CS. You want to measure coping but your protocol’s too long: Consider the brief cope. Int J Behav Med. 1997;4. doi:10.1207/​s15327558ijbm0401_​6 93. Ellis A. Reason and Emotion in Psychotherapy. Lyle Stuart; 1962. 94. Wood AM, Maltby J, Gillett R, Linley PA, Joseph S. The role of gratitude in the development of social support, stress, and depression: Two longitudinal studies. J Res Personal. 2008;42(4):854–​871. doi:10.1016/​j.jrp.2007.11.003 95. Chan DW. Burnout and life satisfaction: Does gratitude intervention make a difference among Chinese school teachers in Hong Kong? Educational Psychology. 2011;31(7):809–​823. doi:10.1080/​01443410.2011.608525 96. Green JD, Davis JL, Cairo AH, Griffin BJ, Behler AMC, Garthe RC. Relational predictors and correlates of humility: An interdependence analysis. In: Handbook of Humility: Theory, Research, and Applications. Routledge/​Taylor & Francis Group; 2017:165–​177.

102

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97. Emmons RA, McCullough ME. Counting blessings versus burdens: An experimental investigation of gratitude and subjective well-​being in daily life. J Pers Soc Psychol. 2003;84(2):377–​389. doi:10.1037/​0022-​3514.84.2.377 98. Clarke T, Barnes P, Black L, Stussman B, Nahin R. Use of yoga, meditation, and chiropractors among U.S. adults aged 18 and over. NCHS Data Brief, no 325. National Center for Health Statistics. Published 2018. Accessed October 27, 2020. www.cdc.gov/​nchs/​products/​databriefs/​db325.htm 99. Goyal M, Singh S, Sibinga EMS, et al. Meditation programs for psychological stress and well-​being: A systematic review and meta-​analysis. JAMA Intern Med. 2014;174(3):357–​368. doi:10.1001/​jamainternmed.2013.13018 100. Gamaiunova L, Brandt P-​Y, Bondolfi G, Kliegel M. Exploration of psychological mechanisms of the reduced stress response in long-​term meditation practitioners. Psychoneuroendocrinology. 2019;104:143–​151. doi:10.1016/​j.psyneuen.2019. 02.026 101. Lazar SW, Bush G, Gollub RL, Fricchione GL, Khalsa G, Benson H. Functional brain mapping of the relaxation response and meditation. Neuroreport. 2000;11(7):1581–​1585. 102. Williams A, Ness PV, Dixon J, McCorkle R. Barriers to meditation by gender and age among cancer family caregivers. Nursing Research. 2012;61(1):22–​27. doi:10.1097/​ NNR.0b013e3182337f4d 103. Kabat-​Zinn J, Lipworth L, Burney R. The clinical use of mindfulness meditation for the self-​regulation of chronic pain. J Behav Med. 1985;8(2):163–​190. doi:10.1007/​ BF00845519 104. Keng S-​L, Smoski MJ, Robins CJ. Effects of mindfulness on psychological health: A review of empirical studies. Clin Psychol Rev. 2011;31(6):1041–​1056. doi:10.1016/​ j.cpr.2011.04.006 105. Hölzel BK, Carmody J, Evans KC, et al. Stress reduction correlates with structural changes in the amygdala. Soc Cogn Affect Neurosci. 2010;5(1):11–​17. doi:10.1093/​ scan/​nsp034 106. Hölzel BK, Carmody J, Vangel M, et al. Mindfulness practice leads to increases in regional brain gray matter density. Psychiatry Research: Neuroimaging. 2011;191(1):36–​43. doi:10.1016/​j.pscychresns.2010.08.006 107. Raab K. Mindfulness, self-​ compassion, and empathy among health care professionals: A review of the literature. J Health Care Chaplaincy. 2014;20(3):95–​ 108. doi:10.1080/​08854726.2014.913876 108. Ozbay F, Johnson DC, Dimoulas E, Morgan CA, Charney D, Southwick S. Social support and resilience to stress. Psychiatry (Edgmont). 2007;4(5):35–​40. 109. Rippe JM, Nedley N, Ramirez, FE. Emotional Health and Stress Management. In: Lifestyle Medicine. 3rd ed. CRC Press Taylor & Francis Group; 2019. 110. Agudelo LZ, Femenía T, Orhan F, et al. Skeletal muscle PGC-​ 1α1 modulates kynurenine metabolism and mediates resilience to stress-​induced depression. Cell. 2014;159(1):33–​45. doi:10.1016/​j.cell.2014.07.051 111. Jacobson E. Progressive Relaxation: A Physiological and Clinical Investigation of Muscular States and Their Significance in Psychology and Medical Practice. University of Chicago Press; 1938. 112. Ma X, Yue Z-​Q, Gong Z-​Q, et al. The effect of diaphragmatic breathing on attention, negative affect and stress in healthy adults. Front Psychol. 2017;8. doi:10.3389/​ fpsyg.2017.00874

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113. Kawamura A, Yoshiike T, Yoshimura A, et al. Bright light exposure augments cognitive behavioral therapy for panic and posttraumatic stress disorders: A pilot randomized control trial. Sleep Biol Rhythms. 2020;18:101–​ 107. doi:10.1007/​ s41105-​019-​00248-​7 114. Lieverse R, Van Someren EJW, Nielen MMA, Uitdehaag BMJ, Smit JH, Hoogendijk WJG. Bright light treatment in elderly patients with nonseasonal major depressive disorder: A randomized placebo-​controlled trial. Arch Gen Psychiatry. 2011;68(1):61–​ 70. doi:10.1001/​archgenpsychiatry.2010.183 115. Maslach C, Jackson SE, Leiter MP. The Maslach Burnout Inventory Manual. Evaluating Stress: A Book of Resources. Eds. Zalaquett and Wood. New York: Scarecrow Press.1997;3:191–​218. 116. Kane L. Medscape National Physician Burnout & Suicide Report 2020: The Generational Divide. Medscape. Published January 15, 2020. Accessed October 3, 2020. //​www.medscape.com/​slideshow/​2020-​lifestyle-​burnout-​6012460 117. Vetter MH, Salani R, Williams TE, Ellison C, Satiani B. The impact of burnout on the obstetrics and gynecology workforce. Clinical Obstetrics and Gynecology. 2019;62(3):444–​454. doi:10.1097/​GRF.0000000000000452 118. National Academies of Sciences, Engineering, and Medicine; National Academy of Medicine; Committee on Systems Approaches to Improve Patient Care by Supporting Clinician Well-​Being. Taking Action Against Clinician Burnout: A Systems Approach to Professional Well-​Being. National Academies Press (US); 2019. doi:10.17226/​ 25521 119. Rosenstein AH. Hospital administration response to physician stress and burnout. Hospital Practice. 2019;47(5):217–​220. doi:10.1080/​21548331.2019.1688596

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Positive Psychology and Relational Connectedness Liana Lianov, MD, MPH

President, Global Positive Health Institute, Inc. Chair, Happiness Science and Positive Health Committee, American College of Lifestyle Medicine President, Positive Health and Wellness Division, International Positive Psychology Association Vice-​Chair, American Board of Lifestyle Medicine Principal and Founder, HealthType LLC Sacramento, CA 5.1 Introduction to Positive Psychology...............................................................106 5.2 Positive Psychology, Gender, and Culture.....................................................107 5.2.1 Positive Psychology, Gender, and Sex...............................................107 5.2.2 Positive Psychology and Culture........................................................108 5.3 Positive Psychology Throughout the Lifespan...............................................108 5.3.1 Adolescence.......................................................................................108 5.3.2 Pregnancy...........................................................................................108 5.3.3 Menopause.........................................................................................109 5.3.4 Aging..................................................................................................109 5.4 Positive Emotions, Healthy Lifestyles, and Well-​Being................................109 5.4.1 The Reciprocal Relationship between Positive Emotions and Healthy Lifestyles........................................................................109 5.4.2 Positive Psychology Activities That Promote Positive Emotions......110 5.5 Types of Positive Psychology Interventions...................................................110 5.5.1 The PERMA Framework....................................................................110 5.5.2 Mindfulness........................................................................................110 5.5.3 Exposure to Nature.............................................................................111 5.6 Practical Application of Positive Psychology Approaches in Health Care.................................................................................................111 5.6.1 Measures of Happiness and Related Constructs................................111 5.6.2 Variety, Dosing, and Person-​Activity Fit of Positive Psychology Interventions...................................................................112 5.7 Positive Psychology Approaches in Interactions with Patients......................113 5.7.1 Coaching Health Behavior Change with Positive Psychology...........113 5.7.2 Modeling Positive Psychology in the Exam Room............................113 DOI: 10.1201/9781003110682-6

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5.8 Positive Psychology Strategies For Health Care Workers’ Well-​Being.........114 5.8.1 Medical Practitioner Well-​Being and Patient Care.............................114 5.8.2 Positive Psychology Interventions for Medical Practitioners............114 5.8.2.1 P –​Positive Emotions..........................................................114 5.8.2.2 E –​Engagement...................................................................115 5.8.2.3 R –​Relationships.................................................................115 5.8.2.4 M –​Meaning........................................................................115 5.8.2.5 A –​ Accomplishment............................................................115 5.9 Positive Psychology Resources......................................................................116 5.9.1 Academic and Nonprofit Organizations.............................................116 5.9.2 Positive Psychology Websites, Apps, and Programs..........................116 5.10 Summary and Conclusion..............................................................................116

KEY POINTS • Positive psychology-​ based activities including social connection, that lead to positive emotions, not only improve emotional health but also offer direct physiologic benefits, enhance physical health, and increase longevity. • Positive emotions and healthy behaviors, such as a whole food, plant-​based diet and physical activity, have a reinforcing reciprocal relationship. • Unlike studies in some other elements of health care, studies in the field of positive psychology often have an overrepresentation of women and, hence, are relevant to the female gender. • More studies are needed to examine the impact of positive psychology on diverse cultural populations and age groups, and in non-​mental health care settings. • Medical practitioners can briefly assess patients’ levels of flourishing with brief measures, such as the Satisfaction with Life Scale, and monitor the status of this health element, as positive activities and healthy lifestyles are being adopted. • The positive emotions, engagement, relationships, meaning and accomplishment (PERMA) framework can be used as a guide for recommending or prescribing positive activities in a total healthy lifestyle. • When recommending positive activities, practitioners need to consider each patient’s culture and personal preferences, as well as the variety and dosing of these activities. • Medical practitioners can incorporate positive psychology techniques into coaching health behaviors and can model positive approaches in the exam room.

5.1  INTRODUCTION TO POSITIVE PSYCHOLOGY Positive psychology-​ based activities, including social connections, can promote positive emotions and improve well-​being beyond the traditional behavioral health approach. Standard behavioral health techniques focus on removing or reducing the burden of negative elements, such as anxiety, depression, post-​traumatic stress, or

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other negative psychological states. The underlying assumption views negative and positive affect as different ends of the same continuum. However, positive affect is not simply the absence of negative affect and offers potential well-​being benefits over and above removal of the negative affect.1 This enhanced approach is the realm of positive psychology.

5.2  POSITIVE PSYCHOLOGY, GENDER, AND CULTURE Research in positive psychology overrepresents women and hence the recommendations are applicable to women. However, more research is needed from a spectrum of cultures.

5.2.1 Positive Psychology, Gender, and Sex Women have traditionally been underrepresented in much of the health care research.2 However, this trend is shifted in positive psychology studies. One review looked at 1,628 positive psychology articles, of which 972 were empirical, and 796 of these empirical studies reported the gender composition of study participants. In aggregate 60.2% of the total study sample were women; and of the empirical research 81.3% were women. Therefore, the conclusions and recommendations derived from this research can be viewed as relevant, applicable, and empowering for women. Although authorship by female researchers is relatively low,3 the influence of women in the field is growing, with some of the best-​known leading researchers being female, including Barbara Fredrickson, Sonja Lyubomirsky, and Sarah Pressman. Of the 1,628 articles, 37 (2.3%) had a feminist orientation and addressed women’s issues, such as reproductive, physical and mental health of women, parenthood, and victimization of women. Less than 1% addressed the marginalization or oppression of women and women’s position in society. The most popular topics were overall well-​being, life satisfaction, coping, post-​traumatic growth, and positive development of young girls. Some other topics covered were hope, positive relationships, character strengths, forgiveness, and coping with childhood abuse. Early studies of how positive psychology can benefit women include the study of positive psychology in coping strategies post-​violence,4 resilience during adolescence,5 and impact of spiritual well-​being on behavioral outcomes of homeless women.6 Many constructs in positive psychology are traditionally considered feminine in nature, such as compassion, forgiveness, kindness, social intelligence, and relationships. The field has the potential to be leveraged to help women thrive in the face of adversity, such as victimization, violence, and abuse. Also, the field is uniquely positioned to highlight behavioral and psychological gender issues that have been marginalized, including positive intergroup relationships and valuing differences.7.8 However, additional research is needed to address the impact of positive psychology approaches on gender identity. Also the relationship of the positive health element as it relates to the biologic sex phenotype, including chromosomes, hormones, and sex organs, has not yet been studied.

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5.2.2 Positive Psychology and Culture Much of the published research, especially in positive psychology, is criticized due to its emphasis on the western point of view.9,10 Future research needs to study a variety of cultural viewpoints, as well as different ethnic populations. The review study mentioned in the previous section found that 56% of the1,628 articles described studies conducted in English-​speaking western countries. Only seven of the articles dealt with issues intersecting gender and race.3 Positive psychology is a relatively young field and has much to uncover about the impact of these interventions for different genders, cultures, and in various environments, including health care settings and as part of health care treatments.

5.3  POSITIVE PSYCHOLOGY THROUGHOUT THE LIFESPAN Positive interventions have potential beneficial effects in all ages. However, much more research is needed to draw strong conclusions about specific interventions and their benefits in each age group or life stage.

5.3.1 Adolescence An alternative approach to existing cognitive behavioral therapies that may not be well-​suited for adolescents is positive psychology. While online programs may not yet be empirically supported,11 adolescent coaching integrated with positive psychology strategies may provide an opportunity to help teen girls learn and adopt approaches that can maximize their potential and improve their well-​being. Challenges during adolescence, including academic pressure, bullying, family discord, peer pressure, future goal setting, and poor body image, 12,13,14, can be addressed by teaching practical strategies that leverage positive psychology for effectively coping and even thriving. Building positive experiences of happiness, gratification and fulfillment, and positive individual traits can support adolescent well-​being and growth.15 Positive psychology interventions (PPIs) have the potential to support girls struggling with self-​ esteem, friendships, and future orientation. Girls can learn techniques, such as savoring and positive reminiscing and loving-​kindness meditation, to increase positive feelings.16 Also friendship in adolescence can enhance connectivity, empathy, and communication and conflict resolution skills,13,17 and lead to increased self-​esteem, better school achievement, fewer behavioral problems,18, and greater feelings of self-​worth and social competence.19

5.3.2 Pregnancy Very few quality published studies have addressed the use of positive psychology during pregnancy. One study of a 5-​week online PPI formulated for pregnant women found lower depression and pregnancy-​related anxiety and greater life satisfaction and social support post-​intervention.20 Much more research using robust measurements and interventions is needed in this population before we can draw conclusions specific to pregnant women.21

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5.3.3 Menopause Positive psychology and related positive well-​being approaches can be used to boost resilience in the face of midlife challenges.22 Researchers have noted a significant direct relationship between quality of life and meaning in life, self-​efficacy, body area satisfaction, and health evaluation among menopausal women.23 However, one study could not separate the effects of age and stage of menopause on women’s view of key positive well-​being factors, such as purpose in life.24 Another study found that perimenopausal and postmenopausal women did not feel as positive about their roles in life as premenopausal women. By contrast, an earlier community-​based sample of women revealed that they perceived menopause as a life crisis laden with opportunities for self-​accomplishment and positive changes in lifestyle.25 Hence, more research is needed to clarify the role of positive life elements and positive psychology across different menopausal stages.

5.3.4 Aging Positive psychology approaches may help decrease psychological effects of aging, reduce anxiety about life’s ending, support a sense of having lived a full, satisfying and meaningful life, and adjust to changes in life roles.26 Unfortunately, a 2017 review found very few high-​quality positive psychology studies in the geriatric population.27 The few studies available revealed similar results of PPIs in older age groups of 50 years and above as in younger ones. One study of 163 women aged 50–​79 years tested the impact of four self-​administered online PPIs (i.e., gratitude visit, three good things, three funny things, and using signature strengths in a new way) conducted over a week on happiness and depressive symptoms compared with a placebo control exercise about early memories. Three out of the four interventions (gratitude visit, three good things, and using signature strengths in a new way) increased happiness, whereas two interventions (three funny things and using signature strengths in a new way) led to a reduction of depressive symptoms.28 Another study in India involving 200 women and men aged 60–​80 years revealed that high levels of hope were a robust predictor of subjective well-​being.22

5.4  POSITIVE EMOTIONS, HEALTHY LIFESTYLES, AND WELL-​BEING Positive emotions and overall well-​being are closely interlinked. Although further research is needed to uncover nuances of the benefits of certain PPIs in a spectrum of populations and in health care settings, medical practitioners can harness this close relationship to enhance disease treatment and promote total well-​being.

5.4.1 The Reciprocal Relationship between Positive Emotions and Healthy Lifestyles Positive emotions, such as joy, gratitude, and pride, drive and support health behavior, improve emotional well-​being, increase reinforcing health resources,16,29,30,31,32,33,34

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and improve adherence to healthy behaviors.35,36 Positive emotions have also been associated with better health outcomes,37,38 decreased health care utilization,39 increased preventive care,40 and increased longevity.41,42,43 Potential underlying mechanisms include lower inflammation, stronger immunity,1,44 greater telomere length,45,46 and better endocrine and gene regulation.47 Evidence also supports the reverse; healthy behaviors are associated with positive emotions. Hence, positive emotions and healthy behaviors have a reinforcing, reciprocal link. For example, individuals who exercise and eat a diet high in vegetables report greater happiness,48,49 and, in turn, self-​reported happiness can lead to healthier food choices.35 Positive emotions can expand social, physical, and cognitive resources,33 which reinforce healthy behaviors and increase positive emotions in an upward positive spiral.32

5.4.2 Positive Psychology Activities That Promote Positive Emotions Because positive activities support healthy behaviors and have direct physiologic benefits, they should be considered an essential Lifestyle Medicine intervention. Interventions can be “prescribed” to patients who can learn the skills through digital and live instructional programs independently and regularly practice these skills, like physical training.

5.5  TYPES OF POSITIVE PSYCHOLOGY INTERVENTIONS A broad spectrum of PPIs are available; some induce calm and self-​regulation, while others produce a sense of vigor and vitality. A combination of these interventions can lead to emotional well-​being, life satisfaction, physical health, and longevity.50 More research is needed regarding the types of interventions best suited for different well-​ being goals and for individuals from various cultural backgrounds and personality preferences.

5.5.1 The PERMA Framework One way to categorize the wide variety of positive activities is by using the PERMA framework.51 This practical acronym describes five well-​being pillars based in positive psychology: • • • • •

Positive emotion: engage in experiences that elicit positive feelings. Engagement: conduct activities that produce a sense of full immersion or flow. Relationships: develop social connections and relationships. Meaning: engage in activities that align with one’s sense of purpose. Accomplishment: set and work towards meaningful goals.

5.5.2 Mindfulness Mindfulness, which is defined as paying attention to present moment experience with nonjudgment,52 is another intervention in the positive psychology and emotional

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well-​being field. Most mindfulness-​based interventions are based on research from the mindfulness-​based stress reduction (MBSR) program shown to have physiologic and psychologic benefits. Awareness of breath and body sensations and mindful movement53 are examples. These types of practices have been successfully used to address a variety of conditions, such as anxiety,54 depression,55 pain, stress, and substance abuse.56,57,58 Meditation practices are a subset of mindfulness. Loving-​kindness meditation59 and compassion meditation exercises, in particular, enhance positive emotional states of kindness and compassion60 with psychological and physical benefits. Brief loving-​ kindness practice has been shown to produce higher positive affect, more positive self-​evaluations,61 and reduce depressive symptoms.62 As with other interventions, when recommending these practices, practitioners need to keep in mind patient preferences, culture, spiritual and religious beliefs, and other individual differences.

5.5.3 Exposure to Nature The connection between exposure to nature and emotional and mental health has been increasingly demonstrated. Forest bathing, the Japanese practice called shinrin-​ yoko, is getting more attention as an important well-​being practice. A meta-​analysis of 32 studies concluded that exposure to natural environments leads to less negative and greater positive affect.63 A calming effect64 and lower mental fatigue with attention to natural landscapes rather than urban environments65 have also been reported. In our current society where individuals spend increasingly more time on digital devices, time in nature may be considered a frontline therapy for improving emotional well-​being.

5.6  PRACTICAL APPLICATION OF POSITIVE PSYCHOLOGY APPROACHES IN HEALTH CARE Despite the potential large impact of genetics of 50–​80% in study populations,66,67,68 research suggests that individuals can engage in a variety of intentional activities to increase their personal happiness levels and improve their well-​being.69,70 Even short boosts in happiness levels can offer physiologic benefits, such as increasing heart rate variability.

5.6.1 Measures of Happiness and Related Constructs While research on happiness and flourishing measures is ongoing, medical practitioners may consider conducting brief assessments, such as the Satisfaction with Life Scale.71 Sharing the results with patients may spark a discussion about the role of positive activities on physical health and explore patient readiness to include such activities in treatment or health maintenance plans. Measuring the frequency of positive activities, for example, gratitude and mindfulness practices and meaningful or flow activities, may be a more reliable indicator of progress than measuring fleeting emotional states.31,36

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Prescriptions of Interventions Aligned with the PERMA Framework Practitioners can recommend positive activities that align with PERMA. Well-​ studied activities include gratitude practice and acts of kindness,72 which may protect against rumination, loneliness, and other risk conditions, and increase positive thoughts and behaviors and need satisfaction.73 These activities can be learned at any stage in life to garner both mental and physical health benefits. Flow is a mental state that occurs when a perceived challenge matches personal skills of an activity (e.g. gardening, dancing, making art, and playing a musical instrument) so that the individual is fully engaged at optimal capacity. This state is associated with high levels of happiness.74,75 Social support and feeling connected is the most powerful of the PERMA pillars.76 Social connectivity has been associated with a healthy body mass index, improved blood sugars, greater cancer survival, decreased cardiovascular mortality, lower depressive symptoms, and improved overall mental health. Inquiring about quantity and quality of social activities and interactions and discussing ways to increase them are steps to facilitating total well-​being.77 A sense of meaning in life is another key pillar of the PERMA model.78 Research suggests that higher levels of meaning have a positive influence on biological, psychological, and behavioral outcomes, including protection against heart disease in those at risk,39,79,80 and greater use of preventive health care services.40 Religious beliefs and spiritual transcendence have an anxiety-​reducing outcome, particularly regarding mortality,81 increase positive affect and a sense of purpose in life, hold across cultures82 and correlate with decreased mortality.42 The last pillar of the PERMA model that contributes to flourishing is a sense of accomplishment when achieving goals through skills and effort. Encouraging patients to set achievable goals and celebrate successes is essential to promoting well-​being.51

5.6.2 Variety, Dosing, and Person-​Activity Fit of Positive Psychology Interventions A number of factors can help increase the likelihood that the PPI will lead to improved emotional well-​being. Among these factors are the patient’s culture, variety and “dosage” of activities, interest level and ease of performing activities, and alignment with personal strengths. Patients can be encouraged to participate in a variety of positive activities to avoid hedonic adaptation and lower positive emotions.83 Study participants asked to vary their weekly acts of kindness reported greater increases in well-​being than those who did the same kindness activity every week.84 Active appreciation and savoring of the positive emotion can also slow adaptation.,84,85 When recommending these types of activities, practitioners also need to consider the individual’s cultural background. One study found that South Koreans fared better if they performed acts of kindness before writing a letter of gratitude, whereas the

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reverse was true of the US participants.86 Much more research is needed to decipher the impact of various interventions on happiness and health across different cultures. The level of benefit from PPIs is also impacted by “dosing” (frequency and intensity of the activity). In one study, individuals who performed five acts of kindness all in one day derived greater increase in well-​being than those who did them throughout the week.87 In another study, individuals who counted blessings once a week had greater well-​being gains than those who counted them three times a week.87 Sustainability, and hence greater benefit, can be garnered by helping patients identify “person activity-​fit,” activities that align with an individual’s personality and strengths.88,89,90 Patients may be directed to take the Values in Action (VIA) character strengths survey90 and the Myers–​Briggs Type Indicator for insights about their strengths and personality-​based preferences.91

5.7  POSITIVE PSYCHOLOGY APPROACHES IN INTERACTIONS WITH PATIENTS Positive psychology can serve as an essential tool in coaching health behavior change, including motivational interviewing, to aim at achieving desired life outcomes, rather than avoiding negative consequences. Modeling positivity in the exam room not only enhances positive emotions that drive adherence, but also can lead to immediate physiologic benefits and satisfying interactions in the health care setting for both patients and practitioners.

5.7.1 Coaching Health Behavior Change with Positive Psychology Focusing on what is going well, rather than on what is wrong, is fundamental to positive psychology interactions.92 Practitioners can point out successes, even partial successes, to reinforce patent’s self-​efficacy and build energy to persist.93,94 This positive psychology approach to coaching can be integrated with motivational interviewing94 to overcome ambivalence, harnessing the power of positive emotions, and use personal strengths to achieve goals. Positive images of the future fuel hope and the drive to find solutions, and boost self-​empowerment to make change.95,96 The vision shifts from weight loss or tobacco cessation, for example, to how this change enhances the individual’s life. Connecting health behaviors to intrinsically satisfying activities is also an effective positive psychology-​based approach to health behavior change. While the PERMA model has mainly been used as a framework for promoting flourishing,97 it can also be used as a guide for making this behavioral connection. When people experience positive emotions during health-​related behaviors, they become more flexible and creative in ways that activate and support future health behaviors.33 Intrinsically rewarding feelings and health behaviors offer potential for long-​term behavioral maintenance.33,36,98

5.7.2 Modeling Positive Psychology in the Exam Room With empirical evidence that positive emotions are associated with a myriad of health benefits; fewer emergency room and hospital admissions; lower incidence of drug

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and alcohol use; buffering against depression; speedy recovery from illness, injury, and stress; and increased longevity,33,87 it behooves practitioners to seek ways to facilitate positive activities and emotions in the exam room and beyond. For example, highlighting what is working shifts the practitioner–​patient interactions to empower individuals toward positive health and to be at their best.92

5.8  POSITIVE PSYCHOLOGY STRATEGIES FOR HEALTH CARE WORKERS’ WELL-​BEING Medical practitioner burnout is widespread, common, with potential dangerous consequences, lower well-​being and life satisfaction, and greater likelihood of depression, alcohol and drug use, and suicide.99 Under such circumstances, the goal of thriving and flourishing could seem quite daunting. However, before such situations worsen and require interventions by mental health professionals, practitioners can help avoid this condition by incorporating a range of wellness approaches, even into their busy lives. In conjunction with organizational health care system changes that better support practitioners systemically, individual self-​care that includes positive psychology has the potential to enhance health professionals’ well-​being. A healthy lifestyle with regular, intentional positive activities can help buffer against burnout, build a capacity for growth, and promote a flourishing life.29,100,101

5.8.1 Medical Practitioner Well-​Being and Patient Care When medical practitioners are burned out, patients report receiving lower quality care and less satisfaction.102 Positivity helps medical practitioners to be more open-​ minded and creative when diagnosing patients and finding solutions or creating action plans.101,103 Moreover, prescribing a healthy lifestyle has a greater impact on the patient when the practitioner models those behaviors.99,104 Interactions with patients that are positive and show compassion are more likely to help patients better understand and adhere to treatment plans, and experience less anxiety and enhanced well-​being.105

5.8.2 Positive Psychology Interventions for Medical Practitioners Medical practitioners can apply the PERMA framework for themselves, as well as their patients, to increase the likelihood of flourishing,51 which is detailed below.

5.8.2.1 P –​Positive Emotions Positive interactions and experiences interjected consistently into daily routines that lead to a boost in positive emotions can enhance job engagement and satisfaction. Examples of such positive activities include playing upbeat music during surgery, taking a moment to play with a young patient, or starting the workday with the team doing a brief reflection of gratitude. In addition, hope and optimism are important positive emotions that practitioners can spark through the learned skill106,107 by directing attention toward possible positive future outcomes.104,105

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5.8.2.2 E –​Engagement Immersion in an activity that creates a sense of engagement or flow at work can promote health.108 Practitioners can harness this element of positive psychology by remaining mindfully present while conducting medical procedures or interacting with patients. In restrictive, fast-​paced environments, finding engagement at work might be challenging. Hence, fostering opportunities for flow outside of work, such as perfecting a craft or sport, might be more feasible. Planning to do these activities with friends and family can also expand the social connectivity element of the PERMA frameworks.

5.8.2.3 R –​Relationships Social isolation, both actual and perceived, triggers pain centers in the brain in a similar way as physical pain and is a risk factor of mortality.109,110 Conversely, strong social connections and having friends are associated with life satisfaction, well-​being, and longevity.111,112,113,114 Although medical practitioners interact with patients much of their work day, having friends at work can increase engagement, collaboration, and productivity, and spur more positive interactions with patients.115 Health care teams can engage in regularly scheduled breaks and lunches for socialization, conduct retreats, and participate in after-​hours social events (in-​person or virtual) to sustain the team’s well-​being.

5.8.2.4 M –​Meaning Meaningful work creates fulfillment and improves mental health, well-​being, and longevity.116,117,118,119 One strategy that health workers can use to reconnect with work-​ related meaning is to reflect on their “why” 120 and re-​awaken their compassion as a powerful tool to invoke their sense of meaning.121 Finding meaning outside of the medical profession can also help combat burnout and contribute to work–​life balance.100, 118 Volunteering in the community and becoming involved in children’s school activities are ways to balance family needs and instill a sense of meaning. Reframing life experiences from the spiritual or religious perspective is another powerful avenue toward meaning and spiritual growth.112,113,114,122

5.8.2.5 A –​Accomplishment Individuals possess a need to be competent, achieve mastery, and meet their goals.123 Feelings of accomplishment means using skills and effort to realize success.51 The health care arena provides many opportunities to strive for mastery and goal attainment, for example, new certifications, educational achievements, building business-​related competencies, leadership development, or other professional advancements. Seeking accomplishment outside of work may offer additional well-​ being rewards, for example, mastering a musical instrument or new form of art, learning a new physical skill, or writing a blog.

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5.9  POSITIVE PSYCHOLOGY RESOURCES Health practitioners have a number of credible resources that they can turn to for education in positive psychology, as well as practical resources for their patients.

5.9.1 Academic and Nonprofit Organizations Several academic and nonprofit institutions offer informative, comprehensive websites that contain links to useful articles, seminal research, and tools, and serve as excellent launch pads for practitioners who would like to learn more. Examples include the University of Pennsylvania’s Positive Psychology Center, Yale University’s Center for Emotional Intelligence, and the Lee Kum Sheung Center for Health and Happiness at Harvard T.H. Chan School of Public Health. Opportunities for further training, degrees, and certification in areas related to positive psychology are offered by the Benson Henry Institute for Mind Body Medicine (advanced training in stress management and resiliency), Stanford University’s Center for Compassion and Altruism Research and Education (compassion cultivation training), and the University of Pennsylvania (the Masters in Applied Positive Psychology). The International Positive Psychology Association (IPPA) offers online and live educational opportunities about research on topics of positive psychology and health and more. Leading peer-​reviewed journals include the Journal of Positive Psychology, the Journal of Positive Psychology and Well-​Being, and the Journal of Happiness Studies.

5.9.2 Positive Psychology Websites, Apps, and Programs A simple way to begin incorporating positive psychology into clinical practice is to prescribe regular positive activities, such as gratitude journaling. Credible websites and digital programs offer a variety of research summaries, assessments, techniques, tools, and online communities to support your positive psychology “prescriptions.” Patients can be encouraged to explore them. Examples include the Greater Good Science Center, which provides science summaries and articles on evidence-​based practices, and the Live Happy Magazine, which offers a publication, podcasts, tips on positive living, and an online community. Overuse of social media and digital devices can be a harbinger of isolation, inattention, depression, and anxiety. However, smartphones deliver an easily accessible format to help promote healthy behaviors, including positive activities. Preliminary research suggests that vetted digital applications can promote positive mood changes and behavioral outcomes.124,125 A few well-​respected apps include Headspace, Calm, and Happify.

5.10  SUMMARY AND CONCLUSION Positive psychology-​based approaches can improve emotional, mental, and physical health and lead to a new construct of health that achieves flourishing. The empirical evidence in this relatively new, but growing, field is relevant for the female gender, in that women are overrepresented in many of these studies. Although much more

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research is needed to identify specific strategies that offer the best outcomes for subpopulations, early data suggest that these approaches are relevant throughout the lifespan, including teenage girls, pregnant women, pre-​, peri-​, and postmenopausal women, and among the elderly. Health care practitioners can harness the field to promote total well-​being by assessing levels of flourishing, recommending positive activities, engaging in positive interactions with patients, coaching health behavior with positive life goals, and last, but not least, applying positive psychology strategies for their self-​care. Teaching and role modeling these principles to students and residents and advocating for health system changes that support total well-​being of both patients and practitioners are actions that practitioners can take to advance this aim. Such changes are essential during a time of skyrocketing emotional and mental health crises in the general population, as well as high rates of physician and health professional burnout. Inadequate insurance coverage or reimbursement for these elements of well-​being presents a challenge. However, a shift in framing practitioner–​patient interactions to bolster positive emotions, offer brief interventions, and refer to outside resources is well worth considering to improve health and well-​being outcomes.

REFERENCES 1. Pressman SD, Black LL. Positive emotions and immunity. In Segerstrom SC, ed. The Oxford Handbook of Psychoneuroimmunology. 1st ed. Oxford University Press, 2012. 2. Matlin MW. Writing and rewriting about the psychology of women. Sex Roles. 2010;62:166–​172. doi.org/​10.1007/​s11199-​010-​9741-​2 3. Rao MA, Donaldson, SI. Expanding opportunities for diversity in positive psychology: An examination of gender, role and ethnicity. Canadian Psychology 2015;56(3):271–​282. doi.org/​10.1037/​cap0000036 4. Oosthuizen CM, Wissing MP. Prevalence of violence against women: Distress, coping and psychological well-​being. Surviving the fire? South African Journal of Psychology. 2005;35:637–​656. doi.org/​10.1177/​008124630503500403 5. Johnson NG. On treating adolescent girls: Focus on strengths and resiliency in psychotherapy. Journal of Clinical Psychology 2003;59:1193–​1203. doi.org/​10.1002/​ jclp.10210 6. Frisman L, Ford J, Hsiu-​Ju L, Mallon S, Chang R. Outcomes of trauma treatment using the TARGET model. Journal of Groups in Addiction & Recovery. 2008:3(3):285–​503. doi.org/​10.1080/​15560350802424910 7. Biwas-​Diener R. From the equator to the North Pole: A study of character strengths. Journal of Happiness Studies. 2006;7:293–​310. doi:10.1007/​s10902-​005-​3646-​8 8. van Eden C, Wessing MP, Dreyer J, et al. Validation of values in action inventory of strengths for youth (VIA-​Youth) among South African learners. Journal of Psychology in Africa. 2008;18:143–​154. doi.org/​10.1080/​14330237.2008.10820181 9. Constantine MG, Sue DW. Factors contributing to optimal human functioning in people of color in the United States. The Counseling Psychologist. 2006;34:228–​244. doi.org/​10.1177/​0011000005281318 10. Christopher JC, Hickinbottom S. Positive psychology, ethnocentrism, and the disguised ideology of individualism. Theory & Psychology. 2008;18:563–​589. doi.org/​10.1177/​ 0959354308093396

118

118

Liana Lianov

11. Burckhardt R, Manicavasagar V, Batterham PJ, Miller LM, Talbot E, Lum A. A web-​ based adolescent positive psychology program in schools: Randomized controlled trial. J Med Internet Res. 2015;17(7):e187. doi.org/​10.2196/​jmir.4329 12. Riera M, Di Prisco J. Field Guide to the American Teenager. 1st ed. Perseus Publishing; 2000. 13. Simmons R. Odd Girl Out: The Hidden Culture of Aggression in Girls. 1st ed. Harcourt Inc.; 2002. 14. Thompson M, Barker T. The Pressured Child: Freeing Our Kids from Performance Overdrive and Helping Them Find Success in School and Life. Reprint 1st ed. Ballantine Books; 2005. 15. Peterson C. A Primer in Positive Psychology (Oxford Positive Psychology Series). 1st ed. Oxford University Press; 2006. 16. Fredrickson BL, Cohn MA, Coffey KA, Pek J, Finkel SM. Open hearts build lives: Positive emotions, induced through loving-​ kindness meditation, build consequential personal resources. Journal of Personality and Social Psychology. 2008;95(5):1045–​1062. doi.org//​10.1037/​a0013262 17. Siegel DJ. Brainstorm: The Power and Purpose of the Teenage Brain. 1st ed. Penguin Group; 2013. 18. Berndt J, Keefe K. Friends’ influence on adolescents’ adjustment in school. Child Development. 1995;66:1312–​1329. doi.org/​10.2307/​1131649 19. Berger J, 2014. From Paralyzed to Catalyzed: Supporting Adolescent Girls through Positive Psychology Coaching. Master of Applied Positive Psychology (MAPP) Capstone Projects. 57. Capstones 8-​5-​2014, University of Pennsylvania, University of Pennsylvania Scholarly Commons. http://​repository.upenn.edu/​mapp_​capstone/​57. Accessed October 9, 2020. 20. Corno G, Etchemendy E, Espinoza M, et al. Effect of a web-​based positive psychology intervention on prenatal well-​ being: A case series study. Women Birth. 2018;31(1):e1–​e8. doi.org/​10.1016/​j.wombi.2017.06.005 21. O’Leary K. The effect of positive psychological interventions on psychological and physical well-​being during pregnancy. DClinPsych Thesis, University College Cork, 2015.. https://​cora.ucc.ie/​bitstream/​handle/​10468/​2118/​OLearyK_​ PhD2015.pdf?sequence=4. Accessed September 19, 2020. 22. Budhiraja A, Midha P. Hope and spirituality as portals to subjective well-​being among geriatrics. Indian Journal of Positive Psychology. 2015;6(2):175–​177. 23. Jafary F, Farahbakhsh K, Shafiabadi A, Delavar A. Quality of life and menopause: Developing a theoretical model based on meaning in life, self-​ efficacy beliefs, and body image. Aging Ment Health. 2011;15(5):548056. doi.org/​10.1080/​ 13607863.2010.548056 24. Deeks AA, McCabe MP. Well-​ being and menopause: An investigation of purpose in life, self-​acceptance and social role in premenopausal, perimenopausal and postmenopausal women. Qual Life Res. 2004;13(2):389–​398. doi.org/​10.1023/​ B:QURE.0000018506.33706.05 25. Defey D, Storch E, Cardozo S, Díaz O, Fernández G. The menopause: Women’s psychology and health care. Social Science and Medicine. 1996;42(10):1447–​1456. https://​doi.org/​10.1016/​0277-​9536(95)00344-​4 26. Pandey JM, Garg S. Positive psychology and aging. In Vijaya Prasad B, Akbar S., eds. Advances in Medical Diagnosis, Treatment, and Care (AMDTC) Book Series. Handbook of Research on Geriatric Health, Treatment, and Care. 57th ed. IGI Publishing/​IGI Global, 2018:1–​16.

119

Positive Psychology

119

27. Sutipan P, Intarakamhang U, Macaskill A. The impact of positive psychological interventions on well-​being in healthy elderly people. J Happiness Stud. 2017;18:269–​ 291. doi.org/​10.1007/​s10902-​015-​9711-​z 28. Proyer RT, Gander F, Wellenzohn S, Ruch W. Positive psychology interventions in people aged 50–​79 years: Long term effects of placebo-​controlled online intervention on well-​being and depression. Aging and Mental Health 2014;18(8):997–​1005. doi. org/​10/​1080/​13607863.2014.899978 29. Fredrickson BL. The role of emotions in positive psychology: The broaden-​and-​ build-​theory of positive emotions. American Psychologist 2001;56:218–​226. doi.org/​ 10.1037/​0003-​066X.56.3.218 30. Cohn MA, Fredrickson BL. In search of durable positive psychology interventions: Predictors and consequences of long-​term positive behaviour change. J Posit Psychol. 2010;5(5):355–​366. doi.org/​10.1080/​17439760.2010.508883 31. Kok BE, Fredrickson BL. Upward spirals of the heart: Autonomic flexibility, as indexed by vagal tone, reciprocally and prospectively predicts positive emotions and social connectedness. Biol Psychol. 2010;85:432–​436. doi.org/​10.1016/​ j.biopsycho.2010.09.005 32. Kok BE, Coffer KA, Cohn MA, et al. How positive emotions build physical health: Perceived positive social connections account for the upward spiral between positive emotions and vagal tone. Psychol Sci. 2013;24(7):1123–​ 1132. doi.org/​ 10.1177/​0956797612470827 33. Fredrickson BL. Positive emotions broaden and build. Advances in Experimental Soc Psychol. 2013;47:1–​53. doi.org/​10.1016/​B978-​0-​12-​407236-​7.00001-​2 34. Redwine LS, Henry BS, Pung MA, et al. PPilot randomized study of a gratitude journaling intervention on heart rate variability and inflammatory biomarkers in patients with stage B heart failure. Psychosom Med. 2016;78(6):667–​676. doi.org/​ 10.1097/​PSY.0000000000000316 35. Gardner MP, Wansink B, Kim J, Park SB. Better moods for better eating? How mood influences food choice. J Consum Psychol. 2014;24(3):320–​335. doi.org/​10.1016/​ j.jcps.2014.01.002 36. Van Cappellen P, Rice EL, Catalino LI, Fredrickson BL. Positive affective processes underlie positive health behavior change. Psychol Health 2018;33:77–​97. doi.org/​ 10.1080/​08870446.2017.1320798 37. Kubzansky LD, Huffman JC, Boehm JK, et al. Positive psychological well-​being and cardiovascular disease. JACC health promotion series. J Am Coll Cardiol. 2018;72(12):1382–​1396. doi.org/​10.1016/​j,acc.2018.07.042 38. Yeung JWK, Zhang Z, Kim TY. Volunteering and health benefits in general adults: Cumulative effects and forms. BMC Public Health 2018;18:8. doi.org/​10.1186/​ s12889-​017-​4561-​8 39. Kim ES, Sun JK, Park N, Kubzansky LD, Peterson C. Purpose in life and reduced risk of myocardial infarction among older US adults with coronary heart disease: A two-​year follow-​up. J Behav Med. 2013;36(2):124–​133. doi.org/​10.1007/​ s10865-​012-​9406-​4 40. Kim ES, Strecher VJ, Ryff CD. Purpose in life and use of preventive health care services. Proc Natl Acad Sci. 2014;111(46):16331–​16336. doi.org/​10.1073/​ pnas.1414826111 41. Danner DD, Snowden DA, Friesen WV. Positive emotions in early life and longevity: Findings from the nun study. J Pers Soc Psychol. 2001;80(5):804–​813. doi.org/​ 10.1037/​0022-​3514.80.5.804

120

120

Liana Lianov

42. Chida Y, Steptoe A. Positive psychological well-​being and mortality: A qualitative review of prospective observational studies. Psychosom Med. 2009;70:741–​756. doi. org/​10.1097/​PSY.0b013e31818105ba 43. Eichstaedt JC, Schwartz HA, Kern ML, et al. Psychological language on twitter predicts county-​level heart disease mortality. Psychol Sci. 2015;26(2):159–​169. doi. org/​10.1177/​0956797614557867 44. Brod S, Rattazzi L, Piras G, D’Acquisto F. ‘As above, so below’ examining the interplay between emotion and the immune system. Immunology. 2014;143:311–​318. doi. org/​10.1111/​imm.12341. 45. Puterman E, Epel E. An intricate dance: Life experience, multisystem resiliency, and rate of telomere decline throughout the lifespan. Soc Pers Psychol Compass. 2012;6(11). doi.org/​10.1111/​j.1751-​9004.2012.00465.x 46. Blackburn E. The Telomere Effect: A Revolutionary Approach to Living Younger, Healthier, Longer. 1st ed. Onion Spring; 2018. 47. Nelson-​ Coffey K, Fritz MM., Lyubomirsky S, Cole SW. Kindness in the blood: A randomized controlled trial of the gene regulatory impact of prosocial behavior. Psychoneuroendocrine. 2017;81:8–​13. doi.org/​10.1016/​j.psyneuen.2017.03.025 48. Jacka FN. Association of Western and traditional diets with depression and anxiety in women. Am J Psychiat. 2010;167:305–​511. doi.org/​10.1176/​appi.ajp.2009.09060881 49. Jacka FN. The association between habitual diet quality and the common mental disorders in community-​dwelling adults: The Hordaland Health Study. Psychosom. Med. 2011;73(6):483–​490. doi.org/​10.1097/​PSY.0b013e318222831a 50. Xu J, Robert RE. The power of positive emotions: It’s a matter of life or death –​subjective well-​being and longevity over 28 years in a general population. Health Psychol. 2010;16(8):867–​873. doi.org/​10.1037/​a0016767 51. Seligman, M. Flourish: A Visionary New Understanding of Happiness and Well-​Being. 1st ed. Atria Books; 2012. 52. Kabat-​Zinn J. Wherever You Go, There You Are: Mindfulness Meditation in Everyday Life. 1st ed. Hachette Books; 2010. 53. Kabat-​ Zinn J. An outpatient program in behavioral medicine for chronic pain patients based on the practice of mindfulness meditation: Theoretical considerations and preliminary results. Gen Hosp Psychiat. 1982;4(1):33–​47. doi.org/​10.1016/​ 0163-​8343(82)90026-​3 54. Evans S, Ferrando S, Findler M, Stowell C, Smart C, Haglin D. Mindfulness-​ based cognitive behavioral therapy for generalized anxiety disorder. J Anxiety Disord.2008;22(4):716–​721. doi.org/​10.1016/​j.janxdls.2007.07.005 55. Teasdale JD, Segal ZV, Williams JM, Ridgeway VA, Soulsby, JM, Lau MA. Prevention of relapse/​recurrence in major depression by mindfulness-​based cognitive therapy. J Consult Clin Psychol. 2000;68(4):615. doi.org/​10.1037/​0022-​006x.68.4.615 56. Creswell JD. Mindfulness interventions. Ann Rev Psychol. 2017;68:491–​516. doi.org/​ 101146/​annurev-​psych-​042716-​051139 57. Engert V, Ko BE, Papassotiriou I, Chrousos GP, Singer T. Specific reduction in cortisol stress reactivity after social but not attention-​based mental training. Sci Adv. 2017;3(10):e1700495. doi.org/​10.1126/​sciadv.1700495 58. Goldberg SB, Tucker RP, Greene PA, et al. Mindfulness-​based interventions for psychiatric disorders: A systematic review and meta-​ analysis. Clin Psychol Rev. 2018;59:5260. doi.org/​10.1016/​j.cpr.2017.10.011 59. Zeng A, Chiu CPK, Wang R, Oei TPS, Leung FYK. The effect of loving kindness meditation on positive emotions: A meta-​analytic review. Front. Psychol. 2015;6:1693. doi.org/​10.3389.fpsyg.2015.01693

121

Positive Psychology

121

60. Zeng X, Chio FHN, Oei TPS, Leung FYK, Xiangping L. A systematic review of associations between amount of meditation practice and outcomes in interventions using the four immeasurables meditations. Front Psychol. 2017;8:141. doi.org/​10.3389/​ fpsyg.2017.00141 61. Hutcherson CA, Seppala M, Gross JJ. Loving-​kindness meditation increases social connectedness. Emotion. 2008;8(5):720–​724. doi.org/​10.1037/​a0013237 62. Shahar B, Szepsenwol O, Zilcha-​Mano S, et al. A wait-​list randomized controlled trial of loving-​kindness meditation programme for self-​criticism. Clin Psychol Psychother. 2015;22(4):346–​356. doi.org/​10.1002/​cpp.1893 63. McMahon EA, Estes D. The effect of contact with natural environments on positive and negative affect: A meta-​analysis. J Posit Psychol. 2015;(6):507–​519. doi.org/​ 10.1080/​17439760.2014.994224 64. Kuo M. How might contact with nature promote human health? Promising mechanisms and a possible central pathway. Front Psychol. 2015;6 :1093. doi:10.3389/​ fpsyg.2015.01093 65. Pearson DG, Craig T. The great outdoors? Exploring the mental health benefits of natural environments. Front Psychol. 2014;5(1178):1–​4. doi.org/​10.3389/​fpsyg.2014.01178 66. Braungart JM, Plomin R, DeFries JC, Fulker DW. Genetic influence on tester-​rated infant temperament as assessed by Bayley’s Infant Behavior Record: Nonadaptive and adaptive siblings and twins. Dev Psychol.1992;28:40–​47. doi.org/​10.1037/​ 0012-​1649.28.1.40. 67. Roysamb E, Harris JR, Magnus P, Vitterso J. Subjective well-​being sex specific effects of genetic and environmental factors. Pers Indiv Differ. 2002;32:211–​233. doi.org/​ 10.1016/​S0191-​8869(01)00019-​8 68. Lykken D, Tellegen A. Happiness is a stochastic phenomenon. Psychol Sci. 1996;7:186–​189. doi.org/​10.1111/​j.1467-​9280.1996.tb00355.x 69. Sin NL, Lyubomirsky S. Enhancing well-​being and alleviating depressive symptoms with positive psychology interventions: A practice-​ friendly meta-​analysis. J Clin Psychol. 2009;65(5):467–​487. doi.org/​10.1002/​jclp.20593 70. Layous K, Sheldon KM, Lyubomirsky S. The prospects, practices, and prescriptions for the pursuit of happiness. In Joseph S, ed. Positive Psychology in Practice, Promoting Human Flourishing, Education, and Everyday Life. 2nd ed. Wily & Sons; 2015. 71. Diener E, Emmons, RA, Larsen RJ, Griffin S. The satisfaction with life scale. J Pers Assess.1985;48(1):71–​75. doi.org/​10.1207/​s15327752jpa4901_​13 72. Hirshberg MJ, Goldberg SM, Schaefer SM, Flook L, Findley D, Davidson RJ. Divergent effects of brief contemplative practices in response to an acute stressor: A randomized controlled trial of brief breath awareness, loving-​kindness, gratitude or an attention control practice. PloS One. 2018;13(12):e0207765. doi.org/​10.17605/​OSF. IO/​GV5RC 73. Lyubomirsky S, Layous K. Do simple positive activities increase well-​being? Curr Dir Psychol Sci. 2013;22:57–​62. doi.org/​10.1177/​0963721412469809 74. Csikszentmihalyi M, Csikszentmihalyi IS. Optimal Experience: Psychological Studies of Flow in Consciousness. 1st ed. Cambridge University Press; 1988. 75. Csikszentmihalyi M, Larson R. Flow and the Foundations of Positive Psychology: The Collected Works of Mihaly Csikszentmihalyi. 1st ed. Springer; 2014. 76. Vaillant GE. Aging Well: Surprising Guideposts to a Happier Life from the Landmark Harvard Study of Adult Development. 1st ed. Little, Brown Spark; 2003. 77. Martino J, Pegg J, Frates EP. The connection prescription: Using the power of social interactions and the deep desire for connectedness to empower health and wellness. Am J Lifestyle Med. 2016;11(6):466–​475. doi.org/​10.1177/​1559827615608788

122

122

Liana Lianov

78. Steger MF, Frazier P, Oshi S, Kaler M. The Meaning in Life Questionnaire: Assessing the presence of and search for meaning in life. J Couns Psychol. 2006;53:80–​93. doi. org/​10.1037/​0022-​0167.53.1.80 79. Roepke AM, Jayawickreme E, Riffle OM. Meaning and health: A systemic review. Appl Res Qual Life 2014;9(4):1055–​1079. doi.org/​10.1007/​s11482-​013-​9288-​9 80. Cohen R, Bavishi C, Rozanski A. Purpose in life and its relationship to all-​cause mortality and cardiovascular events: A meta-​analysis. Psychosom Med. 2016;78(2):122–​ 133. doi.org/​10.1097/​PSY.0000000000000274. 81. Soenke M, Landau MJ, Greenberg J. Sacred armor: Religion’s role as a buffer against the anxieties of life and the fear of death. In Pargament K, Exline J, Jones J, eds. APA Handbooks in Psychology: APA Handbook of Psychology, Religion, and Spirituality: Vol. 1. 1st ed. American Psychological Association; 2013. 82. Falb MD, Pargament, KI. Religion, spirituality, and positive psychology: Strengthening well-​being. In Pedrotti JT, Edwards LM, eds. Perspectives on the Intersection of Multiculturalism and Positive Psychology. 1st ed. Springer; 2014:143–​157. 83. Sheldon KM, Lyubomirsky S. Achieving sustainable increases in happiness: Change your actions, not your circumstances. J Happiness Stud. 2006;7:55–​ 86. doi.org/​ 10.1007/​s10902-​005-​0868-​8 84. Sheldon KM, Lyubomirsky S. The challenge of staying happier: Testing Hedonic-​ Adaptation Prevention (HAP) model. Pers Soc Psychol B. 2012;38:670–​680. doi.org/​ 10.1177/​0146167212436400 85. Lyubomirsky S, Dickerhoff R, Boehm JK, et al. Becoming happier takes both will and a proper way: An experimental longitudinal intervention to boost well-​being. Emotion. 2011;11:391–​402. doi.org/​10.1037/​a0022575 86. Layous K, Lee H, Choi I, Lyubomirsky S. Culture matters when designing a successful happiness-​increasing activity: A comparison of the United States and South Korea. J Cross Cultural Psychol. 2013;44(8):1294–​1303. doi.org/​10l1177/​ 0022022113487591 87. Lyubomirsky S, King L, Diener E. The benefits of frequent positive affect: Does happiness lead to success? Psychol Bull. 2005;131(6):803. doi.org/​ 10.1037/​0033-​2909.131.6.803 88. Deci EL, Ryan RM. The “what” and “why” of goal pursuits: Human needs and the self-​determination of behavior. Psychol Inquiry. 2000;11(4):227–​268. doi.org/​1207/​ S15327965PLI1104_​01 89. Sheldon KM, Elliot AJ, Kim Y, et al. What is satisfying about satisfying events? Testing 10 candidate psychological needs. J Pers Soc Psychol. 2001;80325–​80339. doi.org/​10.1037/​0022-​3514.80.2.325 90. Park N, Peterson C. Character strengths: Research and practice. J Coll Character. 2009;10(4). doi.org/​10.2202/​1940-​1639.1042 91. Lianov L. Roots of Positive Change: Optimizing Healthcare with Positive Psychology. 1st ed. HealthType LLC with American College of Lifestyle Medicine; 2019. 92. Biswas-​Diener R. Practicing Positive Psychology Coaching: Assessment, Activities and Strategies for Success. 1st ed. John Wiley & Sons; 2012. 93. Snyder CR, Rand, KL, Sigmon DR. Hope theory. Handbook of Positive Psychology. Oxford University Press; 2002:257–​276. doi.org/​10.1521/​jscp.2000.19.1.11 94. Reynolds R, Palmer S, Green S. Positive psychology coaching for health and wellbeing. In Green S, Palmer S, eds. Positive Psychology Coaching in Practice. 1st ed. Rutledge; 2019. 95. Boyatzis RE, Akrivou K. The ideal self as the driver of intentional change. J Manage Development. 2006;25(7):624–​642. doi.org/​10.1108/​02621710610678454.

123

Positive Psychology

123

96. McQuaid,M, Niemiec R, Doman F. A character strengths-​based approach to positive psychology. Positive psychology coaching for health and wellbeing. In Green S, Palmer S, eds. Positive Psychology Coaching in Practice. 1st ed. Rutledge; 2019. 97. Falecki D, Leach C, Green S. PERMA-​powered coaching: Building foundations for a flourishing life. In Green S, Palmer S, eds. Positive Psychology Coaching in Practice. 1st ed. Routledge; 2019. 98. Kaufman C. Positive psychology: The science at the heart of coaching. In Stober D, Grant A, eds. Evidence-​Based Coaching: Putting Best Practices to Work for Your Clients. 1st ed. John Wiley & Sons; 2006. 99. Patel RS, Bachu R, Adikey A, Bachu R, Malik M, Shah M. Factors related to physician burnout and its consequences: A review. Behav and Brain Sci. 2018;8(11):98. doi.org/​10.3390/​bs8110098 100. Cameron KS, Dutton JE, Quinn RE. Positive Organizational Scholarship: Foundations of a New Discipline. 1st ed. Berrett-​Koehler Publishers; 2003. 101. Fredrickson BL. Positivity: Top-​Notch Research Reveals the Upward Spiral That Will Change Your Life. 1st ed. Three Rivers Press; 2009. 102. Shanafelt T, Goh J, Sinsky C. The business case for investing in physician well-​being. JAMA Intern Med. 2017;177(12):1826–​1832. doi.org/​10.1001/​ jamainternmed.2017.4340 103. Estrada CA, Isen AM, Young MJ. Positive affect facilitates integration of information and decreases anchoring in reasoning among physicians. Org Behav Hum Dec.1997;72(1):117–​135. 104. Lobelo F, de Quevedo IG. The evidence in support of physicians and health care providers as physical activity role models. Am J Lifestyle Med. 2016;10(1):36–​52. doi.org10.1177/​1559827613520120 105. Amutio-​ Kareaga A, Garcia-​ Campayo J, Delgado LC, Hermosilla D, Martinez-​ Taboada C. Improving communication between physicians and their patients through mindfulness and compassion-​ based strategies: A narrative review. J Clin Med. 2017;6(3):33. doi.org/​10.3390/​jcm6030033 106. Seligman MEP. Learned Optimism: How to Change Your Mind and Your Life. Reprint 1st ed. Vintage; 2006. 107. Lopez SJ. Making Hope Happen: Create the Future You Want for Yourself and Others. Reprint 1st ed. Atria Books; 2013. 108. Christian M, Slaughter J. Work engagement: A meta-​analytic review and directions for research in an emerging area. Acad Manag Proc. 2011;2007(1):1–​6. doi.org/​ 10.5465/​AMBPP.2007.26536346 109. Eisenberger N. The neural bases of social pain: Evidence for shared representations with physical pain. Psychosom Med. 2012:74(2):126–​135. doi.org/​10.1097/​ PSY.0b013e3182464dd1 110. Holt-​Lunstad J, Smith TB, Baker M, Harris T, Stephenson D. Loneliness and social isolation as risk factors for mortality: A meta-​analytic review. Perspect Psychol Sci. 2015 Mar:10(2):227–​237. doi.org/​10.1177/​1745691614568352 111. Diener E. Subjective well-​ being. Psychol Bull. 1984;95(3):542–​ 575. doi.org/​ 10.1037/​0033-​2909.95.3.542 112. Poloma MM, Pendleton BF. Religious domains and general well-​being. Soc Indic Res. 1990;22:255–​276. doi.org/​10.1007/​BF00301101 113. Idler EL, Kasl SV. Religion among disabled and nondisabled persons I: Cross-​ sectional patterns in health practices, social activities, and well-​being. J Gerontol: Soc Sci. 1997:52B(6):S294–​S305. doi.org/​10.1093/​geronb/​52B.6.S294

124

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114. Krause N. Religious meaning and subjective well-​being in late life. J Gerontol: Soc Sci. 2003:58B(3):S160–​S170. doi.org/​10.1093/​geronb/​58.3.S160 115. Rath, T. Vital Friends: The People You Can’t Afford to Live Without.1st ed. Gallup Press; 2006. 116. Wrzesniewski A., McCauley C, Rozin P, et al. Jobs, careers, and callings: People’s relations to their work. J Res Pers. 1997;31:21–​33. doi.org/​10.1006/​jrpe.1997.2162 117. Schwartz M, Carroll, A. Corporate social responsibility: A three-​domain approach. Business Ethics. 2003;13:503–​530. doi.org/​10.5840/​beq200313435 118. Post S. Altruism, happiness, and health: It’s good to be good. Int J Behav Med. 2005;12(2):66–​77. doi.org/​10.1207/​s15327558ijbm1202_​4 119. Wrzesniewski A, Lobuglio N, Dutton JE, Berg JM. Job crafting and cultivating positive meaning and identity in work. In Bakker AB, ed. Advances in Positive Organizational Psychology: Vol 1. 1st ed. Emerald Group Publishing; 2013:281–​302. 120. Sinek S, Mead D, Docker P. Find Your Why: A Practical Guide for Discovering Purpose for You and Your Team. 1st ed. Penguin Books; 2017. 121. Worline M, Dutton JE, Sisodia R. Awakening Compassion at Work: The Quiet Power That Elevates People and Organizations. 1st ed. Berrett-​Koehler Publishers, Inc., 2017. 122. Koenig HG, King DE, Carson VB. Handbook of Religion and Health. 2nd ed. Oxford University Press, Inc.; 2012. 123. Deci EL, Ryan RM. Intrinsic Motivation and Self-​Determination in Human Behavior. 1st ed. Plenum Press; 1985. 124. Vandelanotte C, Müller AM, Short CE. Past, present, and future of eHealth and mHealth research to improve physical activity and dietary behaviors. J Nutr Educ Behav. 2016;48(3):219–​228. doi.org/​10.1016/​j.jneb.2015.12.006 125. Lin Y, Tudor-​Sfetea C, Siddiqui S, Sherwani Y, Ahmed M, Eisingerich AB. Effective behavioral changes through a digital mHealth App: Exploring the impact of hedonic well-​being, psychological empowerment and inspiration. JMIR Mhealth Uhealth, 2018;6(6): e10024. doi.org/​10.2196/​10024

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Avoiding Risky Substances and Environmental Exposures Natasha DeJarnett, PhD, MPH

Assistant Professor, Christina Lee Brown Envirome Institute, University of Louisville Louisville, KY

Neha Pathak, MD, DipABLM

Co-​Chair, Global Sustainability Committee, American College of Lifestyle Medicine Atlanta, GA 6.1 Introduction....................................................................................................126 6.1.1 Substance Use and Environmental Exposures...................................126 6.2 Substance Use and Women’s Health..............................................................127 6.3 Environmental Exposures and Women’s Health............................................127 6.3.1 Air Exposures.....................................................................................127 6.3.2 Water Exposures.................................................................................129 6.3.3 Soil Food Exposures...........................................................................131 6.3.4 Personal Care Product Exposures......................................................132 6.3.5 Plastics................................................................................................134 6.3.6 Equity/​Justice.....................................................................................135 6.7 Conclusion......................................................................................................136 6.7.1 Recommendations..............................................................................136

KEY POINTS • Biopsychosocial differences can play a role in health impacts from substance use and environmental exposures in women. • Women are uniquely affected by exposures throughout their lifespan, in part, due to impacts on reproductive and gynecologic health, including age of menarche, fertility, pregnancy, lactation, and onset of menopause. • Medical practitioners should assess substance use and environmental exposures to provide appropriate anticipatory guidance as part of a comprehensive evaluation promoting a healthy lifestyle. DOI: 10.1201/9781003110682-7

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• Prevention and treatment approaches should be tailored to respect differences in life experiences and culture. • More research that includes women throughout the lifespan is needed to fully understand differences in exposure, health effects, along with prevention and treatment strategies.

6.1  INTRODUCTION 6.1.1 Substance Use and Environmental Exposures Notable differences exist between men and women regarding the risk of exposure to and health impacts from substance use and environmental exposures. A complex combination of biopsychosocial factors plays a role in the effects of various exposures on the health of women. For example, women may be at higher risk of substance use-​related health impacts due to biological differences in the absorption, metabolism, and clearance of certain toxic substances from the body. Women may also be at higher risk of exposure to certain environmental hazards due to “socially accepted” use of a wide variety of personal care products and cosmetics. Additionally, reproductive and gynecologic concerns pose unique health risks throughout the lifespan. Understanding the research behind these differences can help health professionals guide women toward a healthy lifestyle through appropriate prevention, treatment, and recovery strategies.

FIGURE 6.1  Risky substances and environmental exposures

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6.2  SUBSTANCE USE AND WOMEN’S HEALTH For a brief overview of substance use and women’s health, see the supplemental materials.

6.3  ENVIRONMENTAL EXPOSURES AND WOMEN’S HEALTH The environments around us can greatly impact women’s health. These environments can facilitate positive health outcomes when they reflect healthy community design, have access to clean air and safe water, and are free from disease-​carrying vectors and pests. On the other hand, there are multiple exposures in the environment that can adversely affect health. Populations most susceptible to environmental exposure include older adults, communities of color, people living in impoverished communities, tribal and indigenous communities, and people with disabilities. In addition, pregnant women, infants, and children bear a higher burden associated with exposures. To add to environmental risks, climate change has been defined as the greatest global health challenge of this century.1 This is because it not only degrades the environment, but also harms health, exacerbates inequities, and compromises the economy. Children are especially susceptible to environmental exposures because their organ systems are still developing, they have a higher burden of exposure because they take in more air and water per body weight than adults, they are likely to play on the ground, and they depend on adults for their care and decision-​making. Pregnant women who are exposed to environmental exposures bear a higher risk of adverse pregnancy outcomes for children with birth defects or developmental diseases. Infants are susceptible for reasons similar to that of children, they can also be exposed to some environmental exposures that can leach into the breastmilk, and their oral exploratory habits can lead to them ingesting toxic substances. In addition, toxic substances that can cross the placental barrier put developing fetuses at increased risk of adverse health outcomes. The following sections will explore health outcomes associated with toxic environmental exposures through air, water, climate change, soil/​food, personal care products, and plastics across different periods in the lifespan of women, including childhood, adolescence, preconception, pregnancy/​lactation, and menopause. Information on the health threats of climate change across the lifespan of women is presented in supplemental material.

6.3.1 Air Exposures Inhalation of airborne toxic exposures can adversely affect health across the lifespan of women. Pollutants of concern commonly found in ambient air can include particulate matter, oxides of nitrogen, benzene and a mixture of traffic-​related air pollution. Coarse particulate matter (PM10, particulates with an aerodynamic diameter of 10 µm or less) can reach the upper airway passage stem including the nose and throat. Fine particulate matter (PM2.5, particulates with an aerodynamic diameter of 2.5 µm or less) can be inhaled and deposited in the lower respiratory system

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(lungs, and lung alveoli). Ultrafine particulate matter (UPM, particles with an aerodynamic diameter of less than 0.1 µm) has the potential to be translocated in the bloodstream. PM2.5 exposure sources can derive from the combustion of fossil fuels, tailpipe emissions, and close roadway proximity. Short-​and long-​term exposures to PM2.5 are associated with cardiovascular diseases, respiratory diseases, and premature mortality.2–​7 Humans are exposed to oxides of nitrogen through the combustion of fossil fuels, particularly vehicular exhaust, as well as industrial emissions related to food, metals, manufacturing, and power plants. In addition, indoor exposure sources can include gas cooking appliances and heaters as well as tobacco smoke. Benzene is an air pollutant that can be traced in industrial emissions, vehicular emissions, and tobacco smoke. Benzene is a known carcinogen that also demonstrates adverse effects with chronic diseases like cardiovascular disease. Living in close proximity to major roadways or exposure to traffic-​related air pollutants has been associated with adverse cancer, cardiovascular, and respiratory disease risks. The Health Effects Institute estimated that air pollution was responsible for 476,000 deaths of newborns during their first month of life.8 Results from the Children’s Health Study identified that children aged 10–​18 years that resided in areas with the highest PM levels in the cohort were approximately five times more likely to have low forced expiratory volume in 1 second (FEV1), indicating adverse adolescent lung development.9 Children exposed to high levels of PM are more likely to develop chronic obstructive pulmonary disease (COPD) as adults.10 Children exposed to nitrogen dioxide (NO2) have demonstrated increased lower respiratory symptoms (shortness of breath with wheezing, chronic wheezing, chronic coughing, chronic phlegm, or bronchitis), with a stronger association being demonstrated in girls.11 Asthma onset12, asthma exacerbations,13 and virus-​induced asthma exacerbations14 are additional outcomes children face with NO2 exposure. Children living in inner city environments also demonstrated decreased lung function with increased 5-​day average concentrations of NO2, sulfur dioxide, and PM2.5.15 In addition, NO2’s respiratory threats to children are also significantly associated with school absences.15,16 Women exposed to a 10 µm/​m3 increase in PM2.5 over the course of pregnancy have demonstrated adverse pregnancy outcomes, including 5% higher odds of low birth weight, 10% higher odds of preterm birth, and 15% higher odds of small for gestational age.17 Increased exposure to NO2 and PM2.5 during pregnancy has demonstrated neuropsychological impairment in infants at 15 months of age, affecting motor and neuron development.18 Pregnant women with higher exposure to NO2 have significantly increased odds for developing gestational diabetes and preeclampsia.19 Adverse outcomes in pregnancy associated with exposure to benzene include decreased birth weight20,21 and head circumference,20 potentially leaving children at risk of adverse neurodevelopmental outcomes22 and cognitive developmental delays.23 An association exists between breast cancer incidence and long-​term exposure to vehicular traffic emissions.24 Traffic-​related air pollution exposure was associated with higher incidence of hypertension and diabetes among African-​American women in Los Angeles.25 Traffic exposure is also associated with increased risk of diabetes mellitus onset in women.26 For populations living in close proximity to a major roadway, not only is exposure to traffic-​related pollutants a health concern, but road

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noise can also be hazardous to health. Exposure to road traffic noise has been found to raise the risk of hypertension in women aged 30–​45 years.27 In postmenopausal women, a 10 µm/​m3 of PM2.5 exposure has been associated with a 24% increase in incident of cardiovascular events and a 76% increased risk of cardiovascular disease mortality.28 In addition, long-​term exposure PM10–​2.5 is associated with more rapid cognitive decline in postmenopausal women.29 Women aged over 55 years demonstrate increased incidence of breast cancer associated with exposure to PM2.5, PM10, and nitrogen oxides.30 Exposure to a 5 ppb increase in NO2 exposure is associated with approximately 24% increased breast cancer risk in postmenopausal women.31 In addition, women with long-​term higher exposure to NO2 demonstrate increased breast cancer risk.32 Women exposed to higher traffic emissions at the time of menarche are more likely to develop postmenopausal breast cancer.33 Women aged 55 years with long-​term exposure to traffic-​related air pollutants have demonstrated significantly higher COPD risk.34 Proximity of a major roadway increases postmenopausal women’s risk of incident hypertension, especially for those living within 50 m of a major roadway.35 Indoor air quality can be improved by the use of air conditioning, filters, and ventilation; decreasing the sources of fossil fuel combustion sources in homes, like gas stoves; and tobacco smoke cessation. Populations can limit exposure to outdoor pollutants by avoiding outdoor activities during poor air-​quality alerts, especially populations that have higher susceptibility including children, pregnant women, and older adults.36 Outdoor air quality can be improved through air pollution mitigation. Air quality sampling, monitoring, and issuing air quality alerts will help vulnerable groups know to limit outdoor activities on poor air quality days. Investing in clean energy will result in less air-​harming emissions. Interventions like tree planting can also improve air quality by uptaking pollutants in the air.

6.3.2 Water Exposures Clean water is essential for life; however, challenges in water infrastructure and wastewater management, along with population growth changes, can threaten access to and quality of drinking water.37 Key water quality contaminants include lead, mercury, and emerging substances including per-​and poly-​fluoroalkyl substances (PFAS). Lead is a neurotoxic metal that poses a great long-​term threat to fetuses, infants, and children. In addition to contaminated water, exposure sources include soil and dust along with lead-​based paints and manufacturing. Mercury is a toxic substance formed naturally in the environment as well as anthropogenically. It can be released from the burning of fossil fuels, can be mined from the earth, is used in thermometers, and is used medicinally in dental restorative amalgam (silver) fillings. In the environment, mercury can settle into water or soil. It is a persistent pollutant and can bioaccumulate in fish (methylmercury) and biomagnifies up the food chain.38 Populations, therefore, are exposed through water that contaminates food, as well as air and soil.38 PFAS are a class of widespread persistent contaminants, often called “forever chemicals” due to their lengthy half-​life in the environment. People can be exposed through contaminated drinking water (predominant exposure source)

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as well as through occupational exposures. The presence of PFAS in our environments can be quite ubiquitous due to its presence in industry, in waste infrastructure, and in consumer products, including use as a flame retardant, marking its presence in textiles, firefighting foam, airplanes, anti-​stick cookware, and food packaging. PFAS is a blood contaminant, a possible carcinogen, an immunotoxin, a metabolic toxin, and a potential endocrine disruptor.39 Exposure to lead during fetal development is associated with brain injury and functional decrements at lower doses compared to adults. In utero exposure is associated with impaired cognitive and language development (in combination with manganese exposure)40 and sociability41 in infants. In utero exposure to lead is associated with modified DNA methylation and may be more likely to occur in female infants compared to males, suggesting a potential risk for future offspring.42 Fetuses and infants are susceptible to mercury exposure because of the damage it causes to the central nervous system,38 which can be permanent,42,44 regardless of whether the exposure occurs pre-​or postnatally.45 In addition, PFAS can transfer to infants through breastmilk and cord blood.39 Perfluorooctanoic acid (PFOA), another perfluorochemical, exposure during pregnancy has been linked with gestational diabetes.46 The impacts of lead exposure on children’s health have been extensively investigated. Children with elevated exposure to lead reveal challenges in concentration, memory, and cognition.47 Lead levels in children have declined in the United States, but lead levels remain higher for African-​American children and impoverished children.48 Lead demonstrates an inverse relationship with intelligence quotient (IQ) in children, where higher lead is associated with lower IQ levels.49 There is no safe level of lead exposure. Even low doses of childhood lead exposure are linked with decreased IQ.50 PFAS is associated with immune deficits in children.51 Children exposed to elevated PFOA demonstrate dyslipidemia, including increased total cholesterol and low-​density lipoprotein levels.52 Mercury levels have been found to be nearly fourfold higher in women of childbearing age who consumed fish three or more times in the past 30 days compared to women who consumed no fish during that period.53 Women exposed to mercury are more likely to have poor reproductive outcomes, including reduced fecundability, increased preterm birth, and increased spontaneous abortions.54 Endocrine system impacts in women include decreased luteinizing hormone, estradiol, progesterone, and prolactin, and increased menstrual disorders. In terms of in vitro fertilization outcomes, mercury exposure is associated with decreased follicle count, number of oocytes, number of eggs, and ovarian response to gonadotropin-​releasing hormone.54 Higher PFAS exposure has been linked with greater weight regain in women, adding evidence to support the impacts of PFAS on metabolism and body weight regulation.55 Exposure to PFAS can be detected in the plasma and serum of women, and exposure to PFAS-​contaminated drinking water is associated with increased levels PFAS detected in their plasma.56 Across the lifespan, however, women have periods where there is more or less PFAS detected in their bodies. Menstrual bleeding and parity are associated with lower PFAS levels, potentially indicating that menstruation and parturition may provide mechanisms of excretion PFAS.57,58

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Mitigation of lead exposure requires a healthy housing policy that ensures homes do not have lead-​based paint or contaminated soil. In addition, lead service line replacement is recommended to alleviate the risk of lead leaching from service lines and contaminating drinking water. For early detection, it is recommended that children are screened early and regularly. Chelation therapy can reduce blood lead levels, but evidence does not indicate neurodevelopmental and cognitive benefits.59,60 The greatest benefit is in preventing lead exposure altogether. To reduce mercury exposures, it is recommended that pregnant women or women who intend to become pregnant follow state advisories with regard to fish consumption. Occupational exposures can be reduced through personal protective equipment, engineering controls, and through elimination of the use of mercury. For example, composite fillings are offered in place of amalgam fillings in dentistry. In New Zealand, the use of amalgam fillings decreased from 52.3% in 1997 to 7.1% in 2017,61 and thereby reduced staff and patient exposure to mercury. In addition, doctors can encourage their patients to reduce personal exposures to PFAS by recommending that they limit the use of coated products, including nonstick cookware. If there is a known breach of PFAS into the local drinking water supply, physicians can recommend alternative water sources for drinking, cooking, or brushing teeth. In addition, people should not consume fish that may have been caught from a contaminated water source or crops grown in contaminated soil. Providers can also recommend that patients avoid food packaged in material containing PFAS along with stain-​resistant carpet, and water-​ repellent clothing.

6.3.3 Soil Food Exposures Hazardous exposures in soil have the potential to become hazardous in the food supply, leaving populations at risk for ingesting toxic substances. Contaminants in soil include metals like lead, cadmium, copper, and zinc. Sources of metal contamination can originate from industrial activity or can derive naturally. Food insecurity also threatens health. Food insecurity reflects the lack of access to healthy nutrients or over-​consuming non-​nutritious food. Therefore, underweight, overweight, and obese populations could all represent malnutrition. Communities in food deserts lack access to fresh fruits and vegetables, and may, conversely, have an abundance of fast food and convenience foods, leaving the population with few healthy options. However, having access to healthy food is essential because healthier diets can reduce the risk of chronic diseases. Contaminated food and malnutrition can harm health across the lifespan of women. Contaminated soil can increase children’s exposure to hazards, particularly metals. Children who lived near a smelter factory had soil contaminated with lead and arsenic and also demonstrated high blood lead levels.62 Malnourishment can increase the risk of infectious disease, immunodeficiency, gastrointestinal illness, and mortality from respiratory infections in children.63 Anemia, asthma, and poor oral health are also linked with food insecurity.64 Mental health threats of food insecurity in children include aggression, depression, anxiety, suicidal ideation, and cognitive and behavioral challenges.64 Food insecurity in children is associated with “fair-​to-​poor” health

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and higher odds of hospitalization in infants and toddlers.65 Nutritional status is an environmental risk factor for pregnant women. Overweight and obesity status are associated with adverse pregnancy outcomes, including gestational diabetes and pre-​ eclampsia.66 It is also important to consider cultural factors that influence exposure to potentially contaminated soil. For example, pica during pregnancy is reported at high rates women of low socioeconomic status born in Mexico.67 Reducing exposures to contaminated soil can involve advising patients not to track soil in the house. Because children are more likely to play on the floor and have oral exploratory habits, contaminated soil tracked in the house on shoes can become ingested by children. One way to not track soil in the house is to remove shoes upon entry. Additionally, households can be advised to sanitize floors often. Food insecurity can be addressed by policy change that ensures healthy food options in schools and communities.

6.3.4 Personal Care Product Exposures Cosmetics are products that can be applied to the body ranging from skin to hair care. According to the US Food and Drug Administration (FDA): It’s against the law for a cosmetic to contain any ingredient that makes the product harmful when consumers use it according to directions on the label, or in the customary or expected way… Under U.S. law, cosmetic products and ingredients, other than color additives, do not need FDA approval before they go on the market. Cosmetic manufacturers have a legal responsibility for the safety and labeling of their products.68

The FDA prohibits the use of the following toxic substances in cosmetics due to their sensitization, irritant, and carcinogenic qualities, including bithionol, chlorofluorocarbon propellants, chloroform, halogenated salicylanilides (di-​, tri-​, metabromsalan and tetrachlorosalicylanilide), hexachlorophene, mercury compounds, methylene chloride, prohibited cattle materials, sunscreens in cosmetics, vinyl chloride, and zirconium-​containing complexes.68 Additional toxicants of concern in cosmetics include heavy metals (lead, arsenic, and cadmium), endocrine disruptors (phthalates, bisphenol-​A, triclosan, persistent organic pollutants, etc.), parabens, phenols, and formaldehyde. Women aged 18–​34 years are considered heavy buyers of beauty products, consuming more than 10 products annually.69 The topical use of cosmetics products can result in dermal exposures to toxic substances. In addition, cosmetics can be ingested. It is estimated that many women will ingest 2 lbs of lipstick in their lifetime if they use five tubes annually from age 16 to 60 years.70 Lead levels in lipstick can affect blood lead levels in children.71 Endocrine disrupting hormones are associated with adverse effects on child development, including early reproductive tract development, pubertal development, neurodevelopment, and obesity, and are commonly found in cosmetics and personal care products.72 The National Institute of Environmental Health Sciences found that Latina girls exposed daily to personal care products (including makeup, soaps, hair products, oral hygiene products, and sunscreen) demonstrated higher levels of

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endocrine disruptors detected in their urine, putting these girls at higher risk due to their critical age in hormonal development.73 Reproductive disorders associated with endocrine disruptors are associated with exposures in long-​term exposures early in life or in adulthood.74 In addition to associations with decreased fertility and fecundity in women, exposure to endocrine disrupting chemicals is also associated with adverse effects on pregnancy outcomes, brain development, and reproductive development and function.72 In addition, endocrine disrupting chemicals are associated with the trans-​generational transfer of harmful to exposures.75 Women exposed to phthalates and phenols in the first trimester demonstrate altered mRNA expression in placental tissue, an indication of their potential to cross the placental barrier and that mRNA regulation may be a mechanism of endocrine disrupting effects in fetuses.76 Ovarian disorders that may be affected by endocrine disruptors include altered cyclicity, aneuploidy, endometriosis, and polycystic ovary syndrome.75 Uterine disorders, including uterine fibroids, are associated with endocrine disruptors.75 Placental function disorders and adverse pregnancy outcomes include early pregnancy loss, recurrent spontaneous abortion, and fetal growth restriction.75 Endocrine disruptors are also associated with disorders of the breast, including breast cancer and reduced duration of lactation.75 Certain personal care products, by nature of their use and chemical content, are associated with adverse health outcomes for women. Frequent use of hair dye may increase cancer risk, particularly for African-​American women.77 Even before pregnancy, hair dye use can contribute to adverse reproductive health risks. A study of pregnant women revealed hair dye use prior to pregnancy was associated with low birth weight, particularly for women who had experienced irregular periods or had higher body mass index (BMI).78 Triclosan, an antimicrobial used in antibacterial soap, hand sanitizer, toothpaste, and mouthwash, is associated with increased risk of gestational diabetes.79 Women who douche are at greater risk for ovarian cancer.80 Chemical hair straighteners are linked with increased risk of breast cancer.77 The use of hair relaxers is also associated with uterine leiomyomata (fibroids) in African-​ American premenopausal women.81,82 Multiple studies have indicated that perineal use of talc-​based baby powder is associated with increased risk of ovarian cancer.83 Skin lightening creams that contain mercury are associated with renal and central nervous system toxicity along with dermatologic complications in women, but data on dermal contact with mercury in skin lighteners and reproductive outcomes does not draw clear conclusions.84 These exposures not only affect the users, but there are also occupational exposures to personal care products that affect risk. Occupational exposures for cosmetologists and manicurists indicate increased risk for gestational diabetes as well as placenta previa.85 It is recommended to reduce exposures to cosmetics or personal care products that contain metals, endocrine disrupting chemicals, parabens, and phenols. Exposure in children during sensitive phases of development could have long-​term effects on their reproductive system. It is also recommended to limit exposure to personal care products containing endocrine disrupting chemicals, phenols, parabens, bisphenol A, and metals. Providers can inform patients about resources that can inform individual decision-​making around personal care product use. The California Safe Cosmetics

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Program Products Database provides publicly available information on potential hazards in personal care products.1 The Environmental Working Group hosts a web page and smart phone app, EWG’s Skin Deep®, where consumers can search their database of personal care products and identify ingredient concerns around cancer, reproductive and developmental toxicity, allergies and immunotoxicology, use restrictions, contamination concerns, irritation, occupational hazards, persistence and bioaccumulation, organ system toxicity (nonreproductive), enhanced skin toxicity, ecotoxicology, endocrine disruption, neurotoxicity, and multiple, additive exposure sources.2

6.3.5 Plastics Plastics are widely used in many of our daily tasks. In fact, plastics have improved quality of life by supporting infrastructure by delivering clean water to homes; bringing forth advancements in medical device manufacturing and medication packaging; facilitating conveniences like water bottles and containers that help preserve food; and affording technological advancements in televisions, cellphones, and computers. However, the production, usage, and storage of plastics pose growing concerns for human health. Communities that live on the fence lines of plastics manufacturers or extraction facilities bear a disproportionate burden of exposure, industrial accidents or incidents, and death.86 Those residing in fence line communities are often impoverished or people of color.86 Key community exposures resulting from plastic manufacturing include 1,3-​butadiene, benzene, styrene, toluene, ethane, propylene, and polycyclic aromatic hydrocarbons (PAH).86 In addition, there are additives used in plastics associated with health harms including plasticizers, such as bis(2-​ethylhexyl) phthalate (DEHP) and bisphenol A (BPA), vinyl chloride, benzene, phenol, brominated flame retardants, per-​and poly-​fluoroalkyl substances, phthalates, and lead heat stabilizer.86 Certain toxic substances are also known to leach from plastics, including antioxidants, UV stabilizers, and nonylphenol.86 In addition, the end-​of-​life of plastics also poses health threats by contaminating drinking water sources with microplastics, contributing to growth in municipal waste, and hazardous emissions from waste incineration and recycling. In addition to consumer products, children can be exposed to plastics via their toys. Children living near plants that emit 1,3-​butadiene have higher rates of cancer, including lymphatic leukemia and acute myeloid leukemia.86,87 Toluene exposure can increase children’s nervous and reproductive systems. Bisphenol A (BPA) is commonly found in the blood of children (CDC’s National Health Examination Study identified it in 92% of children and adults). This endocrine disruptor harms endocrine system functionality in young children. BPA can affect brain development and behavior in children exposed before or after birth.86 Phthalates are another endocrine disruptor used as a plastic additive to make plastic soft and pliable and is associated with reproductive, respiratory, and nervous system disorders, and learning and behavior difficulties.86 Because phthalates can be found in children’s toys, children may ingest them due to their oral exploratory habits. Similarly, polybrominated diphenyl ethers (PBDE) are found in children’s toys and can disrupt thyroid function

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and are associated with hyperactivity and poorer attention in children.86,88 Lead is an additional additive in plastics, found in jewelry and window blinds, and is associated with cognitive deficits in children. Pregnant women who worked in the reinforced plastics industry and had higher styrene exposure than their counterparts had infants with lower birth weight.89 Pregnant women exposed to phthalates are at increased risk of preterm birth and shorter gestation.90–​92 Toluene is associated with adverse developmental effects in children exposed in utero, including central nervous system dysfunction, deficits in attention, and birth defects including minor craniofacial and limb anomalies.86,93 Children exposed to lead can have reduced growth after birth.86 Older women can be sensitive to exposures to plastic chemicals due to their increased likelihood of preexisting chronic illnesses. The links between endocrine disruptors and obesity are consistent through older age. Phthalates are associated with increased abdominal fat distribution in women aged 70 years and above.94 Decreasing exposure to plastics can involve the reduction of utilization of single-​ use plastics like grocery bags and disposable cups when possible. In addition, health professionals can advocate for manufacturers of medical supplies to utilize life cycle assessments to identify the best processes and materials for public health and the environment, beginning with the extraction of raw materials through end of life. Physicians can encourage patients to not microwave plastics or Styrofoam or use them with hot liquids. The public should be aware that consumer products and packaging, including food packaging, can expose families to endocrine disrupting chemicals and carcinogens and to limit exposure to these as much as possible. In addition, it is important for the general population to be aware that plastics may contain untested additives, and to not assume that all products have been proven safe.

6.3.6 Equity/​Justice Environmental health services help ensure safe air to breathe, clean water to drink, and environments protected from disease-​carrying vectors in communities worldwide. However, systemic racism undermines the health gains of environmental health services, causing inequities in the distribution of these essential public health services. Furthermore, systemic racism plays a role in where environmental health hazards are located. Race is the most powerful predictor of where hazardous toxic air, water, and soil exist in the United States. Hazardous industrial polluters and major roadways are more likely to be in close proximity to communities of color and impoverished communities. Because toxic exposures place a higher health burden on pregnant women, infants, children, and older adult women, hazardous exposures in these communities further magnify the health disparities already faced by these uniquely susceptible populations. Racism is a source of toxic stress. Maternal exposure to discrimination, vicarious racism, is associated with poor health outcomes in children.95 Perceived racism is an indicator of adverse behavioral and mental health in children.96 Adverse childhood experiences (ACEs) and chronic or toxic stressors97 increase the risk of asthma in children, and research indicates that racism is a factor of chronic stress exposure

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increasing asthma-​related health disparities in African-​American children (as young as ages 1–​6 years).98 Unique to women across the lifespan are exposures to cosmetics. Certain personal care products, often for hair and skin, are directly marketed toward African-​American women. The American Journal of Obstetrics and Gynecology reports that women of color have higher levels of “beauty product-​related environmental chemicals in their bodies.”69 This includes endocrine disrupting chemicals, found in root stimulators, hair lotions, and hair relaxers.99 Pregnant African-​American women, who are especially vulnerable to toxic exposures, have demonstrated higher developmental toxin exposure, namely, phthalates, compared to Caucasians.100 In addition, asthma-​ associated chemicals are frequently detected in these products.99 The use of chemical relaxers and hair dye has been associated with increased risk of breast cancer in African-​American women compared to their Caucasian counterparts.77 Interventions that can address health inequities in environmental toxin exposure must uphold in environmental justice: “Environmental justice is the fair treatment and meaningful involvement of all people regardless of race, color, national origin, or income, with respect to the development, implementation, and enforcement of environmental laws, regulations, and policies.”101 Community-​based participatory research (CBPR) is a powerful intervention that facilitates fair treatment and ensures meaningful involvement through community engagement in the research and decision making process.102 In CBPR, members of the community are involved in problem identification, intervention selection, data collection, all the way through the intervention evaluation. An additional intervention to advance equity is the Health in All Policies Framework. This framework centers on health and equity being included in informing policy decision-​making.103

6.7  CONCLUSION Exposures through air, water, climate, soil and food, personal care products, and plastics can adversely affect health across the lifespan of women. By contrast, healthy air quality, safe water, and access to nutritious food can protect women’s health across the lifespan. Upholding environmental justice and health equity will ensure environmental health benefits across the lifespan but also across populations that are at greater risk and are more susceptible.

6.7.1 Recommendations • Air exposures: • Physicians should educate patients, particularly those who are most sensitive, to avoid outdoor activities during poor air quality days. Patients can access the EPA’s Air Quality Index at www.airnow.gov for local air quality information. • To ensure healthy indoor air quality, providers can recommend that patients reduce the combustion sources in homes, including gas stoves and tobacco smoke.

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• Water exposures: • Water contaminants can include metals and “forever” chemicals. Doctors should warn patients, particularly pregnant women, about the dangers of consuming fish from contaminated water. • Patients can reduce exposure to PFAS by avoiding products known to contain PFAS, including nonstick cookware, food packaged in PFAS-​contained materials, water-​repellent clothing, and stain-​resistant carpet. • Physicians can educate patients on the risk of water contamination following flooding. Patients should be advised to heed boil water advisories that follow an extreme rainfall event. • Soil exposures: • Hazards in soil can be tracked into homes by shoes, wheelchairs, walkers, or strollers. Physicians can advise patients to remove shoes, wear shoe covers, or sanitize wheels upon entry, when possible. In addition, it is advised that people sanitize floors often. • Personal care product exposures: • Providers should recommend that patients avoid products containing metals, endocrine-​disrupting chemicals, parabens, and phenols. • Providers can empower patients to make informed personal care product decisions by using accessible databases including that of the California Safe Cosmetics Program Products and the Environmental Working Group. • Plastic exposures: • Physicians can recommend that patients refrain from the following plastics uses: • Single use plastics, • Microwaving plastics, and • Plastic food packaging. • Equity and justice • Physicians must assess their personal biases and ensure that they are educating all patients on the health threats of hazardous exposures and providing them with the methods to reduce their personal exposures. • Physicians can support community-​based participatory research (CBPR), research that meaningfully involves members of the community in all aspects of research and decision-​making. • Physicians can support Health in All Policies to ensure that health is considered in all policies that can affect health.

NOTES 1 www.cdph.ca.gov/​Programs/​CCDPHP/​DEODC/​OHB/​CSCP/​Pages/​CSCP.aspx 2 www.ewg.org/​skindeep/​

REFERENCES 1. Watts N, Amann M, Arnell N, et al. The 2019 report of the Lancet Countdown on health and climate change: Ensuring that the health of a child born today is not defined

138

138

Natasha DeJarnett and Neha Pathak

by a changing climate. The Lancet. 2019;394(10211):1836–​1878. https://​doi.org/​ 10.1016/​S0140-​6736(19)32596-​6 2. Dockery DW, Pope CA, Xu X, et al. An association between air pollution and mortality in six US cities. New England Journal of Medicine. 1993;329(24):1753–​1759. https://​doi.org/​10.1056/​NEJM199312093292401 3. Brook RD, Rajagopalan S, Pope III CA, et al. Particulate matter air pollution and cardiovascular disease: An update to the scientific statement from the American Heart Association. Circulation. 2010;121(21):2331–​2378. https://​doi.org/​10.1161/​ CIR.0b013e3181dbece1 4. Brook RD, Franklin B, Cascio W, et al. Air pollution and cardiovascular disease: A statement for healthcare professionals from the Expert Panel on Population and Prevention Science of the American Heart Association. Circulation. 2004;109(21):2655–​2671. https://​doi.org/​10.1161/​01.CIR.0000128587.30041.C8 5. Bhatnagar A. Environmental cardiology: Studying mechanistic links between pollution and heart disease. Circulation Research. 2006;99(7):692–​705. https://​doi.org/​10.1161/​ 01.RES.0000243586.99701.cf 6. Bhatnagar A. Environmental determinants of cardiovascular disease. Circulation Research. 2017;121(2):162–​180. https://​doi.org/​10.1161/​CIRCRESAHA.117.306458 7. Pope III CA, Ezzati M, Dockery DW. Fine-​particulate air pollution and life expectancy in the United States. New England Journal of Medicine. 2009;360(4):376–​386. https://​ doi.org/​10.1056/​NEJMsa0805646 8. Institute HE. State of Global Air 2020. Special Report. Boston, MA: Health Effects Institute; 2020. 9. Gauderman WJ, Avol E, Gilliland F, et al. The effect of air pollution on lung development from 10 to 18 years of age. New England Journal of Medicine. 2004;351(11):1057–​ 1067. https://​doi.org/​10.1056/​NEJMoa040610 10. Grigg J. Particulate matter exposure in children: Relevance to chronic obstructive pulmonary disease. Proceedings of the American Thoracic Society. 2009;6(7):564–​569. https://​doi.org/​10.1513/​pats.200905-​026RM 11. Neas LM, Dockery DW, Ware JH, Spengler JD, Speizer FE, Ferris Jr BG. Association of indoor nitrogen dioxide with respiratory symptoms and pulmonary function in children. American Journal of Epidemiology. 1991;134(2):204–​219. https://​doi.org/​ 10.1093/​oxfordjournals.aje.a116073 12. Jerrett M, Shankardass K, Berhane K, et al. Traffic-​related air pollution and asthma onset in children: A prospective cohort study with individual exposure measurement. Environmental Health Perspectives. 2008;116(10):1433–​1438.https://​doi.org/​ 10.1289/​ehp.10968 13. Belanger K, Gent JF, Triche EW, Bracken MB, Leaderer BP. Association of indoor nitrogen dioxide exposure with respiratory symptoms in children with asthma. American Journal of Respiratory and Critical Care Medicine. 2006;173(3):297–​ 303.https://​doi.org/​10.1164/​rccm.200408-​1123OC 14. Chauhan A, Inskip HM, Linaker CH, et al. Personal exposure to nitrogen dioxide (NO2) and the severity of virus-​induced asthma in children. The Lancet. 2003;361(9373):1939–​ 1944. https://​doi.org/​10.1016/​S0140-​6736(03)13582-​9 15. O’Connor GT, Neas L, Vaughn B, et al. Acute respiratory health effects of air pollution on children with asthma in US inner cities. Journal of Allergy and Clinical Immunology. 2008;121(5):1133–​1139. e1131. https://​doi.org/​10.1016/​j.jaci.2008.02.020 16. Pilotto LS, Douglas RM, Attewell RG, Wilson SR. Respiratory effects associated with indoor nitrogen dioxide exposure in children. International Journal of Epidemiology. 1997;26(4):788–​796. https://​doi.org/​10.1093/​ije/​26.4.788

139

Avoiding Risky Substances

139

17. Zhu X, Liu Y, Chen Y, Yao C, Che Z, Cao J. Maternal exposure to fine particulate matter (PM 2.5) and pregnancy outcomes: A meta-​ analysis. Environmental Science and Pollution Research. 2015;22(5):3383–​3396. https://​doi.org/​10.1007/​ s11356-​014-​3458-​7 18. Lertxundi A, Baccini M, Lertxundi N, et al. Exposure to fine particle matter, nitrogen dioxide and benzene during pregnancy and cognitive and psychomotor developments in children at 15 months of age. Environment International. 2015;80:33–​40. https://​ doi.org/​10.1016/​j.envint.2015.03.007 19. Malmqvist E, Jakobsson K, Tinnerberg H, Rignell-​Hydbom A, Rylander L. Gestational diabetes and preeclampsia in association with air pollution at levels below current air quality guidelines. Environmental Health Perspectives. 2013;121(4):488–​493. https://​ doi.org/​10.1289/​ehp.1205736 20. Slama R, Thiebaugeorges O, Goua V, et al. Maternal personal exposure to airborne benzene and intrauterine growth. Environmental Health Perspectives. 2009;117(8):1313–​ 1321. https://​doi.org/​10.1289/​ehp.0800465 21. Chen D, Cho S-​I, Chen C, et al. Exposure to benzene, occupational stress, and reduced birth weight. Occupational and Environmental Medicine. 2000;57(10):661–​667. https://​doi.org/​10.1136/​oem.57.10.661 22. Yanney M, Marlow N. Paediatric consequences of fetal growth restriction. Paper presented at Seminars in Fetal and Neonatal Medicine 2004. https://​doi.org/​10.1016/​ j.siny.2004.03.005 23. Perera FP, Rauh V, Whyatt RM, et al. Effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on neurodevelopment in the first 3 years of life among inner-​ city children. Environmental Health Perspectives. 2006;114(8):1287–​1292.https://​ doi.org/​10.1289/​ehp.9084 24. Mordukhovich I, Beyea J, Herring AH, et al. Vehicular traffic-​related polycyclic aromatic hydrocarbon exposure and breast cancer incidence: The long island breast cancer study project (LIBCSP). Environmental Health Perspectives. 2016;124(1):30–​ 38.https://​doi.org/​10.1289/​ehp.1307736 25. Coogan PF, White LF, Jerrett M, et al. Air pollution and incidence of hypertension and diabetes mellitus in black women living in Los Angeles. Circulation. 2012;125(6):767–​ 772. https://​doi.org/​10.1161/​CIRCULATIONAHA.111.052753 26. Krämer U, Herder C, Sugiri D, et al. Traffic-​related air pollution and incident type 2 diabetes: Results from the SALIA cohort study. Environmental Health Perspectives. 2010;118(9):1273–​1279. https://​doi.org/​10.1289/​ehp.0901689 27. Bendokiene I, Grazuleviciene R, Dedele A. Risk of hypertension related to road traffic noise among reproductive-​age women. Noise and Health. 2011;13(55):371. https://​ doi.org/​10.4103/​1463-​1741.90288 28. Miller KA, Siscovick DS, Sheppard L, et al. Long-​term exposure to air pollution and incidence of cardiovascular events in women. New England Journal of Medicine. 2007;356(5):447–​458. https://​doi.org/​10.1056/​NEJMoa054409 29. Weuve J, Puett RC, Schwartz J, Yanosky JD, Laden F, Grodstein F. Exposure to particulate air pollution and cognitive decline in older women. Archives of Internal Medicine. 2012;172(3):219–​227. https://​doi.org/​10.1001/​archinternmed.2011.683 30. Andersen ZJ, Stafoggia M, Weinmayr G, et al. Long-​term exposure to ambient air pollution and incidence of postmenopausal breast cancer in 15 European cohorts within the ESCAPE project. Environmental Health Perspectives. 2017;125(10):107005. https://​doi.org/​10.1289/​EHP1742 31. Crouse DL, Goldberg MS, Ross NA, Chen H, Labrèche F. Postmenopausal breast cancer is associated with exposure to traffic-​ related air pollution in Montreal,

140

140

Natasha DeJarnett and Neha Pathak

Canada: A case-​control study. Environmental Health Perspectives. 2010;118(11):1578–​ 1583. https://​doi.org/​10.1289/​ehp.1002221 32. Goldberg MS, Labrèche F, Weichenthal S, et al. The association between the incidence of postmenopausal breast cancer and concentrations at street-​level of nitrogen dioxide and ultrafine particles. Environmental Research. 2017;158:7–​15. https://​doi.org/​ 10.1016/​j.envres.2017.05.038 33. Nie J, Beyea J, Bonner MR, et al. Exposure to traffic emissions throughout life and risk of breast cancer: The Western New York Exposures and Breast Cancer (WEB) study. Cancer Causes & Control. 2007;18(9):947–​955. https://​doi.org/​10.1007/​ s10552-​007-​9036-​2 34. Schikowski T, Sugiri D, Ranft U, et al. Long-​term air pollution exposure and living close to busy roads are associated with COPD in women. Respiratory Research. 2005;6(1):152.https://​doi.org/​10.1186/​1465-​9921-​6-​152 35. Kingsley SL, Eliot MN, Whitsel EA, et al. Residential proximity to major roadways and incident hypertension in post-​ menopausal women. Environmental Research. 2015;142:522–​528.https://​doi.org/​10.1016/​j.envres.2015.08.002 36. Anderson JO, Thundiyil JG, Stolbach A. Clearing the air: A review of the effects of particulate matter air pollution on human health. Journal of Medical Toxicology. 2012;8(2):166–​175. https://​doi.org/​10.1007/​s13181-​011-​0203-​1 37. Brooks BW, Gerding JA, Landeen E, et al. Environmental health practice challenges and research needs for US health departments. Environmental Health Perspectives. 2019;127(12):125001. https://​doi.org/​10.1289/​EHP5161 38. Bose-​O’Reilly S, McCarty KM, Steckling N, Lettmeier B. Mercury exposure and children’s health. Current Problems in Pediatric and Adolescent Health Care. 2010;40(8):186–​215. https://​doi.org/​10.1016/​j.cppeds.2010.07.002 39. Sunderland EM, Hu XC, Dassuncao C, Tokranov AK, Wagner CC, Allen JG. A review of the pathways of human exposure to poly-​and perfluoroalkyl substances (PFASs) and present understanding of health effects. Journal of Exposure Science & Environmental Epidemiology. 2019;29(2):13–​47. https://​doi.org/​10.1038/​s41370-​018-​0094-​1 40. Lin C-​C, Chen Y-​C, Su F-​C, et al. In utero exposure to environmental lead and manganese and neurodevelopment at 2 years of age. Environmental Research. 2013;123:52–​ 57. https://​doi.org/​10.1016/​j.envres.2013.03.003 41. Tang HW, Huel G, Campagna D, Hellier G, Boissinot C, Blot P. Neurodevelopmental evaluation of 9-​ month-​ old infants exposed to low levels of lead in utero: Involvement of monoamine neurotransmitters. Journal of Applied Toxicology. 1999;19(3):167–​172. https://​doi.org/​10.1002/​(SICI)1099-​1263(199905/​ 06)19:33.0.CO;2-​8 42. Wu S, Hivert M-​F, Cardenas A, et al. Exposure to low levels of lead in utero and umbilical cord blood DNA methylation in Project Viva: An epigenome-​wide association study. Environmental Health Perspectives. 2017;125(8):087019. https://​doi.org/​ 10.1289/​EHP1246 43. Grandjean P. Methylmercury toxicity and functional programming. Reproductive Toxicology. 2007;23(3):414–​420. https://​doi.org/​10.1016/​j.reprotox.2007.03.002 44. Murata K, Weihe P, Budtz-​ Jørgensen E, Jørgensen PJ, Grandjean P. Delayed brainstem auditory evoked potential latencies in 14-​year-​old children exposed to methylmercury. The Journal of Pediatrics. 2004;144(2):177–​183.https://​doi.org/​ 10.1016/​j.jpeds.2003.10.059 45. Grandjean P, White R. Neurodevelopmental disorders. Children’s health and environment: A Review of the Evidence. World Health Organization and European Environmental Agency, Rome, Italy. 2002:66–​78.

141

Avoiding Risky Substances

141

46. Zhang C, Sundaram R, Maisog J, Calafat AM, Barr DB, Louis GMB. A prospective study of prepregnancy serum concentrations of perfluorochemicals and the risk of gestational diabetes. Fertility and Sterility. 2015;103(1):184–​189. https://​doi.org/​10.1016/​ j.fertnstert.2014.10.001 47. Grandjean P, Landrigan PJ. Developmental neurotoxicity of industrial chemicals. The Lancet. 2006;368(9553):2167–​2178. https://​doi.org/​10.1016/​S0140-6736(06) 69665-​7 48. Health AAoPCoE. Lead exposure in children: Prevention, detection, and management. Pediatrics. 2005;116(4):1036. https://​doi.org/​10.1542/​peds.2005-​1947 49. Schwartz J. Low-​level lead exposure and children’s IO: A meta-​analysis. Environmental Research. 1994;65:42–​55. https://​doi.org/​10.1006/​enrs.1994.1020 50. Needleman HL, Gatsonis CA. Low-​level lead exposure and the IQ of children: A meta-​ analysis of modern studies. JAMA. 1990;263(5):673–​678. https://​doi.org/​10.1001/​ jama.1990.03440050067035 51. Grandjean P, Andersen EW, Budtz-​ Jørgensen E, et al. Serum vaccine antibody concentrations in children exposed to perfluorinated compounds. JAMA. 2012;307(4):391–​397. https://​doi.org/​10.1001/​jama.2011.2034 52. Frisbee SJ, Shankar A, Knox SS, et al. Perfluorooctanoic acid, perfluorooctanesulfonate, and serum lipids in children and adolescents: Results from the C8 Health Project. Archives of Pediatrics & Adolescent Medicine. 2010;164(9):860–​869. https://​doi.org/​ 10.1001/​archpediatrics.2010.163 53. Schober SE, Sinks TH, Jones RL, et al. Blood mercury levels in US children and women of childbearing age, 1999–​2000. JAMA. 2003;289(13):1667–​1674. https://​ doi.org/​10.1001/​jama.289.13.1667 54. Henriques MC, Loureiro S, Fardilha M, Herdeiro MT. Exposure to mercury and human reproductive health: A systematic review. Reproductive Toxicology. 2019;85:93–​103. https://​doi.org/​10.1016/​j.reprotox.2019.02.012 55. Liu G, Dhana K, Furtado JD, et al. Perfluoroalkyl substances and changes in body weight and resting metabolic rate in response to weight-​loss diets: A prospective study. PLOS Medicine. 2018;15(2):e1002502.https://​doi.org/​10.1371/​ journal.pmed.1002502 56. Hu XC, Tokranov AK, Liddie J, et al. Tap water contributions to plasma concentrations of poly-​and perfluoroalkyl substances (PFAS) in a nationwide prospective cohort of US women. Environmental Health Perspectives. 2019;127(6):067006.https://​doi.org/​ 10.1289/​EHP4093 57. Park SK, Peng Q, Ding N, Mukherjee B, Harlow SD. Determinants of per-​and polyfluoroalkyl substances (PFAS) in midlife women: Evidence of racial/​ethnic and geographic differences in PFAS exposure. Environmental Research. 2019;175:186–​ 199. https://​doi.org/​10.1016/​j.envres.2019.05.028 58. Ding N, Harlow SD, Batterman S, Mukherjee B, Park SK. Longitudinal trends in perfluoroalkyl and polyfluoroalkyl substances among multiethnic midlife women from 1999 to 2011: The study of women′ s health across the nation. Environment International. 2020;135:105381. https://​doi.org/​10.1016/​j.envint.2019.105381 59. Dietrich KN, Ware JH, Salganik M, et al. Effect of chelation therapy on the neuropsychological and behavioral development of lead-​exposed children after school entry. Pediatrics. 2004;114(1):19–​26. https://​doi.org/​10.1542/​peds.114.1.19 60. Rogan WJ, Dietrich KN, Ware JH, et al. The effect of chelation therapy with succimer on neuropsychological development in children exposed to lead. New England Journal of Medicine. 2001;344(19):1421–​1426. https://​doi.org/​10.1056/​ NEJM200105103441902

142

142

Natasha DeJarnett and Neha Pathak

61. Broadbent J, Murray C, Schwass D, et al. The dental amalgam phasedown in New Zealand: A 20-​year trend. Operative Dentistry. 2020. https://​doi.org/​10.2341/​ 19-​024-​C 62. Carrizales L, Razo I, Tellez-​Hernandez JI, et al. Exposure to arsenic and lead of children living near a copper-​smelter in San Luis Potosi, Mexico: Importance of soil contamination for exposure of children. Environmental Research. 2006;101(1):1–​10. https://​doi.org/​10.1016/​j.envres.2005.07.010 63. Rodríguez L, Cervantes E, Ortiz R. Malnutrition and gastrointestinal and respiratory infections in children: A public health problem. International Journal of Environmental Research and Public Health. 2011;8(4):1174–​1205. https://​doi.org/​ 10.3390/​ijerph8041174 64. Gundersen C, Ziliak JP. Food insecurity and health outcomes. Health Affairs. 2015;34(11):1830–​1839. https://​doi.org/​10.1377/​hlthaff.2015.0645 65. Cook JT, Frank DA, Berkowitz C, et al. Food insecurity is associated with adverse health outcomes among human infants and toddlers. The Journal of Nutrition. 2004;134(6):1432–​1438.https://​doi.org/​10.1093/​jn/​134.6.1432 66. Nucci LB, Schmidt MI, Duncan BB, Fuchs SC, Fleck ET, Britto MMS. Nutritional status of pregnant women: Prevalence and associated pregnancy outcomes. Revista de saude publica. 2001;35(6):502–​507. https://​doi.org/​10.1590/​ S0034-​89102001000600002 67. Simpson E, Mull JD, Longley E, East J. Pica during pregnancy in low-​income women born in Mexico. Western Journal of Medicine. 2000;173(1):20. https://​doi.org/​10.1136/​ ewjm.173.1.20 68. Administration USFaD. Prohibited & restricted ingredients in cosmetics. www.fda.gov/​ cosmetics/​cosmetics-​laws-​regulations/​prohibited-​restricted-​ingredients-​cosmetics. Published 2020. Accessed October 25, 2020. 69. Zota AR, Shamasunder B. The environmental injustice of beauty: Framing chemical exposures from beauty products as a health disparities concern. American Journal of Obstetrics and Gynecology. 2017;217(4):418.e411–​418.e416. https://​doi.org/​10.1016/​ j.ajog.2017.07.020 70. Mellowship D. Toxic Beauty: The Hidden Chemicals in Cosmetics and How They Can Harm Us. Hachette UK; 2009. 71. Monnot AD, Christian WV, Abramson MM, Follansbee MH. An exposure and health risk assessment of lead (Pb) in lipstick. Food and Chemical Toxicology. 2015;80:253–​ 260. https://​doi.org/​10.1016/​j.fct.2015.03.022 72. Meeker JD. Exposure to environmental endocrine disruptors and child development. Archives of Pediatrics & Adolescent Medicine. 2012;166(10):952–​958. https://​doi.org/​ 10.1001/​archpediatrics.2012.241 73. Berger KP, Kogut KR, Bradman A, et al. Personal care product use as a predictor of urinary concentrations of certain phthalates, parabens, and phenols in the HERMOSA study. Journal of Exposure Science & Environmental Epidemiology. 2019;29(1):21–​ 32. https://​doi.org/​10.1038/​s41370-​017-​0003-​z 74. Crain DA, Janssen SJ, Edwards TM, et al. Female reproductive disorders: The roles of endocrine-​disrupting compounds and developmental timing. Fertility and Sterility. 2008;90(4):911–​940. https://​doi.org/​10.1016/​j.fertnstert.2008.08.067 75. Caserta D, Mantovani A, Marci R, et al. Environment and women’s reproductive health. Human Reproduction Update. 2011;17(3):418–​433. https://​doi.org/​10.1093/​ humupd/​dmq061 76. LaRocca J, Binder AM, McElrath TF, Michels KB. First-​trimester urine concentrations of phthalate metabolites and phenols and placenta miRNA expression in a cohort of

143

Avoiding Risky Substances

143

US women. Environmental Health Perspectives. 2016;124(3):380–​387. https://​doi.org/​ 10.1289/​ehp.1408409 77. Eberle CE, Sandler DP, Taylor KW, White AJ. Hair dye and chemical straightener use and breast cancer risk in a large US population of black and white women. International Journal of Cancer. 2020;147(2):383–​391.https://​doi.org/​10.1002/​ijc.32738 78. Jiang C, Hou Q, Huang Y, et al. The effect of pre-​pregnancy hair dye exposure on infant birth weight: a nested case-​control study. BMC Pregnancy and Childbirth. 2018;18(1):1–​8. https://​doi.org/​10.1186/​s12884-​018-​1782-​5 79. Ouyang F, Tang N, Zhang H-​J, et al. Maternal urinary triclosan level, gestational diabetes mellitus and birth weight in Chinese women. Science of the Total Environment. 2018;626:451–​457. https://​doi.org/​10.1016/​j.scitotenv.2018.01.102 80. Gonzalez NL, O’Brien KM, D’Aloisio AA, Sandler DP, Weinberg CR. Douching, talc use, and risk of ovarian cancer. Epidemiology. 2016;27(6):797–​802. https://​doi.org/​ 10.1097/​EDE.0000000000000528 81. Wise LA, Palmer JR, Reich D, Cozier YC, Rosenberg L. Hair relaxer use and risk of uterine leiomyomata in African-​American women. American Journal of Epidemiology. 2012;175(5):432–​440. https://​doi.org/​10.1093/​aje/​kwr351 82. Berge W, Mundt K, Luu H, Boffetta P. Genital use of talc and risk of ovarian cancer: A meta-​analysis. European Journal of Cancer Prevention. 2018;27(3):248–​257. https://​ doi.org/​10.1097/​CEJ.0000000000000340 83. Penninkilampi R, Eslick GD. Perineal talc use and ovarian cancer. Epidemiology. 2018;29(1):41–​49. https://​doi.org/​10.1097/​EDE.0000000000000745 84. Al-​ Saleh I. Potential health consequences of applying mercury-​ containing skin-​ lightening creams during pregnancy and lactation periods. International Journal of Hygiene and Environmental Health. 2016;219(4–​5):468–​474. https://​doi.org/​10.1016/​ j.ijheh.2016.03.002 85. Quach T, Von Behren J, Goldberg D, Layefsky M, Reynolds P. Adverse birth outcomes and maternal complications in licensed cosmetologists and manicurists in California. International Archives of Occupational and Environmental Health 2015;88(7):823–​ 833. https://​doi.org/​10.1007/​s00420-​014-​1011-​0 86. Azoulay D, Villa P, Arellano Y, et al. Plastic & Health: The Hidden Costs of a Plastic Planet. CIEL; 2019. 87. Walker KM, Coker AL, Symanski E, Lupo PJ. A preliminary investigation of the association between hazardous air. Occupational and Environmental Medicine 2000;57:411–​417. 88. Roze E, Meijer L, Bakker A, Braeckel KNJAV, Sauer PJJ, Bos AF. Prenatal exposure to organohalogens, including brominated flame retardants, influences motor, cognitive, and behavioral performance at school age. Environmental Health Perspectives. 2009;117(12):1953–​1958. https://​doi.org/​10.1289/​ehp.0901015 89. Lemasters GK, Samuels SJ, Morrison JA, Brooks SM. Reproductive outcomes of pregnant workers employed at 36 reinforced plastics companies. II. Lowered birth weight. Journal of Occupational Medicine: Official Publication of the Industrial Medical Association. 1989;31(2):115–​120. 90. Ferguson KK, McElrath TF, Ko Y-​A, Mukherjee B, Meeker JD. Variability in urinary phthalate metabolite levels across pregnancy and sensitive windows of exposure for the risk of preterm birth. Environment International. 2014;70:118–​124. https://​doi.org/​ 10.1016/​j.envint.2014.05.016 91. Ferguson KK, McElrath TF, Meeker JD. Environmental phthalate exposure and preterm birth. JAMA Pediatrics. 2014;168(1):61–​67. https://​doi.org/​10.1001/​ jamapediatrics.2013.3699

144

144

Natasha DeJarnett and Neha Pathak

92. Ferguson KK, Rosen EM, Rosario Z, et al. Environmental phthalate exposure and preterm birth in the PROTECT birth cohort. Environment International. 2019;132:105099. https://​doi.org/​10.1016/​j.envint.2019.105099 93. Agency UEP. Toluene (rev. July 2012). www.epa.gov/​sites/​production/​files/​2016-​09/​ documents/​toluene.pdf. Published 2012. Accessed October 25, 2020. 94. Lind PM, Roos V, Rönn M, et al. Serum concentrations of phthalate metabolites are related to abdominal fat distribution two years later in elderly women. Environmental Health. 2012;11(1):21. https://​doi.org/​10.1186/​1476-​069X-​11-​21 95. Condon EM, Holland ML, Slade A, Redeker NS, Mayes LC, Sadler LS. Associations between maternal experiences of discrimination and biomarkers of toxic stress in school-​aged children. Maternal and Child Health Journal. 2019;23(9):1147–​1151. https://​doi.org/​10.1007/​s10995-​019-​02779-​4 96. Pachter LM, Coll CG. Racism and child health: A review of the literature and future directions. Journal of Developmental and Behavioral Pediatrics: JDBP. 2009;30(3):255. https://​doi.org/​10.1097/​DBP.0b013e3181a7ed5a 97. Barnthouse M, Jones BL. The impact of environmental chronic and toxic stress on asthma. Clinical Reviews in Allergy & Immunology. 2019;57(3):427–​438. https://​ doi.org/​10.1007/​s12016-​019-​08736-​x 98. Jones BL, Staggs V, Woods-​Jaeger B. Chronic stress exposure among young African American children with asthma: Racism is a factor. Annals of Allergy, Asthma & Immunology. 2019;123(5):507–​508.https://​doi.org/​10.1016/​j.anai.2019.08.023 99. Helm JS, Nishioka M, Brody JG, Rudel RA, Dodson RE. Measurement of endocrine disrupting and asthma-​associated chemicals in hair products used by Black women. Environmental Research. 2018;165:448–​458. https://​doi.org/​10.1016/​ j.envres.2018.03.030 100. Bloom MS, Wenzel AG, Brock JW, et al. Racial disparity in maternal phthalates exposure; Association with racial disparity in fetal growth and birth outcomes. Environment International. 2019;127:473–​486. https://​doi.org/​10.1016/​j.envint. 2019.04.005 101. Agency UEP. Environmental Justice. www.epa.gov/​environmentaljustice. Published 2020. Accessed October 26, 2020. 102. Northridge ME, Yankura J, Kinney PL, et al. Diesel exhaust exposure among adolescents in Harlem: A community-​driven study. American Journal of Public Health. 1999;89(7):998–​1002. https://​doi.org/​10.2105/​AJPH.89.7.998 103. Rudolph L, Caplan J, Ben-​Moshe K, Dillon L. Health in All Policies: A Guide for State and Local Governments. American Public Health Association, Washington, DC; 2013.

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Models of Care for Women and Families, Reimbursement, and Telemedicine Haran Sivakumar, MD

Department of Family Medicine UC San Diego Health San Diego, CA

Megan Alexander, MS

Boston University School of Medicine Boston, MA

Allison Theberge

Department of Family Medicine UC San Diego Health San Diego, CA

Deepa Sannidhi, MD

Department of Family Medicine UC San Diego Health San Diego, CA 7.1 In-​Person Visit Structures...............................................................................146 7.1.1 Individual Visits..................................................................................146 7.1.2 Group Medical Visits..........................................................................146 7.2 Telehealth.......................................................................................................147 7.2.1 Televisits.............................................................................................147 7.2.2 Remote Patient Monitoring................................................................148 7.3 Reimbursement Overview..............................................................................148 7.3.1 Grants and Employer-​Funded Programs............................................148 7.3.2 Analyzing Insurance Reimbursement................................................149 7.3.3 Optimizing Insurance Billing.............................................................149 DOI: 10.1201/9781003110682-8

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7.3.4 A Deeper Look at Direct Payment.....................................................150 7.3.5 Membership Fees...............................................................................150 7.3.6 Additional Services............................................................................150 7.4 Summary of Reimbursement..........................................................................151

KEY POINTS • Lifestyle Medicine (LM) visits are well suited for a variety of clinical settings, including in person visits (individual or group medical visits) as well as telehealth. • Telehealth visits are becoming more prevalent in a variety of medical settings and are increasingly being covered by insurers. • Use of adjuvant technology such as remote patient monitoring and mHealth can facilitate data sharing with providers and provide increased opportunities for billing. • LM providers must utilize various forms of billing to maximize reimbursement. This may include traditional billing of insurance in conjunction with alternative models, including a direct membership fee, employer wellness programs, and/​ or grant-​based funding.

7.1  IN-​PERSON VISIT STRUCTURES 7.1.1 Individual Visits When providing in-​person care, Lifestyle Medicine (LM) providers can utilize either the standard individual visit or the group medical visit. Providers should gain familiarity with both options to evaluate potential strengths and challenges for their practice. Factors to take into account include patient accessibility, level of personalization, privacy, staff support, efficiency, and reimbursement. The most common visit structure is the in-​person visit with a single patient. This type of visit is familiar to patients and offers the ability to conduct a complete physical examination, privately discuss sensitive topics, and conduct in-​office procedures. However, many providers report insufficient time to adequately address LM topics. One technique to combat inadequate time is the “flipped classroom” approach, where the patient is provided with resources to self-​educate on LM principles, to be followed up at a future visit. Follow-​up may be done by phone call via staff to check-​in or referral to a dietician or health coach. If time allows for in-​person counselling, billing by time can be utilized to maximize reimbursement.1,21

7.1.2 Group Medical Visits Group medical visits (or shared medical appointments) are clinical encounters in which multiple patients with a common health concern are offered clinical support and education in a group setting. This visit structure is increasingly common and is endorsed by major medical associations, including the American Academy of Family Physicians (AAFP). Group visits increase access to appointments, allow for

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additional time to discuss LM topics, and give patients a setting to share successes and obstacles with their peers. They also minimize patient wait times and maximize provider time by allowing providers to educate multiple patients simultaneously. Many women’s health topics lend themselves to this structure. Group prenatal care is well established and supported by the American College of Obstetricians and Gynecologists (ACOG) as an alternative to individual visits and is particularly well studied in the Centering Pregnancy™ model.3 Other potential topics include parenting, chronic pain, menopause, weight management, and sexual concerns. Logistically, a group medical visit can be conducted with 10–​15 patients and would last from 1 to 2 hours. One may anticipate an appropriate no-​show rate and consider “overbooking” accordingly. Successful execution of the group medical visit requires advanced planning and adequate support. For this reason, group visits are best led by a team, such as a clinical professional along with a behavioral specialist. Group visits also offer opportunity for increased reimbursement, as each patient may be billed for an individual office visit, so long as each patient is already established within the practice and the billing clinician engages with each individual during the group visit.4,5 To bill for an individual office visit during a group visit, the billing clinician can engage with the patient in various ways, including addressing new complaints, conducting an examination, and placing medical orders. More information implementing group visits can be found in the supplemental materials section.

7.2  TELEHEALTH A new and promising adjunct to traditional in-​person visits can be found through telehealth, which can broadly be defined as any health-​related service that uses electronic and communication technology to remotely deliver health information.6 This includes communication that is “synchronous,” such as real-​time video televisits; “asynchronous,” such as store-​and-​forward messaging; remote patient monitoring (RPM); and mobile health or “mHealth”.7–​9 The Agency for Healthcare Research and Quality found that the greatest evidence for telehealth effectiveness lies in behavioral health communication regarding chronic disease and mental health.

7.2.1 Televisits Adoption of televisits is on the rise. According to surveys, physician use of virtual visits doubled between 2016 and 2019, from 14% to 28%.10,11 And promisingly, there is evidence of high satisfaction rates and comparable patient outcomes for a variety of ambulatory applications.9 The coronavirus disease 2019 (COVID-​19) pandemic notably increased the prevalence of televisit use, including for obstetrics and gynecology (OB/​GYN) care with American College of Obstetricians and Gynecologists (ACOG) promoting televisits during the pandemic.12 Televisits are well suited for LM, as many visits are focused on behavioral change and thus do not require an in-​person physical examination. For patients, televisits are more convenient, requiring no transportation and less time away from other responsibilities. From a provider prospective, they require minimal overhead, increase accessibility to previously unreachable remote patients, and allow for more frequent

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follow-​ups. There are numerous applications of LM televisits to women’s health, such as family planning and preconception counselling,6,13 select prenatal care visits with incorporated mobile health technology, and care for postpartum depression.14 Reimbursement for televisits is a changing landscape, particularly since the COVID-​ 19 pandemic, and varies by state in terms of regulations.

7.2.2 Remote Patient Monitoring RPM enables patients to electronically share medical data collected via handheld or wearable devices or a phone application. Examples include blood pressure cuffs, glucose monitors, and weight scales.15,16 Its use is becoming more widespread as practitioners recognize the advantages of more data-​informed care adjustments and enhanced patient engagement.10 It also serves as an additional revenue source. More information on RPM and mHealth can be found in the supplemental materials section.

7.3  REIMBURSEMENT OVERVIEW The largest survey of LM practitioners to date demonstrated that as of 2018 over half (57%) of LM practitioners were uncompensated for their time, with many others undercompensated.17 Thus, for the clear majority of practitioners, LM becomes a pursuit of passion incurring a financial loss. That loss can be offset by devoting time to other forms of clinical practice; however, this may increase the odds of burnout while limiting the scale of the LM practice. For those wishing to practice LM in a more scalable, sustainable, and financially viable manner, many must look beyond traditional payment models. Providers of LM that are appropriately compensated tend to combine a variety of revenue streams, which may include traditional insurance, along with grants, direct payment, and employer-​funded wellness programs. Of the compensated LM providers, the highest percentage (60%) cites direct payment as a revenue stream compared to billing insurance (54%), employer-​funded programs (21%), and grants (11%).17

7.3.1 Grants and Employer-​Funded Programs The lack of prevalence of grants as a revenue source is not surprising. Grants are not readily available and tend to be competitive to obtain, often requiring institutional support and resources. They require significant upfront work to apply, and there is no guarantee that year to year they will be awarded, making them an unreliable source of revenue. Additionally, there is concern of bias against women and minorities in the grant application process.18 As a result, only a subset of LM providers realistically compete for them. LM providers at academic institutions with a track record of securing grant funding may have more predictable success with this revenue stream. Employer-​funded wellness programs were almost twice as prevalent as grants as a source of revenue but only used by a minority of providers.17 Availability is similarly the limiting factor. Securing a partnership with an employer can be challenging

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and requires significant upfront work. Compared to grants, there is more revenue reliability with employer wellness programs. If an employer has a good experience with an LM practice, they are more likely to continue renewing.19 With the rise in prevalence of high deductible plans, more employers are now using supplemental wellness programs to keep employees engaged and satisfied in their health. If the insurance market continues to favor high deductible plans, wellness programs may become more reliable revenue sources for LM practices.20

7.3.2 Analyzing Insurance Reimbursement Billing insurance is commonly what comes to mind when considering a practice’s revenue stream, and it is among the most popular sources of revenue for compensated LM providers. However, at a prevalence rate of 54%, it is far less common than most would expect.17 There are several possible reasons for this. It is well established that the insurance landscape has consistently undervalued LM and undercompensated LM providers. This may lead some providers to bypass insurance altogether in favor of other revenue streams; others may limit LM to a small percentage of their practice, leaving little incentive to bother with the hassle of billing insurance for LM; and still others may simply not know how to bill appropriately for LM.21 For LM providers who wish to bill insurance, they could benefit from implementing some of the strategies discussed in this chapter. To recap, these strategies include optimizing group visits, appropriately billing, not underbilling individual office visits, and using telehealth to capture additional patients, while utilizing technology such as remote physiologic monitoring.

7.3.3 Optimizing Insurance Billing For group visits, billing can be optimized by ensuring patient attendance is in the double digits and deploying both a physician and another healthcare worker who can effectively bill for separate charges (e.g., a physician to bill for the office visit and a psychologist to bill for psychotherapy). For individual visits, the single most important intervention is ensuring providers are aware of the criteria for insurance billing, based on each level of visit, and appropriately billing. Additionally, many providers fail to realize that they can bill multiple codes for a single office visit, such as current procedural terminology (CPT) codes, specific behavioral screenings, and specific forms of counseling (including obesity, nicotine, etc.).22–​24 Details on current billing codes can be found in the supplemental materials. Telehealth reimbursement varies based on payer and state laws, with reimbursement typically less than or equal to office visits. Regardless, telehealth can be leveraged to capture patients who otherwise could not show up to an office visit (e.g., a patient with transportation difficulties). Remote physiologic monitoring is best deployed via nonphysician clinical staff since reimbursement is less than that of a physician office visit. However, the monitoring system should broadly fall under physician supervision. RPM can be billed monthly, assuming that appropriate monitoring systems are in place and that it is billing on a day when no other office

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visits occur.25 If implemented correctly, RPM can provide a stable monthly revenue stream independent of office visits.

7.3.4 A Deeper Look at Direct Payment Based on survey data from 2018, there is a high prevalence of direct payment among compensated LM providers. For those accustomed to traditional medical practices, direct payment can seem foreign, or even off-​putting. This even appears to be the case for most LM providers. Despite it being the preferred source of revenue for compensated LM providers, overall over 74% of all LM providers do not receive any direct payment. Among those providers who forego direct payment, over 77% end up being completely uncompensated.17 Given that direct payment is the largest revenue stream, it is unsurprising that opting out puts providers at a high risk of being uncompensated. There are a myriad of ways to incorporate direct payment but ultimately strategies for direct payment can be distilled into membership fees and additional services.

7.3.5 Membership Fees Membership fees are fairly straightforward. They are fees billed to all patients in a practice, usually on a monthly or an annual basis, and provide a consistent and predictable revenue stream. There are two models for membership fees: charging membership fees in addition to billing insurance or in place of billing insurance. Advantages of continuing insurance billing include maintaining multiple revenue streams and keeping the membership fees low.21 The fees in this model are typically comparable to the cost of digital subscription services (e.g., Netflix or Amazon Prime). The alternative model, having the membership fee replace insurance billing, necessitates a significantly higher fee but also has numerous advantages. These include streamlining billing, thereby reducing practice overhead significantly, having very predictable costs for patients (avoiding surprise insurance billing) and very predictable revenue for the practice. This can also be an attractive option for uninsured patients or those with high deductibles. The membership fees in this model are typically around the price of a gym membership.26

7.3.6 Additional Services The other approach to soliciting direct payment involves additional services. Examples of additional services could include time with a dietitian or health coach, sessions with a personal trainer, cooking classes, access to digital content such as recipes or a forum, asynchronous communication, monitoring of wearable technology, and specialty group visits. The revenue from additional services is less predictable or consistent than practice-​wide membership fees, but has the advantage of being more flexible, and only requires a subset of the practice providers to participate. Depending on the service, the practice can charge patients on a fee-​for-​service basis, a monthly basis, or an annual basis.21

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7.4  SUMMARY OF REIMBURSEMENT Reimbursement is a nuanced subject, but it is imperative to understand for all providers. This is especially true for LM providers who are frequently undercompensated for their efforts. Given the current insurance landscape, most LM practitioners cannot anticipate being fully compensated if they exclusively rely on a system that undervalues their skill sets. And when providers are not appropriately compensated, it increases the risk of burnout and limits their ability to help their patients.27 So, what can LM providers do to ensure adequate compensation when selecting models of care? Forgoing insurance altogether in favor of direct payment membership is an elegant option worth exploring and certainly viable for some practices.26 Realistically, however, most practices will still find themselves billing insurance. For these practices, procuring appropriate compensation will likely require two elements. The first element is ensuring adequate optimization of insurance billing. This entails leveraging the increased billing of group visits, billing for additional services like RPM, and maximizing office visits via telehealth billing, time-​based billing, preventive counseling billing, and behavioral screening coding. 22–​24,28 The second element is identifying at least one additional revenue stream. This could come from grant funding if an LM provider practices in an institution with a strong track record of procuring grants or from employer wellness programs if an LM provider is able to partner with local employers.20 If neither of these options is feasible, direct payment can always serve as the additional revenue stream. This can be achieved by charging patients a low membership fee or marketing additional services.21 Ideally, one day, insurance billing will be simplified and reimbursement will be increased to reflect the true value of LM. But until then, LM providers must be both savvy and innovative when designing practices. Care must be taken to be creative and open-​minded when considering and diversifying revenue streams. And when insurance is billed, it must be done so strategically and meticulously to ensure appropriate compensation and ultimately optimal patient care.

REFERENCES 1. Motley E. Building a thriving lifestyle medicine practice within a primary care clinic: A model for aspiring lifestyle medicine practitioners. Am J Lifestyle Med. 2020;14(2):133–​136. doi:10.1177/​1559827620904868. 2. Jensen LL, Drozek DS, Grega ML, Gobble J. Lifestyle medicine: Successful reimbursement methods and practice models. Am J Lifestyle Med. 2018;13(3):246–​252. Published 2018 Dec 10. doi:10.1177/​1559827618817294. 3. ACOG Committee Opinion No. 731: Group Prenatal Care. Obstet Gynecol. 2018;131(3):e104–​e108. doi:10.1097/​AOG.0000000000002529. 4. Trickett KH, Matiaco PM, Jones K, Howlett B, Early KB. Effectiveness of shared medical appointments targeting the triple aim among patients with overweight, obesity, or diabetes. J Am Osteopath Assoc. 2016;116(12):780–​787. doi:10.7556/​jaoa.2016.153. 5. Thacker HL, Maxwell R, Saporito J, Bronson D. Shared medical appointments: Facilitating interdisciplinary care for midlife women. J Womens Health (Larchmt). 2005;14(9):867–​870. doi:10.1089/​jwh.2005.14.867.

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6. Dosaj A, Thiyagarajan D, Ter Haar C, et al. Rapid implementation of telehealth services during the COVID-​19 pandemic. Telemed J E Health. 2021;27(2):116–​120. doi:10.1089/​tmj.2020.0219. 7. McCauley JL, Swartz AE. Reframing telehealth: Regulation, licensing, and reimbursement in connected care. Obstet Gynecol Clin North Am. 2020;47(2):227–​239. doi:10.1016/​j.ogc.2020.02.001. 8. Kichloo A, Albosta M, Dettloff K, et al. Telemedicine, the current COVID-​19 pandemic and the future: A narrative review and perspectives moving forward in the USA. Fam Med Com Health. 2020;8:530. doi:10.1136/​fmch-​2020-​000530. 9. Implementing telehealth in practice: ACOG Committee opinion summary, number 798. Obstet Gynecol. 2020;135(2):493–​494. doi: 10.1097/​AOG.0000000000003672. 10. American Medical Association. AMA Digital Health Care 2016 & 2019 Study findings. www.ama-​assn.org/​system/​files/​2020-​02/​ama-​digital-​health-​study.pdf (2020). 11. American College of Physicians (ACP). 2020 ACP member survey about telehealth implementation. 2020. www.acponline.org/​system/​files/​documents/​practice-​res ources/​health-​information-​technology/​telehealth/​acp-​telehealth-​survey-​results-​2020-​ march.pdf. 12. American College of Obstetricians and Gynecologists. COVID-​ 19 FAQs for obstetricians-​gynecologists, obstetrics. Washington, DC: ACOG; 2020. www.acog. org/​clinical-​information/​physician-​faqs/​covid-​19-​faqs-​for-​ob-​gyns-​obstetrics. 13. Thompson TA, Sonalkar S, Butler JL, Grossman D. Telemedicine for family planning: A scoping review. Obstet Gynecol Clin North Am. 2020;47(2):287–​316. doi:10.1016/​j.ogc.2020.02.004. 14. Worley LLM, Wise-​Ehlers A. Telepsychiatry in obstetrics. Obstet Gynecol Clin North Am. 2020;47(2):333–​340. doi:10.1016/​j.ogc.2020.02.009. 15. Hoppe KK, Thomas N, Zernick M, et al. Telehealth with remote blood pressure monitoring compared with standard care for postpartum hypertension. Am J Obstet Gynecol. 2020;223(4):585–​588. doi:10.1016/​j.ajog.2020.05.027. 16. DeNicola N, Grossman D, Marko K, et al. Telehealth Interventions to improve obstetric and gynecologic health outcomes: A systematic review. Obstet Gynecol. 2020;135(2):371–​382. doi:10.1097/​AOG.0000000000003646. 17. Jensen LL, Drozek DS, Grega ML, Gobble J. Lifestyle medicine: Successful reimbursement methods and practice models. Am J Lifestyle Med. 2019;13(3):246–​252. doi:10.1177/​1559827618817294. 18. Viner N, Powell P, Green R. Institutionalized biases in the award of research grants: A preliminary analysis revisiting the principle of accumulative advantage. Research Policy. 2004;33(3):443–​454. doi:10.1016/​j.respol.2003.09.005. 19. Fronstin P, Dretzka E. Consumer Engagement in Health Care Among Millennials, BabyBoomers, and Generation X: Findings from the 2017 Consumer Engagement in Health Care Survey. 2018. EBRI Issue Brief, No. 444. doi: 10.2139/​ssrn.3160059. 20. Gulati M, Delaney M. The lifestyle medicine physician’s case to self-​ insured employers: A business model for physicians, a bargain for companies. Am J Lifestyle Med. 2019;13(5):462–​469. doi:10.1177/​1559827619843882. 21. Braman M, Edison M. How to create a successful lifestyle medicine practice. Am J Lifestyle Med. 2017;11(5):404–​407. doi:10.1177/​1559827617696296. 22. Henley DE. Coding better for better reimbursement. Fam Pract Manag. Published online January 2003:29–​35. www.aafp.org/​fpm/​2003/​0100/​p29.html. 23. Hughes C. Getting paid for screening and assessment services. Fam Pract Manag. 2017;24(6):25–​29. www.aafp.org/​fpm/​2017/​1100/​p25.html.

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24. Ethilon. 2020 Obesity Counseling Reimbursement Fact Sheet; 2020. www.jnjmedi caldevices.com/​sites/​default/​files/​2020-​Obesity-​Counseling-​Reimbursement-​Fact-​ Sheet-​045443-​191120.pdf. 25. Pershing Yoakley and Associates. Providing and Billing Medicare for Remote Patient Monitoring and Treatment Management; 2021. www.pyapc.com/​wp-​content/​uploa ds/​2021/​01/​Providing-​and-​Billing-​Medicare-​for-​RPM-​and-​Treatment-​Management-​ PYA_​01-​08-​21.pdf. 26. Rowe K, Rowe W, Umbehr J, Dong F, Ablah E. Direct Primary Care in 2015: A survey with selected comparisons to 2005 survey data. Kans J Med. 2017;10(1):3–​6. doi: 10.17161/​kjm.v10i1.8640. 27. Wright AA, Katz IT. Beyond burnout —​Redesigning care to restore meaning and sanity for physicians. New Engl J Med. 2018;378(4):309–​311. doi:10.1056/​ nejmp1716845 28. Wang, K.C. Standard lexicons, coding systems and ontologies for interoperability and semantic computation in imaging. J Digit Imaging. 2018;31:353–​360. https://​doi.org/​ 10.1007/​s10278-​018-​0069-​8.

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Adverse Childhood Events and Trauma-​ Informed Care Robin Ortiz, MD

National Clinician Scholars Program University of Pennsylvania, Children’s Hospital of Philadelphia Philadelphia, PA 8.1 Introduction....................................................................................................155 8.1.1 The Science: Allostasis in Women’s Health.......................................156 8.2 Clinical Presentations: Aces and Trauma in Women’s Health.......................157 8.2.1 ACEs and Women’s General, Mental, and Physical Health...............157 8.2.2 ACEs and Traumatic Experiences in the Pre-​and Perinatal Period..... 157 8.2.3 ACEs and Women’s Lifestyle Pillars.................................................158 8.3 Aces and Trauma Intervention and Response................................................158 8.3.1 Clinical Considerations for Therapy and Intervention Support.........158 8.3.2 Responding with Resilience in Individuals and Communities...........159

KEY POINTS • Adverse childhood experiences (ACEs) such as abuse and household dysfunction in early life predispose to toxic stress that may lead to long-​term impacts on women’s health if not recognized and buffered, particularly in building resilience through social emotional well-​being and healthy relationships. • Given the widespread prevalence of stress, trauma, and ACEs, trauma-​informed care should be practiced universally and it begins with recognition of the clinical implications of adversity in general women’s health practice, pre-​and perinatal health, and the pillars of Lifestyle Medicine. • Screening for ACEs can be helpful to identify risk factors for patients who may experience the effects of toxic stress if done with a trauma-​informed approach including provider training, methods to resist re-​traumatization and promote resilience, and supportive resources.

8.1  INTRODUCTION In 1998, Kaiser Permanente and the Centers for Disease Control surveyed over 17,000 Americans on their exposure to adverse childhood experiences (ACEs), including DOI: 10.1201/9781003110682-9

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physical, sexual, and emotional abuse, physical and emotional neglect, living with someone with mental illness or substance use, witnessing violence to their mother, or being separated from a parent.1 In this study, it was demonstrated that not only was exposure to these experiences common across all socioeconomic domains and races, but those who had experienced more ACEs had a greater likelihood of adult diseases, including heart disease, diabetes, stroke, and cancer –​the leading causes of death in the United States. What’s more? Twice as many women as men reported exposure to four or more of these experiences. ACEs continue to be studied since the original work of Felitti and colleagues, including work that shows the risk of early mortality.2 In some cases, exposure to such traumatic and stressful experiences may cause individuals to acquire symptoms of post-​traumatic stress disorder (PTSD), such as avoidance of stimuli associated with the trauma, easy startle response, recurrent intrusive thoughts, or traumatic nightmares.3 However, this is not necessarily always the case. To understand how ACEs, stress, and trauma impact women’s health and behaviors, important terms are defined and considerations for screening for ACES and resilience are explored in supplementary materials. Given that stress is a much more generalized experience, common to all humans, but is a response that can be formulated after the exposure to ACEs or traumatic experiences, we will focus our discussion on ACEs and trauma and revisit stress in the context of its management when we close our chapter in understanding how to foster resilience across the life course.

8.1.1 The Science: Allostasis in Women’s Health It is commonly known that chronic stress may impact women’s health. For example, it is often cited that stress can be a cause of dysregulation of the menstrual cycle.4 However, the impacts on normal balance in the body, or homeostasis, go well beyond menstruation. Women may have a lower cortisol levels, possibly a flattened cortisol diurnal rhythm, in response to acute stress.5 This dysregulation of the hypothalamic–​ pituitary–​adrenal system associated with chronic stress may get under the skin, literally. Epigenetic changes, or modifications to genes that may alter genetic expression, can be seen as at the site of a chaperone to the glucocorticoid –​or stress molecule –​receptor gene, FKBP5, which is associated with bedtime cortisol in women, but not in men.6 Epigenetic modification through methylation of FKBP5 has been associated with a history of trauma and also the risk of cardiovascular disease (CVD) in people with diabetes.7 This has led to the hypothesis that the association between stress and diseases of lifestyle may be underpinned by allostatic load and epigenetic alterations, a hypothesis that is still up for debate by scientists. For example, cortisol dysregulation in women with chronic pelvic pain and endometriosis may differ by race.8 Importantly, in spite of the fact that the relationship between stress and cortisol alone is complicated and may not support the allostatic load hypothesis directly, cortisol dysregulation is buffered by long-​term physical activity and enriching social environments.9 Although underpinning mechanisms are still to be elucidated, it is clear that stress and trauma directly impact clinical presentations of women’s health.

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8.2  CLINICAL PRESENTATIONS: ACES AND TRAUMA IN WOMEN’S HEALTH 8.2.1 ACEs and Women’s General, Mental, and Physical Health ACEs have been associated with increased medical utility, generalized medical presentations from common ailments, and conditions requiring surgical intervention. For example, one study demonstrated that common conditions seen in women in primary care, such as back pain, headaches, and fatigue, were associated with a history of child physical or sexual abuse.10 It has also been demonstrated that ACEs are associated with overall level of disability in women.11 In women with chronic pain from fibromyalgia, those with a history of abuse in childhood were more likely to have decreased pain threshold and more diffuse pain than those even with a history of abuse in adulthood.12 ACEs impact women’s mental health when combined with other comorbid conditions. Specifically, in women with polycystic ovarian syndrome, those with ACEs are more likely to have a psychiatric comorbidity,13,14 and in 174 incarcerated women in Spain, those with ACEs were more likely to have depression, anxiety, and stress burden compared to colleagues without ACEs.15 Importantly, women with ACEs may require more frequent or severe intervention. For example, of women presenting to sexually transmitted disease screening and testing clinics, 241 black women who had experienced abuse (emotional, physician, or sexual) or had witnessed their own mother’s abuse had earlier age of sexual initiation, more commonly associated with coercion.16 Women with ACEs are also more likely to undergo oophorectomy for a non-​cancer, non-​ovarian indication in women of young age (less than 40 years of age).17 These studies and others in women’s health have led clinicians to call on primary care and women’s health to be more trauma-​informed in practice, as supported by the views of women with ACEs themselves who felt their history of ACEs was important to their health.18

8.2.2 ACEs and Traumatic Experiences in the Pre-​and Perinatal Period Often, the practice of women’s health is intergenerational. Much research has demonstrated that ACEs are just as intergenerational in their impacts on biology and health. In a study of parents and adult offspring, parent (73% mother) survivors of the Holocaust and offspring had correlated levels of epigenetic FKBP5 modification, whereas parent and offspring controls did not have such modifications.19 Using data from over 3,000 women in the National Longitudinal Study of Youth, it was found that ACEs predicted earlier age at first birth, which partially mediated later mid-​ life health.20 Furthermore, women who enter pregnancy with a history of childhood abuse are more likely to have comorbid chronic disease and those with either abuse or household dysfunction in childhood carry a greater risk of psychosocial difficulty throughout pregnancy.21 Childhood experiences also impact prenatal pain intensity and distribution.22 In women with prenatal depression, those with ACEs were also more likely to have gestational diabetes.23 The impacts of ACEs carry past prenatal environments into birth outcomes. Women with at least three ACEs were found more likely to experience miscarriages, with a

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relative risk ratio of 2 for a single miscarriage and 3 for recurrent miscarriages in their lifetime even after adjustment for birth cohort, age at menarche, and childhood socioeconomic status.24 In a study of birth outcomes in 1,848 low-​income women, ACEs were associated with significantly increased odds of having a pregnancy loss, preterm birth, or infant of low birth weight (odds ratio [OR] 1.03–​1.08). Speaking about the equally detrimental impacts of expanded ACEs, immigration stress such as from Immigration and Customs Enforcement (ICE) raids (as in Postville, Iowa, in 2009), the passage of anti-​immigrant laws (as in Arizona in 2010), and federal anti-​ immigrant rhetoric (nationally after 2016) have each been associated with preterm or low birth weight outcomes for immigrant and often Latina non-​immigrant women,25-​27 which demonstrates the potential longitudinal and intergenerational impacts of adversity through its impact on women’s health. The children of women with ACEs are also more likely to have health impacts of those intergenerational experiences. For women followed longitudinally, those with ACEs not only had greater perinatal anxiety, depression, and symptoms of PTSD, but their children were also more likely to have externalizing problems in early life.28,29 Children with maternal history of ACEs have greater risk of developmental delay before age 2 (relative risk 1.18) and later childhood behavioral problems including hyperactivity and emotional disturbance, in a dose-​dependent relationship.30,31

8.2.3 ACEs and Women’s Lifestyle Pillars A large reason to understand the impacts is so that intervention including lifestyle modification can impact their long-​term outcomes. Before one can intervene with lifestyle, it is important to recognize that not only women’s health problems but also their lifestyle pillars are impacted by ACEs. A list of examples (isolated examples, not meant to be all inclusive or a near-​exhaustive review) is presented in Table 8.1. Obesity and CVD are conditions particularly associated with lack of attainments of all lifestyle pillars, which may be mediated by ACEs exposure. Obesity is associated with a history of ACEs, importantly independent of socioeconomic or income status, including for pre-​pregnancy obesity.42,43 While those with flattened cortisol curve associated with stress and depression may be at risk of diabetes and CVD, the CVD risk in diabetics is associated with stress pathway epigenetic modification that may be mitigated by exercise.7,44

8.3  ACES AND TRAUMA INTERVENTION AND RESPONSE 8.3.1 Clinical Considerations for Therapy and Intervention Support Trauma and ACEs are best addressed through a multidisciplinary care approach. Importantly, if evidence of trauma symptoms3 is identified at any age, the first-​line intervention should be a referral for trauma-​informed cognitive behavioral therapy (CBT).45 Clinicians may identify individuals in need of therapy with or without active symptoms in many ways. For example, women with many (e.g., four or more) ACEs by history, positive symptoms of PTSD, or exposure to intimate partner violence (IPV) may each serve as reasons to refer to trauma-​informed CBT. Reasons to refer

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TABLE 8.1 ACEs Exposure Is Associated with Women’s Lifestyle Pillars Pillar Healthy eating

Impact

Differential gut microbiome, though those who ate omega-​3 PUFAs had a buffer to inflammatory IL-​6 response to stress despite prior ACEs exposure history. Physical activity Muscle weakness not compensated by the adoption of healthy behaviors in adulthood. Sleep Childhood sexual abuse impacts sleep disturbances 10 years later in adult women. Stress management Intergenerational impact of maternal ACEs on child behavior problems is exacerbated by emotional distress and aggravation. Substance use Binge drinking. Relationships High ACEs burden is associated with intimate partner violence (IPV) in general and IPV victimization severity and both depression and posttraumatic symptoms; relationship quality in racially diverse couples mediated the association between ACEs and health later in life; mothers feel that school and social relation building mitigates their child’s consequences of exposure to immigration trauma

Reference Hantsoo32

Cheval33 Kajeepeta34 Schickedanz31

Timko35 Willie36 Jones37 Cannon38 Li39 Wheeler40 Perez-​ Aronsson41

may also be disclosed as a part of a history when a provider is aware that commonly presenting conditions in women may be associated with adversity and trauma as this chapter, in part, aims to achieve. For children, the American Academy of Child and Adolescent Psychiatry recommends choosing a therapy type that is trauma-​focused and that includes parent/​caregiver participation.46 Ultimately, recognition of the need to refer for support and the type of intervention are at the discretion of the provider and one should always seek insight from reliable resources or referrals if uncertain in guiding clinical care. Given this topic is beyond the scope of this chapter, more information about symptoms of trauma, post-​traumatic stress disorder, and CBT for children and adults can be found through the American Academy of Pediatrics, the National Child Traumatic Stress Network, and the American Psychological Association.47-​49

8.3.2 Responding with Resilience in Individuals and Communities Resilience is the ability to adapt to change. It is viewed that resilience may buffer against the health outcomes commonly associated with ACEs.50 Resilience can be a quality that can be inherent in personal assets, such as self-​esteem or mindfulness traits, or built through interventions strengthening social-​emotional skills and relationships. Though the most impactful buffer against ACEs and toxic stress is a healthy relationship at any time in one’s life, from early life through young adulthood

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and adult life, as this can mediate poor health including inflammation, adiposity measures, and physical inactivity.51 However, the mastery of stress as can be attained through mindfulness practices, for example, in parenthood can also mediate the association between later trauma exposure (like IPV) and physical health.52,53 Now armed with this understanding we can start with simply asking patients what happened to them rather than insinuating that something is wrong with them followed by supporting them to identify how they can put space and time between their experience of stress and trauma and its possible effects (Figures 8.1 and 8.2). These types of identifiers can then be intervened on with the best chance of success when there is stakeholder engagement through family support, such as through involving children and family members in meal preparation, healthy exercise competitions among loved ones, finding time for self or family mindfulness practices, and building environments conscious of sleep hygiene. The key to allowing any solutions to be readily available equitably to all individuals and groups is to create resilient communities, which must be done together through policy, practice, and procedures.55,56 Examples of improving women’s health include home visiting to pregnant women and families with newborns, parenting training programs in mindfulness and positive parenting, IPV prevention, teen pregnancy prevention programs, mental illness and substance abuse treatment, high-​quality childcare programs, and sufficient income support for lower income families.55 Community resilience is the key to build up resilience, foster healthy lifestyles, and combat the epidemic of mortality in the United States. Perhaps with understanding adversity and resilience clinicians will be better able to help patients change and maintain lifestyle change.

“What happened to you?” Motivational interviewing meets psycho-social determinants of health Smoking cessation

May identify environmentally induced stress/trauma triggers

Adherence to a plant-based diet

May identify underpinnings of unhealthy food choices (e.g. unaddressed emotions or childhood beliefs about body image)

Increasing activity and exercise

May identify environmental barriers (e.g. lack of safety exercising outdoors or lack of social support)

FIGURE 8.1  Clinical applications of a trauma-​informed approach in Lifestyle Medicine. Examples of the use of motivational interviewing with a trauma-​informed approach. Asking the historical context literally or metaphorically through the applications of considering what might have happened to a client or patient may contextualize what psychosocial determinants of health predispose an individual to certain behaviors or lifestyle change choices and may help address barriers or inform interventions toward a patient-​centered outcome. (Reprinted with permission from: Ortiz, R. 2019. Building resilience against the sequelae of adverse childhood experiences, American Journal of Lifestyle Medicine. 13(5):470–​479.)

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Adverse Childhood Events EVENT  EXPERIENCE  EFFECT

EXPERIENCE Environment

Self Self + Environment

Pause

EVENT Space

Pause

EFFECT Time

Resilience: Effect ≠ Adverse

FIGURE 8.2  Clinical applications of a trauma-​informed approach in Lifestyle Medicine. Interrupting the toxic stress response. Building self-​resilience through mindfulness or cognitive behavioral approaches may allow the reprogramming of one’s stress response such that when a potentially stressful experience provoking event occurs, a space or pause can be taken that may push time and a buffer (orange triangle) between the self and environment to prevent the effect from being lasting or detrimental to health on long term. (Adapted with modifications from Ortiz 2019 AJLM.54 (Reprinted with permission from: Ortiz, R. 2019. Building Resilience Against the Sequelae of Adverse Childhood Experiences, American Journal of Lifestyle Medicine. 13(5): 470–​479.)

CONFLICT OF INTEREST Dr. Robin Ortiz reported receiving personal fees for her consulting work with the Aurrera Health Group on the ACEs Aware Initiative.

REFERENCES 1. Felitti VJ, Anda RF, Nordenberg D, et al. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. The Adverse Childhood Experiences (ACE) Study. Am J Prev Med. 1998;14(4):245–​258. DOI: 10.1016/​s0749-​3797(98)00017-​8. 2. Brown DW, Anda RF, Tiemeier H, et al. Adverse childhood experiences and the risk of premature mortality. Am J Prev Med. 2009;37(5):389–​396.DOI: 10.1016/​ j.amepre.2009.06.021. 3. Valentino K, Berkowitz S, Stover CS. Parenting behaviors and posttraumatic symptoms in relation to children’s symptomatology following a traumatic event. J Trauma Stress. 2010;23(3):403–​407. DOI: 10.1002/​jts.20525. 4. Nagma S, Kapoor G, Bharti R, et al. To evaluate the effect of perceived stress on menstrual function. J Clin Diagn Res. 2015;9(3):QC01–​03. DOI: 10.7860/​JCDR/​2015/​ 6906.5611. 5. Liu JJW, Ein N, Peck K, Huang V, Pruessner JC, Vickers K. Sex differences in salivary cortisol reactivity to the Trier Social Stress Test (TSST): A meta-​analysis. Psychoneuroendocrinology. 2017;82:26–​37. DOI: 10.1016/​j.psyneuen.2017.04.007. 6. Lee RS, Mahon PB, Zandi PP, et al. DNA methylation and sex-​specific expression of FKBP5 as correlates of one-​month bedtime cortisol levels in healthy individuals. Psychoneuroendocrinology. 2018;97:164–​173. DOI: 10.1016/​j.psyneuen.2018.07.003.

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7. Ortiz R, Joseph JJ, Lee R, Wand GS, Golden SH. Type 2 diabetes and cardiometabolic risk may be associated with increase in DNA methylation of FKBP5. Clin Epigenetics. 2018;10:82. DOI: 10.1186/​s13148-​018-​0513-​0. 8. Ortiz R, Gemmill JAL, Sinaii N, et al. Hypothalamic-​ pituitary-​ adrenal axis responses in women with endometriosis-​related chronic pelvic pain. Reprod Sci. 2020;27(10):1839–​1847. DOI: 10.1007/​s43032-​020-​00201-​x. 9. Strahler J, Berndt C, Kirschbaum C, Rohleder N. Aging diurnal rhythms and chronic stress: Distinct alteration of diurnal rhythmicity of salivary alpha-​amylase and cortisol. Biol Psychol. 2010;84(2):248–​256. DOI: 10.1016/​j.biopsycho.2010.01.019. 10. McCauley J, Kern DE, Kolodner K, et al. Clinical characteristics of women with a history of childhood abuse: Unhealed wounds. JAMA. 1997;277(17):1362–​1368. 11. Tay CT, Teede HJ, Loxton D, Kulkarni J, Joham AE. Psychiatric comorbidities and adverse childhood experiences in women with self-​reported polycystic ovary syndrome: An Australian population-​ based study. Psychoneuroendocrinology. 2020;116:104678. DOI: 10.1016/​j.psyneuen.2020.104678. 12. Ortiz R, Ballard ED, Machado-​Vieira R, Saligan LN, Walitt B. Quantifying the influence of child abuse history on the cardinal symptoms of fibromyalgia. Clin Exp Rheumatol. 2016;34(2 Suppl 96):S59–​S66. 13. Tonmyr L, Jamieson E, Mery LS, MacMillan HL. The relation between childhood adverse experiences and disability due to mental health problems in a community sample of women. Can J Psychiatry. 2005;50(12):778–​ 783. DOI: 10.1177/​ 070674370505001207. 14. Tonmyr L, Jamieson E, Mery LS, MacMillan HL. The relationship between childhood adverse experiences and disability due to physical health problems in a community sample of women. Women Health. 2005;41(4):23–​35. DOI: 10.1300/​ J013v41n04_​02. 15. Caravaca-​ Sanchez F, Fearn NE, Vidovic KR, Vaughn MG. Female prisoners in Spain: Adverse childhood experiences, negative emotional states, and social support. Health Soc Work. 2019;44(3):157–​166. DOI: 10.1093/​hsw/​hlz013. 16. Tsuyuki K, Al-​ Alusi NA, Campbell JC, et al. Adverse childhood experiences (ACEs) are associated with forced and very early sexual initiation among Black women accessing publicly funded STD clinics in Baltimore, MD. PLoS One. 2019;14(5):e0216279. DOI: 10.1371/​journal.pone.0216279. 17. Rocca WA, Gazzuola Rocca L, Smith CY, et al. Bilateral oophorectomy and accelerated aging: Cause or effect? J Gerontol A Biol Sci Med Sci. 2017;72(9):1213–​ 1217. DOI: 10.1093/​gerona/​glx026. 18. Purkey E, Patel R, Beckett T, Mathieu F. Primary care experiences of women with a history of childhood trauma and chronic disease: Trauma-​informed care approach. Can Fam Physician. 2018;64(3):204–​211. 19. Yehuda R, Daskalakis NP, Bierer LM, et al. Holocaust exposure induced intergenerational effects on FKBP5 methylation. Biol Psychiatry. 2016;80(5):372–​ 380. DOI: 10.1016/​j.biopsych.2015.08.005. 20. Williams K, Finch BK. Adverse childhood experiences, early and nonmarital fertility, and women’s health at midlife. J Health Soc Behav. 2019;60(3):309–​325. DOI: 10.1177/​0022146519868842. 21. Racine N, Madigan S, Plamondon A, Hetherington E, McDonald S, Tough S. Maternal adverse childhood experiences and antepartum risks: The moderating role of social support. Arch Womens Ment Health. 2018;21(6):663–​670. DOI: 10.1007/​ s00737-​018-​0826-​1.

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22. Drevin J, Stern J, Annerback EM, et al. Adverse childhood experiences influence development of pain during pregnancy. Acta Obstet Gynecol Scand. 2015;94(8):840–​ 846. DOI: 10.1111/​aogs.12674. 23. Schoenaker D, Callaway LK, Mishra GD. The role of childhood adversity in the development of gestational diabetes. Am J Prev Med. 2019;57(3):302–​310. DOI: 10.1016/​ j.amepre.2019.04.028. 24. Demakakos P, Linara-​Demakakou E, Mishra GD. Adverse childhood experiences are associated with increased risk of miscarriage in a national population-​based cohort study in England. Hum Reprod. 2020;35(6):1451–​ 1460. DOI: 10.1093/​ humrep/​ deaa113. 25. Novak NL, Geronimus AT, Martinez-​Cardoso AM. Change in birth outcomes among infants born to Latina mothers after a major immigration raid. Int J Epidemiol. 2017;46(3):839–​849. DOI: 10.1093/​ije/​dyw346. 26. Torche F, Sirois C. Restrictive immigration law and birth outcomes of immigrant women. Am J Epidemiol. 2019;188(1):24–​33. DOI:10.1093/​aje/​kwy218. 27. Gemmill A, Catalano R, Casey JA, et al. Association of preterm births among US Latina women with the 2016 presidential election. JAMA Netw Open. 2019;2(7):e197084. DOI:10.1001/​jamanetworkopen.2019.7084. 28. Atzl VM, Narayan AJ, Rivera LM, Lieberman AF. Adverse childhood experiences and prenatal mental health: Type of ACEs and age of maltreatment onset. J Fam Psychol. 2019;33(3):304–​314. DOI: 10.1037/​fam0000510. 29. Letourneau N, Dewey D, Kaplan BJ, et al. Intergenerational transmission of adverse childhood experiences via maternal depression and anxiety and moderation by child sex. J Dev Orig Health Dis. 2019;10(1):88–​99. DOI: 10.1017/​S2040174418000648. 30. Folger AT, Eismann EA, Stephenson NB, et al. Parental adverse childhood experiences and offspring development at 2 years of age. Pediatrics. 2018;141(4). DOI: 10.1542/​ peds.2017-​2826. 31. Schickedanz A, Halfon N, Sastry N, Chung PJ. Parents’ adverse childhood experiences and their children’s behavioral health problems. Pediatrics. 2018;142(2). DOI: 10.1542/​peds.2018-​0023. 32. Hantsoo L, Jasarevic E, Criniti S, et al. Childhood adversity impact on gut microbiota and inflammatory response to stress during pregnancy. Brain Behav Immun. 2019;75:240–​250. DOI:10.1016/​j.bbi.2018.11.005. 33. Cheval B, Chabert C, Sieber S, et al. Association between adverse childhood experiences and muscle strength in older age. Gerontology. 2019;65(5):474–​484. DOI: 10.1159/​000494972. 34. Kajeepeta S, Gelaye B, Jackson CL, Williams MA. Adverse childhood experiences are associated with adult sleep disorders: A systematic review. Sleep Med. 2015;16(3):320–​ 330. DOI:10.1016/​j.sleep.2014.12.013. 35. Timko C, Sutkowi A, Pavao J, Kimerling R. Women’s childhood and adult adverse experiences, mental health, and binge drinking: The California Women’s Health Survey. Subst Abuse Treat Prev Policy. 2008;3 :15. DOI: 10.1186/​1747-​597X-​3-​15. 36. Willie TC, Kershaw T, Sullivan TP. The impact of adverse childhood events on the sexual and mental health of women experiencing intimate partner violence. J Interpers Violence. 2018:886260518802852. DOI: 10.1177/​0886260518802852. 37. Jones MS, Burge SW, Sharp SF, McLeod DA. Childhood adversity, mental health, and the perpetration of physical violence in the adult intimate relationships of women prisoners: A life course approach. Child Abuse Negl. 2020;101:104237. DOI: 10.1016/​ j.chiabu.2019.104237.

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38. Cannon EA, Bonomi AE, Anderson ML, Rivara FP, Thompson RS. Adult health and relationship outcomes among women with abuse experiences during childhood. Violence Vict. 2010;25(3):291–​305. DOI: 10.1891/​0886-​6708.25.3.291. 39. Li Y, Herbell K, Bloom T, Sharps P, Bullock LFC. Adverse childhood experiences and mental health among women experiencing intimate partner violence. Issues Ment Health Nurs. 2020;41(9):785–​791. DOI: 10.1080/​01612840.2020.1731636. 40. Wheeler NJ, Barden SM, Daire AP. Mediation of childhood adversity and health by relationship quality in diverse couples. Fam Process. 2020;59(3):1243–​1260. DOI:10.1111/​famp.12467. 41. Perez-​Aronsson A, Warner G, Sarkadi A, Osman F. “I’m a mother who always tries to give my children hope”-​Refugee women’s experiences of their children’s mental health. Front Psychiatry. 2019;10:789. DOI:10.3389/​fpsyt.2019.00789. 42. Foster BA, Weinstein K. moderating effects of components of resilience on obesity across income strata in the national survey of children’s health. Acad Pediatr. 2019;19(1):58–​66. DOI:10.1016/​j.acap.2018.08.012. 43. Hollingsworth K, Callaway L, Duhig M, Matheson S, Scott J. The association between maltreatment in childhood and pre-​pregnancy obesity in women attending an antenatal clinic in Australia. PLoS One. 2012;7(12):e51868. DOI:10.1371/​ journal.pone.0051868. 44. Joseph JJ, Golden SH. Cortisol dysregulation: The bidirectional link between stress, depression, and type 2 diabetes mellitus. Ann N Y Acad Sci. 2017;1391(1):20–​34. DOI:10.1111/​nyas.13217. 45. Gartlehner G, Forneris CA, Brownley KA, et al. Interventions for the Prevention of Posttraumatic Stress Disorder (PTSD) in Adults after Exposure to Psychological Trauma. Rockville, MD: Agency for Healthcare Research and Quality (US); April 2013. 46. Schneider SJ, Grilli SF, Schneider JR. Evidence-​based treatments for traumatized children and adolescents. Current Psychiatry Reports. 2013;15(1). DOI:10.1007/​ s11920-​012-​0332-​5. 47. The Medical Home Approach to Identifying and Responding to Exposure to Trauma. American Academy of Pediatrics; 2014. www.aap.org/​en-​us/​documents/​ttb_​ medicalhomeapproach.pdf 48. Posttraumatic Stress Disorder: Cognitive Behavioral Therapy. American Psychological Association. www.apa.org/​ptsd-​guideline/​treatments/​cognitive-​behavioral-​therapy. Published 2020. Accessed December 30, 2020 . 49. Trauma Treatments: Interventions. The National Child Traumatic Stress Network. www.nctsn.org/​treatments-​and-​practices/​trauma-​treatments/​interventions. Published 2020. Accessed December 30, 2020. 50. Traub F, Boynton-​Jarrett R. Modifiable resilience factors to childhood adversity for clinical pediatric practice. Pediatrics. 2017;139(5). DOI:10.1542/​peds.2016-​2569. 51. Yang YC, Boen C, Gerken K, Li T, Schorpp K, Harris KM. Social relationships and physiological determinants of longevity across the human life span. Proc Natl Acad Sci U S A. 2016;113(3):578–​583. DOI:10.1073/​pnas.1511085112. 52. Alvarez C, Perrin N, Lameiras-​ Fernandez M, Rodriguez R, Glass N. Adverse childhood experiences among Latina women and its association with mastery of stress and health. Child Abuse Negl. 2019;93:139–​148. DOI:10.1016/​j.chiabu. 2019.05.004. 53. Ortiz R, Sibinga EM. The role of mindfulness in reducing the adverse effects of childhood stress and trauma. Children (Basel). 2017;4(3). DOI:10.3390/​ children4030016.

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54. Ortiz R. Building resilience against the sequelae of adverse childhood experiences: rise up, change your life, and reform health care. Am J Lifestyle Med. 2019;13(5):470–​479. DOI:10.1177/​1559827619839997. 55. Spotlight: Building Resilient and Trauma-​ Informed Communities –​Introduction. In: Administration SAaMHS, ed. HHS Publication No. (SMA) 17-​5014: Substance Abuse and Mental Health Services Administration; 2017. 56. Administration SAaMHS. SAMHSA’s Concept of Trauma and Guidance for a Trauma-​ Informed Approach. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2014.

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Health Coaching, Motivational Interviewing, and Behavior Change in Women’s Health Mark D. Faries, PhD

Associate Professor and Extension Health Specialist Texas A&M AgriLife Extension ServiceAdjunct Associate Professor Texas A&M School of Public Health College Station, TX

Alyssa Abreu, MS, DrPH

Doctoral Candidate Texas A&M School of Public HealthMedical Student School of Osteopathic Medicine, University of the Incarnate Word College Station, TX

Sarah-​Ann Keyes, MS, PA-​C Assistant Professor School of Health Professions Baylor College of Medicine Houston, TX

Tasnim El Mezain, MS, RDN, NBC-​HWC Health Coach, Centers for Integrative Health University of California San Diego Department of Family Medicine

DOI: 10.1201/9781003110682-10

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Jessica A. Matthews, DBH, MS, NBC-​HWC, DipABLM Associate Professor, Point Loma Nazarene University Director, Integrative Health Coaching, Centers for Integrative Health, Department of Family Medicine, University of California San Diego San Diego, CA

9.1 Introduction....................................................................................................169 9.2 Basic Behavioral Strategies............................................................................169 9.2.1 Medical Triggers................................................................................169 9.2.2 Evidence Review................................................................................170 9.2.3 Motivation Type.................................................................................170 9.2.4 Evidence Review................................................................................171 9.2.5 Self-​Efficacy.......................................................................................171 9.2.6 Evidence Review................................................................................172 9.3 Specific Behavioral Strategies........................................................................172 9.3.1 Pregnancy...........................................................................................172 9.3.2 Menopause.........................................................................................173 9.3.3 Cancer Survivorship...........................................................................173 9.4 Advanced Behavioral Strategies.....................................................................174 9.4.1 Motivational Interviewing..................................................................174 9.4.2 Health and Wellness Coaching...........................................................175 9.4.3 The 5 A’s.............................................................................................176 9.4.4 Referring Patients for Additional Support..........................................177 9.4.5 Team-​Based Approaches....................................................................177 9.4.6 Group Visits........................................................................................177 9.6 Conclusion......................................................................................................178

KEY POINTS • Self-​regulation, defined as the effort to change, alter, or modify one’s own behavior, provides a foundation and framework to build upon with other behavioral strategies for the healthcare provider. • Basic behavioral strategies are those concepts that have an established, evidence base for behavior change in the general patient population, and should be in every healthcare provider’s behavioral toolbox –​including medical triggers, autonomous motivation support, and self-​efficacy. • Specific behavioral strategies are those approaches that are more specific to the individualized barriers and concerns of women’s health, highlighted across pregnancy, menopause, and cancer survivorship. • Advanced behavioral strategies are those that bring a behaviorally focused healthcare approach to another level, including motivational interviewing, health coaching, group visits, and team-​based approaches.

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• Healthcare providers should intentionally consider current phase of life, context, and individual circumstances in the assessment and adaptation of lifestyle prescriptions. • Practical applications for basic, specific, and advanced behavioral strategies are provided in the supplemental material.

9.1  INTRODUCTION The healthcare provider (HCP) has an important and unique role in helping patients toward medication adherence, when lifestyle is the medicine. While the provider–​ patient interaction is a key starting point, the HCP must have a foundation and framework for a growing toolbox of behavior change strategies in women’s health to assist patients in the adoption of lifestyle prescriptions. Self-​regulation provides a solid foundation for the HCP to build upon with other behavioral strategies, and is well suited to be the framework for strategies presented in this chapter. In its most general form, self-​regulation is the effort to change, alter, or modify one’s own behavior.1 For our purposes, self-​regulation is better described as a process of monitoring and changing one’s thoughts, feelings, and behavior to stay in line with a goal or standard, and notably helping patients bridge the intention–​behavior gap.2,3 The more difficult the internal, social, and/​or physical environments are to navigate in order to stay in line with lifestyle prescriptions, the more self-​regulatory capacity and abilities are required, and the higher the probability of self-​regulatory failure. To help, this chapter is organized around basic, specific, and advanced strategies. Basic behavioral strategies are those self-​regulatory concepts that have an established, evidence base for behavior change in the general patient population, and should be in every HCP’s behavioral toolbox. Specific behavioral strategies are those approaches that are more specific to the barriers and concerns that women must navigate, with pertinent examples across pregnancy, menopause, and cancer survivorship. Advanced behavioral strategies are those that bring a behaviorally focused healthcare approach to another level, including motivational interviewing, health coaching, group visits, and team-​based approaches.

9.2  BASIC BEHAVIORAL STRATEGIES 9.2.1 Medical Triggers The process of self-​regulation is theorized to begin when normalcy is interrupted. Normalcy for patients could mean an inactive and stressful lifestyle, with unhealthy diets, and poor sleep quality. The HCP uses diagnoses, screenings, or self-​monitoring tools, such as fitness trackers or dietary logs to interrupt this normalcy, by creating perceived discrepancies from a desired standard. Theoretically speaking, discrepancies from a standard, goal, or value should motivate individuals to reduce the discrepancy –​ideally through healthy behavior choices. More specifically, the feedback processing model of self-​regulation proposes that behavior is part of a feedback loop, in which an input of information relevant to the patient (e.g., blood test results revealing a fasting blood glucose of 125 mg/​dL) allows her to compare that

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information with a standard (e.g., < 100 mg/​dL).4,5 Interacting with an emotional response and presumed motivation, a behavioral output is chosen by the patient to reduce the discrepancy (e.g., eat a healthier diet). After a period of time, input is re-​ compared with the standard, and if a discrepancy persists, then the model of emotion-​ motivation-​behavior loop continues. However, if the discrepancy is reduced (e.g., the patient reaches a fasting blood glucose of 95 mg/​dL), then the motivation either ceases or a new standard is established for the feedback loop to continue. The HCP can be a major influence on this process, providing both the input and the standard, as well as offering a lifestyle prescription to reduce the discrepancy. As a result, health-​related screenings are promoted as a common component of primary and specialized care, hopefully providing motivation for change through lifestyle prescriptions. However, as patient care elucidates, this process is not that simple. The “medical trigger” can help explain the variation in patient emotions, motivation and behavior, provide a foundation for why patient motivation does not always translate into behavior (i.e., the intention–​behavior gap), and guide the HCP on how to proceed when the patient has difficulty adopting the behavioral prescription.

9.2.2 Evidence Review Triggering events have been most commonly and robustly cited in relation to weight loss and control behaviors, especially those related to the diagnosis of risk and health concerns (i.e., medical trigger), improving appearance, and emotional or ongoing discontent.6–​8 In a national weight control registry, over 80% of individuals with long-​term weight loss revealed a medical trigger as the origin of their weight loss commitment.6 Similarly, medical triggers, such as a myocardial infarction, substantially increased smokers’ odds of quitting.9 However, such triggers are complex and do not always produce the productive motivational responses intended with Lifestyle Medicine prescriptions. The perceived discrepancy and associated distress can also lead to behaviors opposing its intent, such as decreased motivation, psychological, social, and behavioral avoidance, denial, hindered emotional regulation, and suppressed eating.5,10–​13 Being weighed or told to lose weight has been reported as reasons for avoiding healthcare, and the perception of being overweight can be a deterrent to health screenings unrelated to body weight, such as cancer screenings.14–​16 Thus, we propose that a “lifestyle medical trigger” is one that emphasizes the vital role of the HCP in being aware of patients’ emotional, motivational, and behavioral responses to health-​related discrepancies, so that individualized attention, counseling, and other behavioral strategies can be employed to maximize positive pursuit of healthy lifestyle prescriptions.

9.2.3 Motivation Type Motivation is commonly conceptualized as a general drive or inclination typically toward achieving a goal or outcome within the foreseeable future. Interestingly, according to self-​determination theory (SDT), the type of motivation a patient has

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could reveal more about future actions than overall motivation.17 The first type is intrinsic motivation, or motivation that comes from within the individual with inherent interest and enjoyment for the behavior. Intrinsic motivation requires little to no self-​ regulation, since the behavior is pursued from the inherent enjoyment that is produced (e.g., reading a good book, watching a favorite television show, going for a walk on a nice day, and eating a favorite dessert). Patients can be intrinsically motivated for both healthy and unhealthy behaviors. Extrinsic motivation indicates that one is motivated for behavior in order to reach a goal, reward, or outcome extrinsic to the behavior itself. It is this type of motivation that HCPs will engage most often with lifestyle prescriptions, such as a patient eating healthier diet for improvements in blood pressure, cholesterol, anxiety/​mood, sleep, or weight control (i.e., extrinsic outcomes). The SDT posits a continuum of more refined subtypes of extrinsic motivation to self-​regulate behavior, which move from “other-​determined” (i.e., “external regulation”) to the most “self-​determined” or autonomous (i.e., “identified regulation” or “integrated regulation”). Other-​determined motivation is based on the achievement of external reward/​goal/​outcome from outside pressure or compliance, and thus can be commonly induced by the HCP. In self-​determined motivation, while one is still in pursuit of an external reward/​goal/​outcome, the pressure or coercion to regulate behavior comes from within, such as that found with achieving personally meaningful goals.

9.2.4 Evidence Review The research into the types of motivation and behavior is robust, with a growing literature in healthy lifestyle behavior. Suffice this brief review to confirm that the research emphasizes that intrinsic motivation and more self-​determined types of motivation are the most positively related with and predictive of behavior –​spanning youth, adults, and older adults. For more formal, systematic reviews on this research, we recommend Teixeira and colleagues and Sheeran and colleagues.18,19 It is important to recognize that not all patients will have the same type of motivation and the same level of autonomous motivation, and motivation is likely to differ based on their readiness for change. For example, a fascinating study examined how motives for exercise change throughout the stages of change.20 In a large group of government employees, the researchers found that inherent enjoyment of exercise (i.e., intrinsic motivation) was the least likely motive for those in precontemplation or contemplation stages, became more of a motive in a stage of preparation for exercise, reduced as a motive in action stages (likely due to negative feelings exercise can produce in new exercisers), and became the main motivator for those in the maintenance stage.

9.2.5 Self-​Efficacy Self-​efficacy is the confidence or judgment of one’s own capabilities to accomplish what one intends, and is commonly divided into preaction/​action, coping, and recovery self-​efficacy.3,21 Preaction or action self-​efficacy is the judgment that an individual has about his/​her ability to perform a specific task, such as achieving recommended physical activity levels, dietary intake, and other lifestyle prescriptions provided by

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the HCP. If high in preaction self-​efficacy, patients imagine success, anticipate potential outcomes of diverse strategies, and are more likely to initiate a new behavior. Coping self-​efficacy is the judgment of one’s ability to cope with external stressors or barriers to continue with the specific task (i.e., maintenance). Recovery self-​efficacy is confidence in the ability to return to act on the task after experiences of failure, lapses, and setbacks.

9.2.6 Evidence Review The higher a patient’s self-​efficacy in a lifestyle activity, the more likely she will intend to perform that activity.21 Similarly, the higher one’s coping and recovery self-​efficacy, the more likely one will be to act on her intentions. Self-​efficacy has been shown to predict physical activity behaviors and healthy eating, and has been associated with increased intention and behavior.22–​26 In one review of psychosocial predictors of fruit and vegetable consumption in adults, self-​efficacy was found to be a stronger predictor of behavior than barriers, intentions, attitudes and beliefs, stages of change, and even autonomous motivation.27 Also, self-​efficacy has been found to be related to or influence progression and regression through the stages of change, across several health behaviors, including smoking cessation, exercise adoption, dietary fat, fruit and vegetable intake, and medication adherence.27–​32

9.3  SPECIFIC BEHAVIORAL STRATEGIES Women experience sizable physiological and psychological transitions throughout the lifespan, including adolescence, adulthood, and the menopausal and postmenopausal period. Women might also experience considerable shifts during pregnancy, and various health threats, such as cancer diagnoses and survivorship. Each transitional phase is unique and is composed of nuanced biopsychosocial specificities with bearings on identity, health, and well-​being. There are unique behavioral challenges and opportunities to provide lifestyle prescriptions and care during each transition, as well as specific behavioral strategies to facilitate more successful self-​regulation of healthy lifestyle changes. Conceptual theories, such as Midlife Women’s Attitudes Toward Physical Activity (MAPA),33 account for a myriad of contextual considerations, including attitudes, background, health status, self-​efficacy, social influence, perceived barriers, and daily life circumstances with respect to lifestyle behaviors. To illustrate this process, we will highlight three lifespan transitions that are representative of unique challenges and opportunities for lifestyle changes, particularly physical activity and healthful dietary patterns: pregnancy, menopause, and cancer survivorship (most commonly, breast cancer).

9.3.1 Pregnancy Pregnancy is a period in the lifespan presenting unique barriers to lifestyle changes and prescriptions. Generally, patients can experience major shifts in physiology and psychology inherent to carrying and bearing a child, alongside mother–​child safety

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concerns, and perceived threats to the safety of the child with healthy lifestyles (e.g., exercising and dietary changes).34–​36 A common theme in the literature is related to pregnancy-​related symptoms, notably variant depending on the stage of pregnancy.37 Concerning physical activity, nausea and vomiting, injury risk, and fatigue as first, second, and third trimester barriers have been reported, respectively.34 Cravings, nausea, vomiting, and lack of knowledge have been cited as significant barriers to healthful dietary patterns during pregnancy.38 Knowledge-​related issues also underpin another thematic barrier identified in the literature, especially with misconceptions about safety of the child with respect to physical activity.37,39 On the other hand, increased awareness of threats to mother and child health might be facilitators of lifestyle changes, and may provide an opportunity for ensuring a positive, flourishing self-​ regulatory experience. In line with autonomy support, additional conducive variables include support from family, partner, and friends, as well as increased knowledge.38

9.3.2 Menopause The menopausal transition is commonly marked by physiological changes with significant impacts on quality of life.40 Unfortunately, these changes also impart increased risks for cardiovascular disease, osteoporosis, cognitive decline, depression, and anxiety –​all of which can be ameliorated and treated with lifestyle changes, including regular physical activity and a healthful dietary pattern.41–​44 Given the comprehensive nature of the changes women experience during menopause, a holistic approach is often recommended for health management in this population that includes access to social and community systems to facilitate and support lifestyle changes.41 For example, the Women in the Southside Health and Fitness (WISHFIT) study demonstrated the importance of lifestyle interventions targeted at individual, social, and community levels.45 More specifically, a health-​oriented social network was proposed to increase contact with women committed to a healthy lifestyle, and a health-​oriented community can be formed with community partners who are educated in the knowledge of menopause and the role of healthy lifestyles. A robust, holistic approach with a strong sense of support and relatedness can help manage a number of self-​reported barriers during this stage of life that could impact the adoption of lifestyle prescriptions. For example, social and familial demands, such as caring for children and aging parents can act as a specific barrier to physical activity.43,46 Reiterating this theme, Segar and colleagues44 reported that the most frequently cited barriers for low physical activity in menopausal women were familial obligations, care taking, and lack of time. Enhancing self-​efficacy has been proposed as a key facilitator against such barriers, where high exercise self-​efficacy can be an especially potent facilitator of physical activity.33,43 Other facilitators of regular physical activity include structure, accountability, and an expectation that physical activity will increase quality of life.44,46

9.3.3 Cancer Survivorship The individualized experience along the continuum from cancer diagnosis to survivorship presents numerous challenges to lifestyle changes, commonly highlighted

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by weight gain and associated distress.5,47–​50 As a result, past research has had difficulty pinning down the leading threats, and subsequently, opportunities for specific behavioral strategies. Perhaps, the most evident and highlighted threats in the literature are related to the physical challenges that are a result of the cancer and its treatment, particularly cancer-​related fatigue (CRF) –​noted to be more disruptive than pain to daily routines.51 Many of the physiological and psychological challenges encountered by breast cancer survivors (BCS) can be treated or prevented with physical activity.52 Importantly, lifestyle changes such as physical activity can alleviate some of the most distressing symptoms reported, including CRF.51 For example, Duijts and colleagues meta-​analytically examined the effectiveness of behavioral techniques and physical exercise on psychosocial functioning (e.g., fatigue) in BCS.53 The effects of behavioral techniques across studies (e.g., cognitive therapy, education, relaxation, counseling, and social support) on fatigue and stress were modest, but stronger for depression and anxiety. However, a significant, moderate effect of physical exercise interventions was observed for fatigue, depression, body image, and health-​related quality of life (HRQoL). Again, we note that individual differences in responses to both behavioral techniques and physical activity were apparent, emphasizing that a “one-​size–​fits-​all” approach in the population is likely to be less effective than an individualized approach. Despite known benefits, the literature unfortunately demonstrates few BCS meet physical activity guidelines (see Chapter 20).54 Perhaps ironically, common barriers cited are fatigue, time, lower physical well-​being, and higher perceived stress –​the same benefits physical activity has been shown to improve.47,51,55 CRF in particular is an often cited issue, and can persist across the continuum of survivorship.9 Enhancing context-​specific self-​efficacy is again proposed as a main behavioral strategy.47,56 Unfortunately, the literature continues to be a bit sparse in identifying specific barriers to healthful dietary patterns regarding BCS, providing an important opportunity for future research.

9.4  ADVANCED BEHAVIORAL STRATEGIES Hopefully, what has become clear thus far is that the successful regulation of the health behavior change journey is an individualized and nonlinear experience influenced by a myriad of factors. As such, it is important for HCPs to be familiar with a variety of more advanced approaches to foster positive and productive partnerships with patients in order to facilitate lasting lifestyle change. This section highlights several evidence-​based, advanced behavioral strategies, each of which can play a valuable role in improving women’s health and well-​being.

9.4.1 Motivational Interviewing Motivational interviewing (MI) is a collaborative communication style utilized to strengthen patients’ motivation and commitment to change.57 This patient-​centered approach requires specific training on core skills and processes to facilitate behavior change. The core skills of MI are open-​ended questions, affirmations, reflections,

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and summaries –​commonly referred to as OARS. By asking patients open-​ended questions, they are encouraged to think openly without persuasion on their genuine answer. Open-​ended questions invite patients to provide thoughtful, narrative like-​ responses, while also maintaining autonomy over the direction of the conversation. Affirmations are statements that accentuate a patient’s strengths, intentions, or efforts. Affirmations also serve as an empathetic approach and encourage more positivity. Reflections convey empathy and interest, letting the patient know that the provider is actively listening and understanding her, while also helping to guide the conversation forward. Summaries provide a recap of what the patient has shared, and can also be utilized to transition from one topic to another within the encounter. MI is particularly effective for patients who are ambivalent about behavior change, in which they express arguments both for and against change (i.e., decisional balance). A critical skill for HCPs to develop is the ability to recognize and effectively respond to sustain talk (e.g., barriers, challenges, and reasons that reflect a desire not to change) and change talk (e.g., motivations, values, and reasons that reflect a desire to change). In doing so, patients are empowered to work through ambivalence, and commit to making a change. For example, for a patient who expresses interest in, and ambivalence toward, adopting healthier eating habits, powerful open-​ ended questions, such as “What are your top three reasons for wanting to eat healthier foods?,” can offer valuable insights into the patient’s unique motivators. Given that it is not uncommon for patients to pair change talk (e.g., “eating healthier gives me more energy”) with sustain talk (e.g., “I don’t have time to cook healthy meals”), it is important for HCPs to recognize that this is not indicative of the patient being difficult or resistant to change, but rather it is a normal aspect of ambivalence. Utilizing reflections –​such as double-​sided reflections (e.g., “You don’t have time to cook healthy meals, and when you eat healthier you feel more energized”) –​can be particularly helpful in eliciting more movement in the direction of change. Research has demonstrated evidence that MI can be more effective than no treatment or traditional advice, and possibly more effective across certain factors than other active treatment among adults for managing chronic diseases and associated risk factors, such as cardiovascular disease, diabetes, hypertension, diet, and physical activity.58,59 However, the effects of MI on patient outcomes can greatly vary due to individual differences, fidelity of MI interventions, HCP competence, training and practice, duration and dose of MI sessions, and high attrition rates that can be common. On the bright side, patient acceptance of MI appears to be very high, thus providing a reasonable approach for the HCP to utilize.

9.4.2 Health and Wellness Coaching Health and wellness coaching empowers patients to develop the knowledge, skills, resources, confidence, and self-​ regulatory abilities to enact and sustain health-​ related behavior changes in order to achieve their self-​determined goals.60–​62 Whether provided in-​person or telephonically, health and wellness coaching has been shown to increase self-​efficacy, improve nutrition behaviors, as well as lower weight, A1c, and blood pressure.62-​65

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The coach role uniquely varies from the professional expert role. An expert approach focuses on what is wrong, and takes the lead in defining the agenda and solving problems –​in which the provider assumes responsibility for the patient’s health and usually works harder than the patient.66 A coach approach, on the other hand, positions the patient as an active partner in their own care, in which the patient is empowered to lead the process of change, and to take ownership of their health and well-​being. A coach recognizes that patients not only have the capacity for change, but also possess valuable insights into their own lives. Furthermore, effective coaching employs positive psychology principles, such as concentrating on what is going right, being optimistic, and practicing gratitude. By establishing growth-​promoting relationships with patients in which they feel supported and empowered to recognize and leverage their strengths, patients can begin to foster possibilities and initiate actions toward further self-​regulatory abilities that support meaningful changes and improved health outcomes.66

9.4.3 The 5 A’s A practical framework HCPs can utilize in a coaching role is known as the 5A’s –​assess, advise, agree, assist, and arrange. Adapted from tobacco cessation interventions in clinical practice, this brief, patient-​centered approach to health behavior counseling shown in Figure 9.1 can be used as a framework to help increase patient motivation and influence mediators of behavioral change. It is noted in the literature, particularly

Refer to exercise specialist or health and wellness coach for additional support

1. Assess

Evaluate current behavior, beliefs and readiness to change

5. Arrange Schedule follow up appointment and refer to relevant professionals, as appropriate

Provide relevant handouts along with printed exercise prescription

2. Advise

5 A's

4. Assist

Address barriers, discuss self monitoring strategies and suppor twith

"What does beina active look like to you?"

Provide pertinent information with patient’s permission

3. Agree "What type of activities do you enjoy doing?"

"Would it be okay if we talked about your current level of physical activity?"

Co-create change plan in alignment with patient needs and preferences

FIGURE 9.1  Applying the 5A’s behavioral counseling framework to address physical activity. (Created from Whitlock EP, Orleans CT, Pender N, Allan J. Evaluating primary care behavioral counseling interventions: An evidence-​based approach. Am J Prev Med. 2002;22(4):267–​284.)

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with weight control from primary care, that HCPs most frequently will advise and assess, but more rarely agree, assist, or arrange.67 Yet, patients seem to desire the assist and arrange aspects the most. These limitations have provided challenges in the limited, longitudinal evidential support for the 5A’s approach, and highlight the need for the HCP wanting to use this approach to follow through with all five steps to optimize effectiveness and meeting patient needs. An example of how a provider can apply the 5A’s in practice in addressing physical activity is included in the online supplemental materials.

9.4.4 Referring Patients for Additional Support While it is of value for providers to utilize a coach approach, given the time constraints placed on patient visits and the need to address multiple agenda items within a limited timeframe, healthcare systems and practices should also consider integrating qualified health and wellness coaches given their unique ability to provide guidance for lifelong positive behavior changes.68 The National Board for Health and Wellness Coaching (NBHWC) in partnership with the National Board of Medical Examiners (NBME) provides national board certification for health and wellness coaches in addition to establishing and maintaining education and training standards to ensure high-​ quality patient care. NBHWC maintains a directory of national board-​certified health and wellness coaches (NBC-​HWC) to help providers easily identify, collaborate with, and refer to qualified coaches who can provide additional support to patients in the behavior change journey.

9.4.5 Team-​Based Approaches More than 40% of physicians in the United States report feeling burnout,69 a side effect correlated with decreased quality of care, patient satisfaction, productivity, and mental health.70 Multifaceted team-​based interventions in primary care are more impactful in motivating optimal lifestyle behaviors in comparison to isolated specialty care.71 A team-​based approach allows healthcare providers to collaborate in providing specific recommendations and guidance for patients to enact and sustain lifestyle changes. Team members can include, but are not limited to, registered dietitians, psychologists, exercise physiologists, and health coaches,71,72 as well as community partners in public health, community health, fitness, and the local extension service that offer accessible health programming for referral. A team approach to Lifestyle Medicine has shown to improve biomarkers, as well as nutrition and physical activity habits.73

9.4.6 Group Visits Group visits, also known as shared medical appointments, are a collaborative model of care in which providers meet with multiple patients simultaneously for chronic disease management.74,75 Given that group visits are longer in duration –​generally from 60 to 120 minutes –​providers are able to spend more time with patients and

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better understand their needs, while patients are able to build a support system and a sense of relatedness among other individuals who struggle with the same condition.76 Group visits can be cost-​effective and patient compliant in family-​based methods and pediatric interventions, including those focused on childhood obesity.77 In addition, group visits have been shown to improve health behaviors, quality of life, biomarkers, health care costs, and patient–​provider relationship, and increase patient self-​efficacy.74 Group visits are a great opportunity for collaboration between specialized HCPs, as well as to focus on Lifestyle Medicine,73 particularly considering that the modifiable risk factors for chronic diseases include physical inactivity, poor nutrition, smoking, drinking, and obesity.78–​80

9.6  CONCLUSION In healthcare, there have been traditional notions about unmotivated or nonadherent patients, such as they don’t see, they don’t know, they don’t know how, and/​or they don’t care.81 However, Lifestyle Medicine has propelled a change in this culture, since behavior change and adherence is recognized as the cornerstone for the effectiveness of lifestyle prescriptions. Yet, a healthy lifestyle change is complex; sensitive to individual differences; influenced by social, cultural, and physical environments; and difficult for many patients to make necessary changes, even in the presence of sincere intention. HCPs guided by Lifestyle Medicine competencies understand the importance of holistic approaches to guide the patient beyond what to do into why and how to adopt healthy lifestyles. However, this also means HCPs must continue to build a strong foundation of basic, specific, and advanced behavioral strategies. HCPs are encouraged to continue growing a toolbox of behavior change strategies through continuing education, professional development, conferences, and personal pursuits, as well as building a team-​based approach that will allow for a more robust, individualized approach to assessments and adaptations of lifestyle prescriptions to enhance medication adherence when lifestyle is the medicine. For additional reading, see supplementary material including a summary table of basic, specific, and advanced behavior change strategies presented in this chapter to serve as a foundation for the HCP to build upon with other strategies.

REFERENCES 1. Hagger MS. Sleep, self-​ regulation, self-​ control and health. Stress Health. 2010;26(3):181. doi: 10.1002/​smi.1345. 2. de Bruin M, Sheeran P, Kok G, et al. Self-​ regulatory processes mediate the intention-​behavior relation for adherence and exercise behaviors. Health Psychol. 2012;31(6):695. doi: 10.1037/​a0027425. 3. Faries MD, Kephart WC. The Intention–​Behavior gap. Lifestyle Medicine. 2019:241. 4. Carver CS, Scheier MF. On the Self-​Regulation of Behavior. Cambridge University Press; 2001. 5. Faries MD, Bartholomew JB. Coping with weight-​ related discrepancies: Initial development of the WEIGHTCOPE. Womens Health Issues. 2015;25(3):267–​275. doi: 10.1016/​j.whi.2015.02.003.

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6. Gorin AA, Phelan S, Hill JO, Wing RR. Medical triggers are associated with better short-​and long-​term weight loss outcomes. Prev Med. 2004;39(3):612–​616. doi: /​ 10.1016/​j.ypmed.2004.02.026. 7. LaRose JG, Leahey TM, Hill JO, Wing RR. Differences in motivations and weight loss behaviors in young adults and older adults in the national weight control registry. Obesity. 2013;21(3):449–​453. doi: 10.1002/​oby.20053. 8. Wing RR, Phelan S. Long-​ term weight loss maintenance. Am J Clin Nutr. 2005;82(1):222S–​225S. doi: 10.1093/​ajcn/​82.1.222S. 9. Wray LA, Herzog AR, Willis RJ, Wallace RB. The impact of education and heart attack on smoking cessation among middle-​aged adults. J Health Soc Behav. 1998:271–​294. doi: 10.2307/​2676339. 10. Maphis LE, Martz DM, Bergman SS, Curtin LA, Webb RM. Body size dissatisfaction and avoidance behavior: How gender, age, ethnicity, and relative clothing size predict what some won’t try. Body Image. 2013;10(3):361–​368. doi: 10.1016/​ j.bodyim.2013.02.003. 11. Millstein RA, Carlson SA, Fulton JE, et al. Relationships between body size satisfaction and weight control practices among US adults. Medscape J Med 2008;10(5):119. 12. Neumark-​Sztainer D, Wall M, Eisenberg ME, Story M, Hannan PJ. Overweight status and weight control behaviors in adolescents: Longitudinal and secular trends from 1999 to 2004. Prev Med. 2006;43(1):52–​59. doi: 10.1016/​j.ypmed.2006.03.014. 13. Schwartz MB, Brownell KD. Obesity and body image. Body Image. 2004;1(1):43–​56. doi: 10.1016/​S1740-​1445(03)00007-​X. 14. Alegria Drury CA, Louis M. Exploring the association between body weight, stigma of obesity, and health care avoidance. J Am Acad Nurse Pract. 2002;14(12):554–​561. doi: 10.1111/​j.1745-​7599.2002.tb00089.x. 15. Beeken RJ, Wilson R, McDonald L, Wardle J. Body mass index and cancer screening: Findings from the English longitudinal study of ageing. J Med Screen. 2014;21(2):76–​81. doi: 10.1177/​0969141314531409. 16. Wee CC, McCarthy EP, Davis RB, Phillips RS. Screening for cervical and breast cancer: Is obesity an unrecognized barrier to preventive care? Ann Intern Med. 2000;132(9):697–​704. doi: 10.7326/​0003-​4819-​132-​9-​200005020-​00003. 17. Deci EL, Ryan RM. Intrinsic Motivation and Self-​Determination in Human Behavior. New York: New York Academic Press; 1985. 18. Teixeira PJ, Carraça EV, Markland D, Silva MN, Ryan RM. Exercise, physical activity, and self-​determination theory: A systematic review. Int J Behav Nutr Phys Act. 2012;9(1):78. doi: 10.1186/​1479-​5868-​9-​78. 19. Sheeran P, Wright CE, Avishai A, et al. Self-​determination theory interventions for health behavior change: Meta-​analysis and meta-​analytic structural equation modeling of randomized controlled trials. J Consult Clin Psychol. 2020. 20. Ingledew DK, Markland D, Medley AR. Exercise motives and stages of change. J Health Psychol. 1998;3(4):477–​489. doi: 10.1177/​135910539800300403. 21. Schwarzer R. Health action process approach (HAPA). Göttingen: Gesundheits psychologie von A bis Z.Hogrefe. 2002:241–​245. 22. McAuley E, Blissmer B. Self-​efficacy determinants and consequences of physical activity. Exerc Sport Sci Rev. 2000;28(2):85–​88. 23. Barg CJ, Latimer AE, Pomery EA, et al. Examining predictors of physical activity among inactive middle-​aged women: An application of the health action process approach. Psychol Health. 2012;27(7):829–​845. doi: 10.1080/​08870446.2011.609595.

180

180

Mark D. Faries et al.

24. Isa T, Ueda Y, Nakamura R, Misu S, Ono R. Relationship between the intention–​ behavior gap and self-​efficacy for physical activity during childhood. J Child Health Care. 2019;23(1):79–​86. doi: 10.1177/​1367493518777297. 25. Culos-​Reed SN, Brawley LR. Self-​Efficacy predicts physical activity in individuals with fibromyalgia 1. J Appl Biobehav Res. 2003;8(1):27–​41. 26. Dutton GR, Tan F, Provost BC, Sorenson JL, Allen B, Smith D. Relationship between self-​efficacy and physical activity among patients with type 2 diabetes. J Behav Med. 2009;32(3):270–​277. doi: 10.1007/​s10865-​009-​9200-​0. 27. Shaikh AR, Yaroch AL, Nebeling L, Yeh M, Resnicow K. Psychosocial predictors of fruit and vegetable consumption in adults: A review of the literature. Am J Prev Med. 2008;34(6):535–​543. 28. Breaux-​Shropshire TL, Brown KC, Pryor ER, Maples EH. Relationship of blood pressure self-​monitoring, medication adherence, self-​efficacy, stage of change, and blood pressure control among municipal workers with hypertension. Workplace Health Saf. 2012;60(7):303–​311. doi: 10.1177/​216507991206000704. 29. Henry H, Reimer K, Smith C, Reicks M. Associations of decisional balance, processes of change, and self-​efficacy with stages of change for increased fruit and vegetable intake among low-​income, African-​American mothers. J Am Diet Assoc. 2006;106(6):841–​849. 30. Hildebrand DA, Betts NM. Assessment of stage of change, decisional balance, self-​efficacy, and use of processes of change of low-​income parents for increasing servings of fruits and vegetables to preschool-​aged children. J Nutr Educ Behav. 2009;41(2):110–​119. 31. Jones F, Harris P, Waller H, Coggins A. Adherence to an exercise prescription scheme: The role of expectations, self-​efficacy, stage of change and psychological well-​ being. Br J Health Psychol. 2005;10(3):359–​378. doi: 10.1348/​135910704X24798. 32. O’Hea EL, Boudreaux ED, Jeffries SK, Taylor CLC, Scarinci IC, Brantley PJ. Stage of change movement across three health behaviors: The role of self-​efficacy. Am J Health Promot. 2004;19(2):94–​102. doi: 10.4278/​0890-​1171-​19.2.94. 33. Im E, Stuifbergen AK, Walker L. A situation-​specific theory of midlife women’s attitudes toward physical activity (MAPA). Nurs Outlook. 2010;58(1):52–​58. 34. Bennett EV, McEwen CE, Clarke LH, Tamminen KA, Crocker PR. ‘It’s all about modifying your expectations’: Women’s experiences with physical activity during pregnancy. Qual Res Sport Exerc Health. 2013;5(2):267–​ 286. doi: 10.1080/​ 2159676X.2013.766812. 35. Ayyala MS, Coughlin JW, Martin L, et al. Perspectives of pregnant and postpartum women and obstetric providers to promote healthy lifestyle in pregnancy and after delivery: A qualitative in-​depth interview study. BMC Womens Health. 2020;20(1):1–​ 9. doi: 10.1186/​s12905-​020-​0896-​x. 36. Gardner B, Croker H, Barr S, et al. Psychological predictors of dietary intentions in pregnancy. J Hum Nutr Diet. 2012;25(4):345–​ 353. doi: 10.1111/​ j.1365-​277X.2012.01239.x. 37. Coll CV, Domingues MR, Gonçalves H, Bertoldi AD. Perceived barriers to leisure-​ time physical activity during pregnancy: A literature review of quantitative and qualitative evidence. J Sci Med Sport. 2017;20(1):17–​25. 38. Fowles ER, Fowles SL. Healthy eating during pregnancy: Determinants and supportive strategies. J Community Health Nurs. 2008;25(3):138–​152. doi: 10.1080/​ 07370010802221727. 39. Connelly M, Brown H, van der Pligt P, Teychenne M. Modifiable barriers to leisure-​ time physical activity during pregnancy: A qualitative study investigating first time

181

Behavior Change in Women’s Health

181

mother’s views and experiences. BMC Pregnancy Childbirth. 2015;15(1):100. doi: 10.1186/​s12884-​015-​0529-​9. 40. Potter B, Schrager S, Dalby J, Torell E, Hampton A. Primary care—​Clinics in office practice. Menopause. 2018;45(4):625–​641. 41. Zender R, Olshansky E. Promoting wellness in women across the life span. Nursing Clinics. 2009;44(3):281–​291. 42. Manios Y, Moschonis G, Katsaroli I, Grammatikaki E, Tanagra S. Changes in diet quality score, macro-​and micronutrients intake following a nutrition education intervention in postmenopausal women. J Human Nutr Diet. 2007;20(2):126–​131. 43. Barnett F, Spinks WL. Exercise self-​efficacy of postmenopausal women resident in the tropics. Maturitas. 2007;58(1):1–​6. doi: 10.1016/​j.maturitas.2007.04.003. 44. Segar ML, Eccles JS, Richardson CR. Type of physical activity goal influences participation in healthy midlife women. Womens Health Issues. 2008;18(4):281–​291. doi: 10.1016/​j.whi.2008.02.003. 45. Dugan SA, Lange-​Maia B, Karavolos K, et al. Design of a lifestyle intervention to slow menopause-​related progression of intra-​abdominal adipose tissue in women: The women in the Southside Health and Fitness (WISHFIT) study. Contemp Clin Trials Commun. 2016;4:74–​83. doi: 10.1016/​j.conctc.2016.07.002. 46. McArthur D, Dumas A, Woodend K, Beach S, Stacey D. Factors influencing adherence to regular exercise in middle-​aged women: A qualitative study to inform clinical practice. BMC Womens Health. 2014;14(1):49. doi: 10.1186/​1472-​6874-​14-​49. 47. Ventura EE, Ganz PA, Bower JE, et al. Barriers to physical activity and healthy eating in young breast cancer survivors: Modifiable risk factors and associations with body mass index. Breast Cancer Res Treat. 2013;142(2):423–​433. doi: 10.1007/​ s10549-​013-​2749-​x. 48. Ballard-​ Barbash R, Friedenreich CM, Courneya KS, Siddiqi SM, McTiernan A, Alfano CM. Physical activity, biomarkers, and disease outcomes in cancer survivors: A systematic review. J Natl Cancer Inst. 2012;104(11):815–​840. doi: 10.1093/​jnci/​djs207. 49. Rock CL, Doyle C, Demark-​Wahnefried W, et al. Nutrition and physical activity guidelines for cancer survivors. CA Cancer J. 2012;62(4):242–​274. doi: 10.3322/​ caac.21142. 50. Davies NJ, Batehup L, Thomas R. The role of diet and physical activity in breast, colorectal, and prostate cancer survivorship: A review of the literature. Br J Cancer. 2011;105(1):S52–​S73. doi: 10.1038/​bjc.2011.423. 51. Berger AM, Gerber LH, Mayer DK. Cancer-​related fatigue: Implications for breast cancer survivors. Cancer. 2012;118(S8):2261–​2269. doi: 10.1002/​cncr.27475. 52. Schmitz KH, Courneya KS, Matthews C, et al. American College of Sports Medicine roundtable on exercise guidelines for cancer survivors. Med Sci Sports Exerc. 2010;42(7):1409–​1426. doi: 10.1249/​MSS.0b013e3181e0c112. 53. Duijts SF, Faber MM, Oldenburg HS, van Beurden M, Aaronson NK. Effectiveness of behavioral techniques and physical exercise on psychosocial functioning and health-​related quality of life in breast cancer patients and survivors—​A meta-​analysis. Psychooncology. 2011;20(2):115–​126. doi: 10.1002/​pon.1728. 54. Ottenbacher AJ, Day RS, Taylor WC, et al. Exercise among breast and prostate cancer survivors—​what are their barriers? J Cancer Surviv. 2011;5(4):413–​419. doi: 10.1007/​ s11764-​011-​0184-​8. 55. Rogers LQ, Vicari S, Trammell R, et al. Biobehavioral factors mediate exercise effects on fatigue in breast cancer survivors. Med Sci Sports Exerc. 2014;46(6):1077. doi: 0.1249/​MSS.0000000000000210.

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56. Huang F, Yang Q, Wang A, Zhang J. Psychometric properties and performance of existing self-​efficacy instruments in cancer populations: A systematic review. Health Qual Life Outcomes. 2018;16(1):241. doi: 10.1186/​s12955-​018-​1066-​9. 57. Miller WR, Rollnick S. Motivational Interviewing Third Edition: Helping People Change. New York: Guilford. 2013. doi: 10.1017/​CBO9781107415324.004 58. Rollnick S, Miller WR, Butler C. Motivational Interviewing in Health Care: Helping Patients Change Behavior. New York: Guilford Press. 2008. 59. Martins RK, McNeil DW. Review of motivational interviewing in promoting health behaviors. Clin Psychol Rev. 2009;29(4):283–​293. doi: 10.1016/​j.cpr.2009.02.001 60. Bennett HD, Coleman EA, Parry C, Bodenheimer T, Chen EH. Health coaching for patients with chronic illness. Fam Pract Manag. 2010;17(5):24. 61. Wolever RQ, Simmons LA, Sforzo GA, et al. A systematic review of the literature on health and wellness coaching: Defining a key behavioral intervention in healthcare. Glob Adv Health Med. 2013;2(4):38–​57. doi:10.7453/​gahmj.2013.042. 62. Gierisch JM, Hughes JM, Edelman D, et al. Search strategy. In: The Effectiveness of Health Coaching [Internet]. Department of Veterans Affairs (US); 2017. 63. Mettler EA, Preston HR, Jenkins SM, et al. Motivational improvements for health behavior change from wellness coaching. Am J Health Behav. 2014;38(1):83–​91. doi: 10.5993/​AJHB.38.1.9. 64. Wolever RQ, Dreusicke MH. Integrative health coaching: A behavior skills approach that improves HbA1c and pharmacy claims-​derived medication adherence. BMJ Open Diabetes Res Care. 2016;4(1). doi: 10.1136/​bmjdrc-​2016-​000201. 65. Kennel J. Health and wellness coaching improves weight and nutrition behaviors. Am J Lifestyle Med. 2018;12(6):448–​450. doi: 10.1177/​1559827618792846. 66. Moore M, Tschannen-​ Moran B, Jackson E. Coaching Psychology Manual. Philadelphia, PA: Wolters Kluwer Health/​Lippincott, Williams & Wilkins; 2010. 67. Sherson EA, Yakes JE, Katalanos N. A review of the use of the 5 a’s model for weight loss counselling: Differences between physician practice and patient demand. Fam Pract. 2014;31(4):389–​398. doi: 10.1093/​fampra/​cmu020. 68. Landry JB, Solmon MA. African American women’s self-​determination across the stages of change for exercise. J Sport Exerc Psychol. 2004;26(3):457–​469. 69. Yates SW. Physician stress and burnout. Am J Med. 2020;133(2):160–​164. doi:10.1016/​ j.amjmed.2019.08.034. 70. Shanafelt TD, Noseworthy JH. Executive leadership and physician well-​being: Nine organizational strategies to promote engagement and reduce burnout. Mayo Clin Proceedings. 2017;92(1):129–​146. doi:10.1016/​j.mayocp.2016.10.004. 71. Rakel D. Integrative Medicine-​E-​Book. Philadelphia, PA: Elsevier Health Sciences; 2017. 72. Kent K, Johnson JD, Simeon K, Frates EP. Case series in lifestyle medicine: A team approach to behavior changes. Am J Lifestyle Med. 2016;10(6):388–​397. doi: 10.1177/​ 1559827616638288. 73. Egger G, Stevens J, Ganora C, Morgan B. Programmed shared medical appointments: A novel procedure for chronic disease management. Aust J Gen Pract. 2018;47(1/​2):71. doi: 10.31128/​AFP-​07-​17-​4283. 74. Frates EP, Morris EC, Sannidhi D, Dysinger WS. The art and science of group visits in lifestyle medicine. Am J Lifestyle Med. 2017;11(5):408–​413. doi: 10.1177/​ 1559827617698091. 75. Kirsh SR, Aron DC, Johnson KD, et al. A realist review of shared medical appointments: How, for whom, and under what circumstances do they work? BMC Health Serv Res. 2017;17(1):113. doi:10.1186/​s12913-​017-​2064-​z.

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76. Axten K, Hawkins K, Tybor DJ, Bernoff J, Altman W. Impact of a novel wellness group visit model on obesity and behavior change. J Am Board Fam Med. 2017;30(6):715–​ 723. doi:10.3122/​jabfm.2017.06.170098. 77. Srivastava G, Palmer KD, Ireland KA, et al. Shape-​up and eat right families pilot program: Feasibility of a weight management shared medical appointment model in African-​Americans with obesity at an urban academic medical center. Front Pediatr. 2018;6:101. doi: 10.3389/​fped.2018.00101. 78. Plotnikoff RC, Karunamuni N, Spence JC, et al. Chronic disease–​related lifestyle risk factors in a sample of Canadian adolescents. J Adolesc Health. 2009;44(6):606–​609. doi:10.1016/​j.jadohealth.2008.11.004. 79. Mewton L, Champion K, Kay-​ Lambkin F, Sunderland M, Thornton L, Teesson M. Lifestyle risk indices in adolescence and their relationships to adolescent disease burden: Findings from an Australian national survey. BMC Public Health. 2019;19(1):60. doi:10.1186/​s12889-​019-​6396-​y. 80. Centers for Disease Control and Prevention (CDC). Lifestyle risk factors. https://​ ephtracking.cdc.gov/​showLifestyleRiskFactorsMain. Updated 2020. Accessed August 25, 2020. 81. Butterworth SW. Influencing patient adherence to treatment guidelines. J Manag Care Pharm. 2008;14(6 Supp B):21–​25. doi: 10.18553/​jmcp.2008.14.S6-​B.21.

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Health Equity and Women’s Health in Underserved Communities Stacie Schmidt, MD

Associate Professor of Medicine, Department of Medicine Emory University School of Medicine Atlanta, GA

Jada Bussey-​Jones, MD, FACP

Professor of Medicine, Division of General Internal Medicine Emory University School of Medicine Atlanta, GA

Tracey L. Henry, MD, MPH, MS, FACP

Assistant Professor of Medicine, Department of Medicine Emory University School of Medicine Atlanta, GA 10.1 10.2

10.3

10.4 10.5

Introduction..................................................................................................186 Lifestyle Medicine and Vulnerable Communities........................................186 10.2.1 Social Determinants of Health.......................................................186 10.2.2 Systemic Racism...........................................................................188 10.2.3 Health Needs of Women in Under-​Resourced Communities........188 Lifestyle Medicine: Women and Health Equity...........................................189 10.3.1 Addressing Health Equity and SDOH...........................................189 10.3.2 Cultural Competence and Responsiveness....................................189 10.3.3 Building Patient Self-​Efficacy and Self-​Management of Chronic Disease.............................................................................190 Lifestyle Medicine: Cultural Responsiveness and Health Equity................195 10.4.1 Benefits of Increased Patient Self-​Efficacy among Women..........195 Conclusion...................................................................................................196

DOI: 10.1201/9781003110682-11

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KEY POINTS • Social determinants of health (SDoH) can limit self-​efficacy levels in underserved/​ underinsured/​ low health literacy populations. Addressing social determinants has been linked to improved health outcomes among vulnerable patient populations. • Healthcare teams can empower patients to overcome these barriers and become “masters of their domain” by building culturally aligned self-​efficacy skills around healthy behaviors for self-​management of chronic disease. • Engagement between community partnerships/​health systems that synergistically address SDoH can enhance patient self-​efficacy around adoption of healthy behaviors. • Developing multidisciplinary, community, and health system partnerships for improving patient self-​efficacy around healthy behaviors in underserved communities is relatively low-​cost, but with potentially high impact.

10.1  INTRODUCTION Applying LM core competencies for women across the life span can translate to profoundly protective effects during pregnancy, childbirth, and beyond. For example, preventing or reversing diabetes in a woman of childbearing age could potentially reduce the risk of preeclampsia and associated adverse birth outcomes by three-​to fourfold; controlling or reversing high blood pressure prior to pregnancy could potentially reduce the chance of preterm birth and perinatal death by nearly three-​and fourfold, respectively.1 Assisting individuals –​particularly women –​to be self-​managers of their physical and emotional health requires both community-​centered and healthcare team-​ centered approaches. Development of problem-​solving abilities uniquely positions individuals to become self-​managers of their own health as they grow into adults. In situations where it is difficult to address the social determinants of health, building self-​management skills allows patients to develop higher levels of self-​efficacy. This in turn helps patients find ways to exert control over their health, even in situations of limited opportunities and multiple constraints.2 Clinicians and their healthcare teams can work to individually empower patients to become self-​managers of their health by assisting patients with building self-​efficacy skills that take into account the social environment and cultural beliefs. A comprehensive LM movement must target not only preventable chronic conditions and specific lifestyle behaviors of diet and exercise, but also build a woman’s resilience to overcome the impact of bias and other social factors on health and behavior and engage diverse women with empathetic, culturally sensitive, and cohesive approaches.1

10.2  LIFESTYLE MEDICINE AND VULNERABLE COMMUNITIES 10.2.1 Social Determinants of Health Social determinants of health (SDOH) are defined by the Centers for Disease Control (CDC) as “the conditions in the places where people live, learn, work, and play” and

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examples of determinants of poor health include unstable housing, low income, unsafe neighborhoods, or substandard education.3 Societal perceptions of minority communities experiencing unmet social needs are ironically shaped by the very political structures that created them. SDOH are frequently the result of systemic racism and years of unjust policies that adversely affect racial and ethnic minority communities.4 Differences in health are striking in resource-​poor communities. Impoverished neighborhoods are affected by limited access to healthy foods and unsafe neighborhoods limit exercise outside of the home.3 Food insecurity is associated with more hypoglycemic events at the end of the month, higher HBa1c levels, and lower scores on indices of health-​related quality of life. Persons with food insecurity face challenges maintaining a nutritionally adequate diet, higher emotional distress related to diabetes management, and lower scores for self-​efficacy or confidence in managing their health.5–​10 Data supports that safe and affordable housing can also decrease the risk for asthma and lead poisoning.11 In addition to access to housing and home ownership, neighborhoods also matter. A study analyzing infant mortality rate (IMR) data by zip code and race in various Texas counties found that zip code is a bigger driver of health than genetic code or even medical care.12 According to the widely accepted medical model of US HHS Healthy People 2030, these non-​medical determinants impact 60% of health outcomes.12 Unfortunately, societal policies and historical injustices keep such communities segregated in terms of resources, access to public transport, housing, and healthy food, among other key resources. Resource-​poor areas are associated with increased advertisements for tobacco and alcohol, food deserts, less healthcare, and poorer performing schools.13

FIGURE 10.1  Examples of social determinants of health.

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10.2.2 Systemic Racism Racism has also impacted health through disparities in the provision of healthcare services to adults with chronic diseases. Minority patients, for example, receive fewer cancer diagnostic tests, cancer treatments, and receipt of analgesics while controlling for the stage of cancer at diagnosis and other clinical factors. Racial and ethnic disparities are found in a range of other diseases, including diabetes care, end-​stage renal disease, and kidney transplantation.4 Preventable and modifiable risk factors for cardiovascular disease, diabetes, and blood pressure drive differences in health among vulnerable populations. Addressing these risk factors through LM could dramatically improve health outcomes within these groups. Research has shown that controlling blood pressure, blood sugar, body fat, and smoking to optimal levels in vulnerable subgroups would reduce disparities in cardiovascular disease deaths by 80%. Additionally, there is an economic motivation to address preventable health disparities. US health disparities have been estimated to cost more than $1.24 trillion.14

10.2.3 Health Needs of Women in Under-​Resourced Communities Worldwide, women are disproportionately affected by inequities, violence, poverty, and preventable health conditions. Markers such as maternal and infant mortality are representative of societal health, social justice, and welfare. In fact, pregnancy-​related mortality ratios are explicitly used by the CDC as an indicator of the nation’s health. By this yardstick, the United States is undergoing a worsening societal crisis.15 Pregnant women in the United States are more likely to die from childbirth-​or pregnancy-​related causes than in other developed nations in the world.1 Consistent evidence supports that such disparate maternal and child health outcomes stem at least partly from the high poverty rate in the United States, which ranks highest among all developed countries (second highest for child poverty), and the status of the United States as one of the most unequal developed societies.1 Subsequently, chronic stress in impoverished communities leads to increased levels of and prolonged exposure to the stress hormone cortisol, causing inflammatory reactions that predispose individuals to chronic disease later in life.16 The impact of systemic racism has been demonstrated during pregnancy, through IMRs, and persists as adverse health outcomes in childhood and adolescence. In the United States, African-​American, Native American, and Alaskan native women die of pregnancy-​related causes at a rate three times that of white women.1 Racism has been linked to birth disparities and mental health problems in children and adolescents. A study by Collins and colleagues suggested that infants of African-​born mothers were similar to infants of US-​born Caucasian mothers in terms of birth weight and survival patterns.17 Within one generation, the protective “African-​born” effect disappeared, and adverse birth outcomes and low birth weight prevalence increased, leading Collins to conclude “There’s something about growing up a black female in the U.S. that’s not good for… childbearing health.”17 Similar trends are seen for Mexican-​American births; increased acculturation to the United States appears to worsen the risk of adverse birth outcomes.1

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African-​American mothers with a college education were twice as likely to die –​ and more likely to suffer severe complications and mortality –​from a pregnancy or childbirth compared with white women without a high school education.1 Furthermore, African-​ American mothers experience more adverse pregnancy outcomes despite being 71% less likely than their White counterparts to smoke during pregnancy and 41% less likely to consume alcohol.1 In the United States, compared with Caucasian counterparts, African-​American babies are more than twice as likely to die in the first year of life, whereas African-​American mothers are three to four times as likely to die from pregnancy.1 As Lu et al. note, “to expect prenatal care, in less than nine months, to reverse the lifelong, cumulative impact of social inequality on the health of African-​American mothers, may be expecting too much of prenatal care.18 Rather, the greatest potential for promoting healthy pregnancy occurs over the lifespan from birth of the future mother to conception. This concept is something LM practitioners are well-​poised to address.

10.3  LIFESTYLE MEDICINE: WOMEN AND HEALTH EQUITY 10.3.1 Addressing Health Equity and SDOH Health equity is defined as the “principle underlying a commitment to reduce—​and ultimately, eliminate disparities in health and in its determinants, including social determinants.”14 Evidence suggests that organized, multilevel, and tailored disease prevention efforts targeting health equity are feasible on local, national, and global levels and can successfully narrow disparities in diverse groups around the world.14 Similarly, multilevel approaches to addressing lifestyle behaviors are most successful when addressing the interconnected influences of individual, peer/​family group, healthcare team, neighborhood resources, and cultural context, thereby increasing the likelihood that patients can sustain behavior changes outside the healthcare setting. Evidence-​based pathways to achieve health equity and improve lifestyle behaviors within vulnerable communities feature two broad themes. The first theme, capacity-​ building partnerships, is a form of community activism that can mitigate poverty, food deserts, and housing insecurity, and improve community safety over time. This is achieved through tenacious intersectional partnerships operating at local, state, and federal levels. Such inter-​sectoral partnerships require coordination, participation, and resources drawn from the social, political, environmental, and economic sectors, building sustainability, momentum, and capacity for community-​ driven LM.14 Examples of such interventions are outlined in Table 10.1.

10.3.2 Cultural Competence and Responsiveness Healthcare providers can engage and empower historically marginalized groups by implementing culturally tailored lifestyle medicine (LM). This can be done through provider outreach in clinical, health system, and community settings, with targeted LM approaches that address lifestyle risk factors for common chronic diseases.14 Table 10.2 outlines practitioner strategies to do so.

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TABLE 10.1 Examples of Capacity-​Building Intersectional Partnerships to Ameliorate the SDOH Local

Mixed land use environmental design promoting diversity and proximity of local destinations (e.g., grocery stores, salons, business offices, healthcare, recreational facilities, greenspaces) Provision of greenspace within mixed land use communities supported by evidence that those who live in greener neighborhoods have improved mortality at every income level.15 Transportation system policies improving street connectivity, sidewalk and trail infrastructure, bicycle infrastructure, and public transit access to promote physical activity.16

State/​Federal

Increasing “emergency” Medicaid program coverage of uninsured mothers beyond 60 days postpartum. Realigning federal allocation of dollars to provide more equitable healthcare to women.1 Redistribute federal allocation of dollars to balance the care of mothers and their infants. For example, as of 2019, only one multidisciplinary hospital care unit was established to care for high-​risk pregnant mothers; 20 such programs existed at that time for high-​risk infants.1

In any of the above settings, it is important to note that cultural responsiveness is a crucial element of provider training and philosophy, as it enables the delivery of tailored services that are “respectful of and responsive to the health beliefs, practices, and cultural needs of diverse patients.”14 Consider, for example, the phenomenon where immigrant Hispanic communities facing adverse social influences of poverty and social stress have lower-​than-​expected rates of maternal and infant mortality. Research on the Hispanic paradox suggests that a strong connection to community and cultural identity are protective factors, able to at least partially “immunize” against negative social influences and stresses.1 Fragmentation and social isolation, on the other hand, can prove detrimental to health status and lifestyle. See supplemental material for an example of “Putting it into Practice.”

10.3.3 Building Patient Self-​Efficacy and Self-​Management of Chronic Disease Unlike acute illnesses, which often can be reversed with specific medical treatments, chronic disease is long-​standing and “requires a high level of patient responsibility for successful day-​to-​day management.”21 Thus, the management of chronic illnesses necessitates “shifting from medical care that is reactive and event-​driven to care that is proactive and planned.”21 This requires patients to identify the personal, psychosocial, and environmental factors impeding them from appropriately caring for their disease, and then learn to overcome these obstacles.21 In fact, outcomes are improved when patients are more self-​sufficient and confident about caring for their medical issues.21–​23

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TABLE 10.2 Advocacy and Implementation of Culturally Tailored Lifestyle Medicine by Practitioners Within the clinic encounter

Encourage all patients to ask questions during the clinic visit. Provide culturally sensitive and linguistically appropriate shared decision-​making tools that facilitate patient-​centered discussions. Engage in conversations with patients to understand if and how they may have unmet social needs: unemployment, unstable housing, food insecurity, etc. Build trust with their female patients by committing to ask about, understand, and respond empathetically to the impact overt or implicit bias on patient behaviors and health. Recognize that implicit bias affects our individual clinician behaviors and interaction with patients, especially among patients of a different gender or race. Do not assume a patient is afflicted by SDOH because of the color of their skin; while minority communities are more affected by poorer SDOH, assuming this to be the case because of a patient’s skin color could further perpetuate racism and implicit bias. LM practitioners can empower pregnant patients in their practice to take an active role in facilitating a healthy birth through mechanisms such as developing birth plans, engaging in stress reduction practices, and partnering with healthcare professionals such as midwives and doulas, who are associated with better birth outcomes and maternal satisfaction.1 Promoting goal-​setting and action planning for health behaviors as tools to build patient self-​efficacy and self-​management of disease.

Within the health system

Consider ways your practice or health system can provide access to care within minority and underserved communities. Advances in telehealth (including phone visits for those without access to Internet services), home visits, and mobile medicine units for the unhoused create innovative ways to educate and empower individuals and communities to achieve healthy lifestyles. Provision of group visits whereby family and friends can attend, for example, address the interconnected influences of levels of individual, peer/​family group, healthcare team, neighborhood resources, and cultural context, and, therefore, increase the likelihood that patients can sustain behavior changes outside the healthcare setting.1,10

Within the community

LM practitioners can engage in advocacy efforts by participating in community boards, meetings, and town halls offered by local women’s groups and stakeholders. Physician advocacy efforts should specifically engage diverse and vulnerable women within their patient population around setting the reform agenda and in the development and presentation of data, stories, concerns, and recommendations to administrators.1

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Self-​management does not focus on patient knowledge about the disease at hand. Rather, it centers on “[allowing] participants to make informed choices, adopt new perspectives and generic skills that can be applied to new problems as they arise, practice new health behaviors, and maintain or regain emotional stability.”24 Such care allows patients to take a central role in managing their disease, moving them from passive to active participants in the clinic setting and at home.21

This is distinct from didactic education, which uses “standard presentations” in the form of pamphlets, videotapes, and prepared lectures to increase patient knowledge. Rather, behavior-​oriented education that incorporates individual patient experiences and difficulties into self-​management plans is better associated with improved disease control.21 A meta-​analysis of 13 studies evaluated therapeutic outcomes among patients receiving didactic versus behavioral education for the following chronic diseases: hypertension, hyperlipidemia, diabetes, obesity, asthma, renal dialysis, and mixed conditions. Didactic education resulted in 57% therapeutic improvement compared to controls. Behavioral education resulted in 78% improvement over controls. This form of education may be particularly relevant for vulnerable patient populations.22 It is important to note, however, that the greater the system constraints in underserved communities, the stronger the perceived self-​ efficacy must be to effect changes. Addressing SDOH and the policies causing them is certainly one piece of this puzzle, but LM practitioners must simultaneously work to empower patients to become effective in their role as self-​manager –​particularly when living with multiple chronic diseases.2 Clinicians typically attribute non-​adherence with treatments for chronic disease to lack of inherent motivation, low health literacy/​education, and financial constraints by patients. They tend to address these barriers by warning patients about negative impacts of uncontrolled disease, providing education on pathophysiology of disease and medications using pamphlets, videos, diagrams, and/​or tackling financial constraints by prescribing low-​cost medications provided by retail pharmacies. It is time for clinicians to assume an LM approach to addressing nonadherence –​one that assumes patients are “coming to the table with the best they can give” and that focuses on empowering patients to choose and set their own SMART goals, while also implementing problem-​solving skills to address any barriers to goal attainment. … It must be noted, however, that improving patient self-​management skills cannot be achieved through one provider, in part because of time constraints, but also because the role of self-​manager requires a high level of knowledge, confidence, and skill by the patient which should be reinforced throughout their healthcare journey.25 Thus, a reshaping of the healthcare system whereby multiple disciplines work collaboratively to deliver well-​rounded, individualized patient care is required. This concept is inherent to the principles of the Chronic Care Model (CCM) proposed by Wagner et al., which focuses on essential elements for improving chronic illness care.26 To achieve collaborative patient-​centered empowerment and enhanced self-​efficacy in addressing chronic disease management, teams must work together in a co-​located, multidisciplinary fashion to incorporate the essential components of collaborative management outlined in Table 10.3.

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TABLE 10.3 Essential Elements for Improving Chronic Illness Care26,27 to Achieve Collaborative Self-​Management of Chronic Disease26–​28 Essential Element Core Components Proactive care management

Collaboration Steps for Implementation

• Defining team member roles • Patients should receive regular clearly follow-​up to ensure they are • Use of nurse care coordinators successfully managing their or certified health educators to disease. This can be achieved provide self-​management support through scheduled phone between clinic visits calls by trained nurses, mailed • Use of patient navigators to reminders, and appointments at proactively ensuring regular regular intervals with primary follow-​up and virtual check-​ins physicians. with patients • Telephone follow-​up in particular has been associated with improved outcomes (e.g., lower cholesterol levels and smoking cessation among patients with coronary artery disease).28

Self-​management • Empowering patients to manage • Define problems that patients support for patients their health and navigate the experience with self-​managing healthcare system their disease. This may relate to • Performing needs assessments patient adherence; involvement • Assisting patients in goal-​setting, in unhealthy behaviors; or action planning, problem-​solving, problems in terms of pain, and follow-​up decreased functioning, and emotional disturbances. • Both the physician’s and patient’s perspective should be addressed, and a mutual decision should be made about the most important issues at hand. 28 • Providers and patients must work collaboratively to establish specific, measurable, achievable, realistic, and timely (SMART) goals that improve care. • A personalized patient action plan should be generated to help participants reach their defined objectives. • Goals are prioritized based not only on the importance of the problem, but also on the patient’s motivation and willingness to correct the issue. (continued)

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TABLE 10.3 (Continued) Essential Elements for Improving Chronic Illness Care26,27 to Achieve Collaborative Self-​Management of Chronic Disease26–​28 Essential Element Core Components

Collaboration Steps for Implementation • It is prudent for providers to work towards one goal at a time, as incorporating multiple changes might overwhelm the patient; it is also important to keep in mind the personal, environmental, and psychosocial obstacles that patients might encounter along the way. 28

Clinical information systems

• Track individual data and • Teams ideally are co-​located for population health data “warm handoffs” and real-​time • Provide reminders to team collaborations when reviewing members and patients regarding population health reports and/​ care management and follow-​up or individualized reports and • Use of data reporting to “identify care plans groups of patients needing • Involved team members should additional care” discuss daily the established • Use of data to facilitate goals and treatment/​support performance monitoring and plans of their patients with care quality improvement efforts gaps, uncontrolled disease, and those in need of additional support or care.26,27

Developing a culture within healthcare that promotes safe, high-​quality, patient-​centered care

• Encourage team members to • Patients should have continual address errors openly access (virtually or in-​person, • Promoting clinical care in and individually or within group accordance with scientific evidence settings) to community and and patient goals. health system “services that • Organizing community resources teach skills needed to carry out to address patient needs and medical regimens, guide health preferences.22 behavior change, and provide emotional support.” • This might be achieved through the use of group classes teaching self-​help skills to a panel of patients, while also allowing time for patients to problem-​ solve through interactive, open dialogue with other participants in similar situations.28

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10.4  LIFESTYLE MEDICINE: CULTURAL RESPONSIVENESS AND HEALTH EQUITY Krishnaswami and colleagues propose a framework by which LM clinicians can implement culturally responsive strategies within their practice and among their healthcare team in the care of vulnerable populations to enhance health equity.14 These practice enhancement strategies are examined in Table 10.4. See supplemental material for an example of “Putting it into Practice.”

10.4.1 Benefits of Increased Patient Self-​Efficacy among Women Perceived self-​efficacy affects patients’ judgments of, and confidence in, their coping capabilities to manage certain behaviors or situations related to their health.29 The majority of women polled in a recent survey reported that they held back from asking questions of their providers because they feared being perceived as difficult (22%), felt rushed (30%), or desired a different plan of care (22%). Such fear undermines the woman’s ability to engage in partnership approaches, such as creating birth plans, that increase a woman’s ability to promote desired elements of a pregnancy.1 Perceived self-​efficacy has been shown to play a significant role in such diverse forms of health

TABLE 10.4 Community-​Engaged Lifestyle Medicine Practice Enhancement Strategies (adapted from Krishnaswami, Sardana, and Daxini14) Short-​term strategies

Medium-​term strategies

Long-​term strategies Multi-​level community approaches

• Learn about patient’s culture and values during clinical encounters. • Acknowledge and link the care provided to those values. • Respect and accommodate cultural practices that inform a patient’s dietary practices. • Ask patients from diverse groups for advice on how to reach and connect with more patients in need of lifestyle medicine. • Arrange local lay health worker(s) to hold cultural humility trainings for clinical staff. • Survey patients on their perception of respect, bias, and tolerance in your practice. • Research and provide recipes and activity advice that include culturally tailored foods, flavors, and spices. • Employ a community health worker or health coach representing diverse/​ vulnerable communities to work with your staff and patients. • Hire diverse staff and healthcare providers. • Hold group and family lifestyle medicine visits. • Identify common places where vulnerable patients eat, work, and move –​ develop strategies to organize educational workshops at these locations. • Create a map of community-​level resources supporting lifestyle medicine. • Utilize technology (apps or text-​message systems) to engage groups of patients outside the clinic in healthy living practices.

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behavior as smoking-​cessation relapse, pain experience and management, success of recovery from myocardial infarction, adherence to preventive health programs, and control of eating and weight.29 A multiple regression analysis of a small pilot study (N=30) evaluating tangible reinforcement for weight loss examined the impact of changes in diet and exercise self-​efficacy on outcomes. The analysis indicated that the strongest predictors of weight loss were (1) treatment attendance by patients and (2) changes in exercise self-​efficacy throughout the course of treatment.30 Healthy behaviors can delay/​prevent the onset of Type 2 diabetes and prevent complications from diabetes. A meta-​ analysis of self-​ management interventions showed that didactic education of diabetes alone does not lead to improved patient outcomes; instead, self-​management interventions promoting adoption of healthy behaviors results in improved glycemic control. However, “real world” settings face challenges when replicating diabetic self-​management programs from clinical trials, given many clinical trials are resource-​intensive and do not focus on interventions benefiting persons of low literacy, limited English proficiency, poverty, or from different ethnicities and cultures.31 See supplemental material for an example of “Putting It into Practice.”

10.5  CONCLUSION Applying LM core competencies for women across the life span can translate into profoundly protective effects during pregnancy and childbirth. Markers such as maternal and infant mortality are representative of societal health, social justice, and welfare. In fact, pregnancy-​related mortality ratios are explicitly used by the CDC as a measure of the nation’s health. CDC data from 2014–​2017 has noted considerable racial and ethnic disparities in pregnancy-​related mortality, due to “several factors including access to care, quality of care, prevalence of chronic diseases, structural racism, and implicit biases.”11 Thus, a prudent and robust LM movement should not only target preventable chronic conditions and specific lifestyle behaviors of diet and exercise, but also build women’s resilience to overcome the impact of bias and other social factors on health and behavior; and engage diverse women with empathetic, culturally sensitive, and cohesive approaches.1

REFERENCES 1. Krishnaswami J, Del C, Colon-​Gonzalez M. Reforming women’s health care: A call to action for lifestyle medicine practitioners to save lives of mothers and infants. Am J Lifestyle Med. 2019;13(5):495–​504. DOI:10.1177/​1559827619838461. 2. Bandura A, Wood R. Effect of perceived controllability and performance standards on self-​regulation of complex decision making. J Pers Soc Psychol. 1989;56(5):805–​814. DOI:10.1037//​0022-​3514.56.5.805. 3. Centers for Disease Control and Prevention. Social determinants of health: Know what affects health. Available at: www.cdc.gov/​socialdeterminants/​. Accessed February 9, 2021.

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4. Serchen J, Doherty R, Atiq O, Hilden D, Health and Public Policy Committee of the American College of Physicians. A comprehensive policy framework to understand and address disparities and discrimination in health and health care: A Policy Paper from the American College of Physicians. Ann Intern Med. 2021;174(4):529–​532. doi:10.7326/​M20-​7219. 5. Seligman HK, Bindman AB, Vittinghoff E, et al. Food insecurity is associated with diabetes mellitus: Results from the National Health Examination and Nutrition Examination Survey (NHANES) 1999–​2002. J Gen Intern Med. 2007 Jul;22(7):1018–​ 1023. DOI:10.1007/​s11606-​007-​0192-​6. 6. Seligman HK, Laraia BA, Kushel MB. Food insecurity is associated with chronic disease among low-​income NHANES participants. J Nutr. 2010;140(2):304–​310. DOI:10.3945/​jn.109.112573. 7. Laraia BA, Food insecurity and chronic disease. Advances in Nutrition. 2013;4(2):203–​ 212. DOI:10.3945/​an.112.003277. 8. Leung CW, Epel ES, Ritchie LD, et al. Food insecurity is inversely associated with diet quality of lower-​income adults. J Acad Nutr Diet. 2014 Dec;114(12):1943–​1953.e2. DOI:10.1016/​j.jand.2014.06.353. 9. Bawadi HA, Ammari F, Abu-​Jamous D, et al. Food insecurity is related to glycemic control deterioration in patients with type 2 diabetes. Clin Nutr. (2012) 31:250–​254. DOI:10.1016/​j.clnu.2011.09.014. 10. Maddigan SL, Feeny DH, Majumdar SR, et al. Understanding the determinants of health for people with type 2 diabetes. Am J Public Health. 2006 Sep;96(9):1649–​ 1655. DOI:10.2105/​AJPH.2005.067728. 11. Centers for Disease Control and Prevention. Ten essential public health services and how they can include addressing social determinants of health inequities. Available at: www.cdc.gov/​publichealthgateway/​publichealthservices/p​ df/T ​ en_E ​ ssential_S ​ ervices_ and_​SDOH.pdf. Accessed February 9, 2021. 12. DeSalvo, K. It’s the Zip Code, Stupid. SGIM Forum. 2019;42(10)1–​3. Available at: https://​connect.sgim.org/​sgimforum/​viewdocument/​its-​the-​zip-​code-​stpd. Accessed February 9, 2021. 13. Byhoff E, Kangovi S, Berkowitz SA, DeCamp M, Dzeng E, Earnest M, Gonzalez CM, Hartigan S, Karani R, Memari M, Roy B, Schwartz MD, Volerman A, DeSalvo K. Society of General Internal Medicine. A Society of General Internal Medicine Position Statement on the Internists’ Role in Social Determinants of Health. J Gen Intern Med. 2020 Sep;35(9):2721–​2727. DOI:10.1007/​s11606-​020-​05934-​8. 14. Krishnaswami J, Sardana J, Daxini A. Community-​engaged lifestyle medicine as a framework for health equity: Principles for lifestyle medicine in low-​resource settings. Am J Lifestyle Med. 2019;13(5):443–​450. DOI:10.1177/​1559827619838469 15. Centers for Disease Control and Prevention. 2020. Pregnancy mortality surveillance system. Available at: www.cdc.gov/​reproductivehealth/​maternal-​mortality/​pregnancy-​ mortality-​surveillance-​system.htm. Accessed February 9, 2021. 16. Trent M, Dooley D, Dougé J. The impact of racism on child and adolescent health. Policy statement: Organizational principles to guide and define the child health care system and/​or improve the health of all children. Pediatrics. 2019;144 (2) e20191765; DOI:10.1542/​peds.2019-​1765. 17. Collins JW Jr, David RJ, Handler A, et al. Very low birthweight in African American infants: The role of maternal exposure to interpersonal racial discrimination. Am J Public Health. 2004;94:2132–​2138. DOI:10.2105/​ajph.94.12.2132.

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18. Lu MC, Kotelchuck M, Hogan V, Jones L, Wright K, Halfon N. Closing the black-​ white gap in birth outcomes: A life-​course approach. Ethn Dis. 2010;20(1 Suppl 2):S2–​S76. https://​pubmed.ncbi.nlm.nih.gov/​20629248/​. 19. Community Preventive Services Task Force. Physical activity: Built environment approaches combining transportation system interventions with land use and environmental design. Available at: www.thecommunityguide.org/​sites/​default/​files/​assets/​ PA-​Built-​Environments.pdf. Accessed January 14, 2021. 20. Bergmans R, Zivan K, Mezuk B. Depression, food insecurity and diabetic morbidity: Evidence from the Health and Retirement Study. J Psychosom Res, 2019 Feb;117:22–​29. DOI:10.1016/​j.jpsychores.2018.12.007. 21. Mazzuca SA. Does patient education in chronic disease have therapeutic value? J Chron Dis. 1982;35(7):521–​529. DOI: 10.1016/​0021-​9681(82)90071-​6. 22. Weingarten SR, Henning JM, Badamgarav E, et al. Interventions used in disease management programmes for patients with chronic illness-​which ones work? Meta-​ analysis of published reports. BMJ. 2002;Oct 26;325(7370):925. DOI: 10.1136/​ bmj.325.7370.925. 23. Petoukhov K. Measuring the effectiveness of interdisciplinary health care teams in a primary care setting: a review of published evidence. Unpublished manuscript. 24. Lorig K. Self-​management of chronic illness: A model for the future. Generations: J Am Soc Aging. 1993;17(3):11–​14. http://​www.jstor.org/​stable/​44877774. 25. Hibbard JH, Mahoney ER, Stockard J, et al. Development and testing of a short form of the patient activation measure. Health Services Research. 2005;40(6 Pt 1):1918–​ 1930. DOI:10.1111/​j.1475-​6773.2005.00438.x. 26. Wagner EH. The role of patient care teams in chronic disease management. British Medical Journal. 2000; 320(7234):569–​572. DOI:10.1136/​bmj.320.7234.569 27. Glasgow RE, Wagner EH, Schaefer J, et al. Development and validation of the patient assessment of chronic illness care (PACIC). Medical Care. 2005;43(5):436–​444. DOI:10.1097/​01.mlr.0000160375.47920.8c. 28. Von Korff M, Gruman J, Schaefer J, et al. Collaborative management of chronic disease. Ann Intern. Med. 1997;127(12):1097–​1102. DOI: 10.7326/​0003-​4819-​12712-​199712150-​00008. 29. O’Leary A. Self-​ efficacy and health. Behav Res Ther. 1985;23(4): 437–​ 451. DOI:10.1016/​0005-​7967(85)90172-​X. 30. Byrne S, Barry D, Petry NM. Predictors of weight loss success. Exercise vs. dietary self-​efficacy and treatment attendance. Appetite. 2012;58(2):695–​698. DOI:10.1016/​ j.appet.2012.01.005. 31. Anderson D., Christison-​Lagay, J. Diabetes self-​management in a community health center: Improving health behaviors and clinical outcomes for underserved patients. Clinical Diabetes. 2008;26(1):22–​27. DOI:10.2337/​diaclin.26.1.22

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Community Engagement and Women’s Health Cheryl True, MD, DipABLM, FACLM True Lifestyle Medicine Clinic, LLC Davenport, IA

Elisabeth Fontaine, MD, DipABLM, FACLM Let’s Lead, LLC Swanton, VT

Erin Phillips, OTD, MSOT, DipABLM Carlow University College of Health and Wellness Program in Occupational Therapy Pittsburgh, PA 11.1 11.2

11.3

Introduction..................................................................................................200 Community Engagement Process................................................................200 11.2.1 Checklist for Community-​Engaged Lifestyle Medicine Prescription....................................................................................201 11.2.2 A Model of Community Engagement...........................................202 Adopting Community-​Engaged Models......................................................203

KEY POINTS • Community engagement begins with relationship building and understanding the key needs of the women and girls in our communities. • The Community-​ Engaged Lifestyle Medicine model can improve health outcomes and reduce health disparities. • Multi-​ sectoral community partnerships and interprofessional collaboration including Lifestyle Medicine providers, healthcare organizations, and academic institutions are effective ways to establish community Lifestyle Medicine programming and promote learning outcomes for student trainees. • Effective resources exist to assist clinician implementation and outcomes measurement.

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11.1  INTRODUCTION Drawing upon the power of community creates a dynamic resource to assist individuals in achieving and sustaining healthy lifestyle behaviors, even in populations with significant health disparities.1 Engaging existing communities or forming de novo communities can amplify messages delivered by the Lifestyle Medicine clinician. Communities represent people with shared or common attitudes, interests, goals, or other characteristics that create bonds that connect them. Communities serve an important role in modern society by supporting the physical and emotional needs of individuals.2 Endless examples exist: those formed due to geographic location, religious preferences, those based upon occupation, gender, age, leisure activities, hobbies, political affiliation, or education. Individuals belong to multiple communities which overlap, creating pathways for exchanges of information and ideas far beyond an individual’s personal realm. Current technology has added an entirely new dimension by granting global access to distant communities in an instant.3 The coronavirus disease 2019 (COVID-​19) global pandemic highlighted the importance of community health, while also revealing an unequal distribution of vulnerabilities, among them social, health and digital inequities, impacting disease consequences, including severity and mortality.3 It is evident that communities have the potential to impact the health of their members and vice versa. Leveraging this relationship could contribute to the adoption of healthier behaviors by the members, leading to better health outcomes for the group. Community engagement, defined as “a process of working collaboratively with groups of people who are affiliated by geographic proximity, special interests, or similar situations, with respect to issues affecting their well-​being,” has “emerged as an increasingly effective strategy for harnessing community potential, particularly in health improvement.”1

11.2  COMMUNITY ENGAGEMENT PROCESS Providers recognize that patients are often eager to adopt healthier behaviors while in the office setting, yet face daily barriers and challenges that hinder their ability to succeed. Evidence suggests that environment plays a significant role in adherence to Lifestyle Medicine recommendations, and that community engagement can help to create a supportive context for sustainable behavior change. The first step in establishing a relationship with the local community is to listen to the needs of the people. In order to understand the needs of a multifaceted society, efforts need to reflect the voices of the healthcare consumers and their unique healthcare needs. Community-​ based participatory research (CBPR), leading to community-​ based interventions (CBIs), takes this step.4 “The process seeks to honor the perspectives, voices, preferences and decisions of the least powerful and most affected stakeholders and program beneficiaries.” 4 The use of CBPR first as a way to gather information, then CBI as a strategy for change, empowers participants to have a voice in their health and wellness, promoting sustainable action. There is a need for CBIs to become mainstream in our efforts to reform the healthcare system and move beyond traditional scientific studies of health to include nonclinical issues. “The social determinants of

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health are the social, economic, political, and environmental conditions to which a great share of health problems are attributed.”5 Key findings from a synthesis of the literature on CBI and community-​engaged scholarship suggest growing support for the use of the CBI framework to enhance community engagement and health equity.6 CBIs can move research to action. A primary example is a Community-​Engaged Lifestyle Medicine (CELM) framework, shown to improve health outcomes and address health disparities.7 The US Department of Health and Human Services Office on Women’s Health (OWH) developed a community-​based initiative entitled Coalition for a Healthier Community (CHC).8 The goals of the CHC are to address gender-​based health inequities and support community-​wide health of women and girls. The Coalition for a Healthier Community for Utah Women and Girls (CHC-​ UWAG) used a gender-​based approach to address obesity rates in women and girls. The CBIs used wellness coaching for healthy eating and physical activity and led to policy initiatives to improve the health of women and girls.9 The New Haven Mental Health Outreach for Mothers (MOMS) established a community partnership to address the mental health needs of women in the reproductive phase of life and the impact on their children.10 Using a community engagement model, the need for diapers was identified as a prominent stressor for mothers living in poverty. By listening and engaging the women of the community, the right programming was created to impact the health of both mother and child. These examples illustrate the power of engaging community stakeholders to mobilize for advocacy, access, and action. Additional action steps for the prescription of CELM in clinical practice are listed below.

11.2.1 Checklist for Community-​Engaged Lifestyle Medicine Prescription The following goals are adapted from the CELM framework outlined by Krishnaswami, Sardana, and Daxini.7 Short-​term goals established for clinical practice: • Create focus groups to identify needs of the community. • Use motivational interviewing and patient-​centered care to listen and learn from your patients and community members. • Identify key stakeholders in the community and build relationships. • Identify the community strengths and services already in place. • Consider serving on local boards of community organizations. • Begin holding group and family Lifestyle Medicine visits. • Identify key locations of community gathering and hold educational groups. • Learn about the culture and values of your clients. • Respect a client’s culture when issuing dietary guidelines. • Use snowball recruitment from current clients to reach more members of the community. Developing community partnerships can be facilitated through the collaborative efforts of healthcare organizations, community agencies, and educational institutions.

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Healthy People 2030 states, “to achieve the health and well-​being of all people, it is essential to involve, as active partners, diverse stakeholders from across the public, private, and nonprofit sectors.”11 A first step can start with interprofessional collaborations at local universities educating healthcare trainees. Collaborations between healthcare and academic settings are mutually beneficial, allowing for student training and experience, while providing cost-​effective community programming. The University of Texas Rio Grande Valley developed a Preventative Medicine residency training in Lifestyle Medicine using community engagement principles to promote healthy behavior change and health equity.12 This innovative program addressed the health and well-​being of the local community, while establishing the necessary curricular objectives and experiential learning to promote student training and implementation of Lifestyle Medicine principles. The University of Southern California and the Chan Division of Occupational Science and Occupational Therapy offer Lifestyle Redesign® programs as evidence-​ based education in areas such as weight management, smoking cessation, hypertension, mental health, and diabetes. In a recent study, the Lifestyle Redesign® occupational therapy program was shown to be effective in enhancing interprofessional service delivery and promoting self-​management to improve health outcomes of patients with diabetes in the primary care setting.13 Education and healthcare collaborations result in clinical-​community linkages that promote healthy living and build health equity for all people.13 A variety of resources to begin the engagement process are available in the online supplemental materials.

11.2.2 A Model of Community Engagement RISE VERMONT (RiseVT) is a model of CBI with a mission to embrace healthy lifestyles to improve the quality of life and reduce healthcare costs where we live, work, learn, and play. RiseVT has expanded to the state level and impacts the lives of people, communities, and populations across Vermont. RiseVT is based on the EPODE14 model, an acronym for the French model Ensemble Prévenons l’Obésité Des Enfants, which translates to “together let’s prevent childhood obesity.” The EPODE model is a large-​scale, coordinated, capacity-​building approach for communities to implement effective and sustainable strategies to promote healthier lifestyles and reduce childhood obesity. This methodology has now been implemented in over 28 countries worldwide, and provides a valuable model that may be applicable to other lifestyle-​related diseases. It fosters a multi-​stakeholder approach: top-​down leadership and bottom-​up mobilization with participation at both local and central levels. Figure 11.1 illustrates the components of the EPODE model and the interactive parts of this community engagement model. It is a dynamic process that requires the dedicated work of multiple stakeholders at a variety of community levels in order to successfully produce the desired impact. EPODE methodology identifies four critical factors that form the pillars of the model. The first is political commitment from the local community up to the state and federal levels. The second is public–​ private partnerships that secure sufficient resources to fund the operation and ensure

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FIGURE 11.1  A schematic of the EPODE model. Used with permission from: Borys JM, Le Bodo Y, Jebb SA, et al. EPODE approach for childhood obesity prevention: Methods, progress and international development. Obes Rev. 2012;13(4):299–​315.

its sustainability. The third is planning, coordinating actions, and providing the social marketing and support services at community level. The fourth and last pillar uses evidence from numerous sources to guide the implementation of the EPODE interventions and evaluate outcomes. Available in the supplemental material is a narrative written by one of the founders of RiseVT. “Coaching a Village to Health: A story of Community-​Based Intervention (CBI) through the lens of a female Physician engaged for the greater good.” This first-​ person account is intended to be a reference for others, a “roadmap,” taking readers from the evolution of an idea through its successful implementation.

11.3  ADOPTING COMMUNITY-​ENGAGED MODELS There are extraordinary challenges to global healthcare as we are faced with increasing burdens of chronic diseases. Relevant, financially feasible, and effective methods to improve and support the health and well-​being of populations are needed, especially to assist women and vulnerable populations disproportionately affected by

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health inequities. The foundational, root-​cause approach of Lifestyle Medicine need not be limited to clinical or hospital settings, but extended by a multi-​sector collaborative approach that meets people where they live, learn, work, and play. Utilizing a community engagement framework brings together interprofessional teams, trainees, stakeholders, and community members to develop a best-​fit approach to reach those who are under-​resourced and most in need. Women have been both leaders in this area and beneficiaries of these interventions that can reach across the lifespan. Multiple resources that provide a roadmap to explore options to expand the application of Lifestyle Medicine exist. In the pursuit of health equity, programs can be tailored to meet the needs of varied populations to offer measurable benefits far beyond the traditional walls of the clinical setting.

REFERENCES 1. Cyril S, Smith BJ, Possamai-​Inesedy A, Renzaho AM. Exploring the role of community engagement in improving the health of disadvantaged populations: A systematic review. Glob Health Action. 2015;8:29842. doi:10.3402/​gha.v8.29842. 2. Tryon C, Pobiner B, Kauffman R. Archaeology and human evolution. Evolution: Education and Outreach. 2010;3(3):377–​386. doi:10.1007/​s12052-010-​0246-​9. 3. Beaunoyer E, Dupéré S, Guitton MJ. COVID-​19 and digital inequalities: Reciprocal impacts and mitigation strategies. Comput Human Behav. 2020;111:106424. doi:10.1016/​j.chb.2020.106424. 4. Zukoski A, Luluquisen M. Participatory evaluation. What is it? Why do it? What are the challenges?. Community Based Public Health Policy Pract. 2002;(5):1–​6. 5. Horowitz CR, Robinson M, Seifer S. Community-​based participatory research from the margin to the mainstream: Are researchers prepared?. Circulation. 2009;119(19):2633–​ 2642. doi:10.1161/​CIRCULATIONAHA.107.729863. 6. Ortiz K, Nash J, Shea L, et al. Partnerships, processes, and outcomes: A health equity-​ focused scoping meta-​review of community-​engaged scholarship. Annu Rev Public Health. 2020;41:177–​199. doi:10.1146/​annurev-​publhealth-​040119-​094220. 7. Krishnaswami J, Sardana J, Daxini A. Community-​engaged lifestyle medicine as a framework for health equity: Principles for lifestyle medicine in low-​resource settings. Am J Lifestyle Med. 2019;13(5):443–​450. doi:10.1177/​1559827619838469. 8. Alexander S, Walker EM. Gender-​based health interventions in the United States: An overview of the coalition for healthier community initiative. Eval Program Plann. 2015;51:1–​3. doi:10.1016/​j.evalprogplan.2015.02.004. 9. Simonsen SE, Ralls B, Guymon A, et al. Addressing health disparities from within the community: Community-​based participatory research and community health worker policy initiatives using a gender-​based approach. Women’s Health Issues. 2017;27 Suppl 1:S46–​S53. doi:10.1016/​j.whi.2017.09.006. 10. Smith MV, Kruse A, Weir A, Goldblum J. Diaper need and its impact on child health. Pediatrics. 2013;132(2):253–​259. doi:10.1542/​peds.2013-​0597. 11. Office of Disease Prevention and Health Promotion. Healthy People 2030. https://​ ww.healthypeople.gov/​2020/​About-​Healthy-​People/​Development-​Healthy-​People-​ 2030/​Framework. Accessed July 23, 2020. 12. Krishnaswami J, Jaini PA, Howard R, Ghaddar S. Community-​engaged lifestyle medicine: Building health equity through preventive medicine residency training. Am J Prev Med. 2018;55(3):412–​421. doi:10.1016/​j.amepre.2018.04.012.

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13. Pyatak E, King M, Vigen CLP, et al. Addressing diabetes in primary care: Hybrid effectiveness-​ implementation study of Lifestyle Redesign® occupational therapy. Am J Occup Ther. 2019;73(5):7305185020p1–​7305185020p12. doi:10.5014/​ajot. 2019.037317. 14. Borys JM, Le Bodo Y, Jebb SA, et al. EPODE approach for childhood obesity prevention: Methods, progress and international development. Obes Rev. 2012;13(4):299–​ 315. doi:10.1111/​j.1467-​789X.2011.00950.x.

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Lifestyle Medicine in the Care of Adolescent Girls Neeta B. Agarwal, MD, FAAP, FAMWA, DipABLM Indiana University School of Medicine Indianapolis, IN

Michelle Dalal, MD, FAAP, DipABLM University of Massachusetts Medical School Milford, MA 12.1 12.2 12.3 12.4 12.5 12.6 12.7 12.8

Introduction..................................................................................................207 Nutrition.......................................................................................................208 Physical Activity..........................................................................................209 Sleep.............................................................................................................210 Stress Management......................................................................................210 Social Connectivity/​Relationships...............................................................211 Substance Use Prevention............................................................................212 Conclusion...................................................................................................212

KEY POINTS • Establishing a healthy lifestyle in adolescence sets up long-​lasting health habits in a woman’s life. • The six pillars of Lifestyle Medicine can serve as a framework for prevention and management of chronic diseases in adolescence just as in other stages of life. • A teen’s healthcare can be supported through team-​based care. • Motivational interviewing and SMART goals are two tools providers may use to facilitate discussion and formulate plans.

12.1  INTRODUCTION The adolescent years are a defining time when integration of Lifestyle Medicine pillars lays the foundation for optimal physical and mental health. This is a critical period when rapid cortical development happens and teens undergo changes in physical, cognitive, emotional, and social realms and develop their own values and belief systems.1 Teens are affected by multiple forces: their family and childhood experience, school and peers, their local and global community, and social media. These forces lay the DOI: 10.1201/9781003110682-13

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foundation of their lifestyle for years to come. In their pursuit of personal goals in education, career, relationships, and beyond, good health habits will prepare them for the emotional and physical challenges of life. Some chronic diseases have an initial nidus in adolescence and might be prevented through lifestyle interventions, particularly whole food, plant-​based (WFPB) nutrition, increasing physical activity (PA), improving sleep, managing stress/​building resilience, increasing social connections, and promoting substance use cessation. There are a variety of settings where teens may learn about a healthy lifestyle. Many will be exposed to information about nutrition and exercise in school settings and community organizations. Clinicians have the opportunity to engage with teen girls at well-​child or adolescent visits as well as urgent visits. Yet, visit rates for well care decline with age, with ~1/​20 teens reporting no usual place of healthcare, and problem-​focused visits begin to rival well visits.2 Notably, many chronic illnesses are tied to stress, including diseases such as obesity, depression, cardiovascular disease, and diabetes. The expansion of telehealth visits may help narrow that gap in socially disadvantaged and rural settings alike. An adolescent’s healthcare team may include general pediatricians, family practitioners, and potentially gynecologists and internists in later teen years. A host of other providers including behavioral health providers, psychologists, psychiatrists, registered dieticians, exercise coaches, subspecialists, nurses, and medical assistants may become vital members of their medical team.

12.2  NUTRITION The teen years are an ideal time for teens to understand the tenets of good nutrition. Healthy eating habits are in a transitional phase from childhood and evolve to fit a teen’s lifestyle. Continuing to encourage regular mealtimes including breakfast, limited fast food, limited sugar-​sweetened beverage consumption, and mindful eating practice such as screen-​free meals are key points to bring up with teens. Even if teens are eating out with friends, healthy choices can be made and need to be taught. Healthy foods for teens include a diet rich in optimal micronutrients and macronutrients, which can be encouraged with the adoption of a WFPB diet. This includes eating foods in their most natural forms and eating a diverse diet rich in fruits and vegetables while limiting intake of processed foods and foods high in salt and sugar. Healthier eating can minimize adolescent nutritional deficiencies. Iron deficiency anemia is one of the leading nutritional deficiencies of adolescent girls, due to poor dietary intake and menstrual losses, and ensuring adequate iron stores by encouraging dietary iron intake can prevent this. Adolescence also is a critical time for bone mass accrual;3 therefore, attention to calcium and vitamin D intake should be optimized through foods. Adequate iron, calcium, and vitamin D intake can all be achieved through consumption of foods such as green leafy vegetables, fruits, nuts and seeds, legumes, plant-​based milk, and whole grains. Vitamin supplements can be considered when adequate dietary intake cannot be achieved. Helping teens have a healthy relationship with food is as important as eating well. This can be encouraged by teaching principles of mindful eating early with tips such

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as “eat slowly,” “taste your food,” “chew slowly,” and eat with focus and without distraction. Apps have been shown to help encourage mindful eating.4 Societal and peer influences can impact perception of one’s own body and can lead to positive or negative self-​image, which can create patterns of disordered eating, leading to anorexia, bulimia, restrictive eating patterns, or body dysmorphic disorder.5 Additionally, the home environment can influence food choices. Studies have shown that having access to healthy foods and having health-​oriented rules at home encourage healthy snack choices.6 This is also an optimal time to encourage skills such as meal planning, preparing foods, and cooking as this is shown to lead to healthier food choices.7 Thoughtful and collaborative discussions about healthy habits can encourage small, incremental lifestyle change and lay the foundation for healthy weight maintenance throughout life. This may include setting smart, measurable, achievable, realistic, and timely (SMART) goals to make changes simple and achievable. It is important to approach discussion of weight with sensitivity, being mindful of the importance of self-​image during teen years.8 Good nutrition and health lead to improved long-​term outcomes for a woman’s education, work, future family, and their community, as well as improved reproductive health.

12.3  PHYSICAL ACTIVITY The Centers for Disease Control recommends 1 hour of PA for children and teens alike. It is recommended that teens participate in aerobic, bone-​strengthening, and flexibility exercise. PA has known benefits on mood, sleep, metabolism/​ energy balance, bone, and muscle health. Global analysis shows that 84.7% of teen girls report insufficient PA.9 This statistic has shown little improvement from 2001 through 2016 as lifestyles remain sedentary with increasing screen time and decreasing PA.9 Incorporating PA in a teen’s day may seem challenging since academics, extracurricular activities, family time, and possibly work compete for their time. When extracurricular activities include PA, such as team or individual sports, there is a greater likelihood of achieving the daily PA goal. Without these organized events, specific attention and planning is needed to ensure PA is a part of daily routine. For some teens dealing with overweight, obesity, or other metabolic diseases, achieving PA goals is part of a treatment plan. While discussion of chronic metabolic disease prevention and risk factor modification may provide limited, short-​lived motivation to start PA, helping teens create long-​term habits by focusing on immediate, tangible benefits is likely to be more effective. Using motivational interviewing in well visits can harness teens’ intrinsic motivation to engage in PA. Some chronic illnesses may pose as barriers to begin exercise, for example, asthma, obesity, chronic headaches, and dysmenorrhea. Musculoskeletal pain, difficulty with coordination, stigma, and coexisting mood concerns may affect motivation and are frequent hurdles to overcome. Working with teens to overcome barriers and highlighting ways to gradually begin a sustainable exercise regimen is a key part of management and illness prevention.

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Regardless of the “why,” engaging the teen in finding a reason to become physically active is most important. Helping teens set SMART goals and following up at short intervals provides accountability. This interval is determined by the urgency –​ whether PA is needed as a treatment or in long-​term adoption of healthy practice. The clinical team may consider visits with team nurses or wellness coaches in individual or group visits to provide follow-​up.

12.4  SLEEP Sleep is another important pillar for teens. Adolescence is a time when many teens tend to biologically shift bedtime to be later and consequently may experience inadequate sleep. This shift in biological pathways favors inflammation and can increase the risk of chronic diseases such as obesity, depression, cardiovascular disease, diabetes, and other diseases. Guidance during this time should encourage consistent sleep times on all days of the week and sleep duration to be 8 to 10 hours daily.10 To encourage good nighttime sleep, screens should be turned off at least 30 minutes prior to sleep, although studies have shown that 90 minutes is an optimal time to induce melatonin production which naturally encourages sleep.11 Having a cool, dark, quiet environment prior to sleep can help improve sleep. Lastly, caffeine intake from soda, coffee, and energy drinks should be discouraged, particularly after noon. If naps are required, they should be limited to reduce the effects on nighttime sleep.

12.5  STRESS MANAGEMENT Stress has been described by Hans Selye as the body’s nonspecific response to any demand. Distress refers to stress caused by unpleasant stimuli, whereas eustress refers to stress caused by positive experiences. Teen years are a time of new experiences and many “firsts”, and as such, there is considerable distress and eustress along the way. External stressors abound –​academic demands and career planning, social stressors including friendships, relationships, and peer pressure, possibly financial struggle and need for balancing employment with school, and injury or illness for some. Internal sources of stress –​those that occur within us –​originate from expectation and our mindset. For teens, internal stress includes identity formation, gender concerns, development of values and beliefs, role in family, and self-​image. Spending one-​on-​one time during well visits provides opportunity for teens to share about these stressors. Screening tools include the Perceived Stress Scale (PSS) and the Pediatric ACEs (adverse childhood experiences) and Related Life Events Screener (PEARLS). Screening for mood with the Patient Health Questionnaire (PHQ-9) for depression, the Generalized Anxiety Disorder (GAD-​7) Question Screener for anxiety, and the Ask Suicide-​Screening Questions (ASQ) may also help identify mood concerns which contribute to stress. Screening for anxiety and depression is important at least once annually at well visits. Some stressors are short-​lived and can trigger fight or flight reactions. Long-​term stress can lead to physiological effects on the body. For girls, stress may influence

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menstrual cycles. Periods may be irregular, heavy, and associated with more pain. Stress may lead to irritability, anger, and difficulty concentrating as well as mood concerns such as depression, anxiety, body dysmorphic disorder, and eating disorders. Stress can lead to physical and mental health changes and can impact important self-​ preservation functions: appetite may change and food choices may be less healthful, sleep may be altered in quality and quantity, and PA may be deprioritized. Teens may engage in risky behaviors, including alcohol and illicit substance use, and relationships may be compromised. The severity of a stress response may be reduced by improved sleep times and adequate quality of sleep, healthy diet, regular exercise, social connectivity, and avoidance of toxic substances. Nutrients including omega-​3 fatty acids and vitamin D found in a WFPB diet, may help with stress management.12 Teaching teens coping strategies for stress management is vital. We should encourage teens to develop balance by including relaxation in their daily activities by spending time outdoors, connecting with others in person when possible, exercising, and enjoying hobbies. Some teens may connect with volunteer organizations, faith-​based organizations, or other age-​appropriate community programs. Providers should also introduce and recommend mindfulness strategies, including mindful breathing exercises, yoga, and meditation. For relaxation to be beneficial and to develop resilience, teens need to develop regular practice. Setting SMART goals and tracking their progress with new habits will help make habits sustainable for the long run. While external stress will be unavoidable, developing strategies to combat stress will have significant impact on their emotional and physical well-​being and help build resilience.

12.6  SOCIAL CONNECTIVITY/​RELATIONSHIPS Social connectivity has been shown to be the greatest predictor of longevity.13 Healthy relationships allow for teens to develop mood regulation, improve self-​esteem, learn social etiquette, manage stress, develop resilience, and reduce risk of anxiety and depression. Teen experience with social connections varies widely. Family is the backbone for many throughout childhood. This changes during adolescence, a period of self-​exploration and potential detachment from family. This process is fundamental in their transformation to independent adulthood but can strain relationships between caregivers and siblings. Helping caregivers understand the developmental patterns of adolescence better will help reduce their frustration. Keeping open communication with daily connection, establishing a family meeting time that is a safe space for discussion, and developing clear family expectations and rules are some ways families with teens can navigate these years. Childhood friendships evolve, new friendships form, romantic interest in others develops, and some may engage in sexual relationships. Creating a safe space during visits to allow for screening for safety, discussion of safe sex practices, sexually transmitted infection risk, and contraceptive care is essential. When family planning is considered, teens need to be aware of the impact of their health including nutrition and activity on pregnancy and offspring.

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Face-​to-​face contact with friends may be replaced by connection through social media. While this is a valuable tool to keep connected with friends and family afar, it also has the potential for negative impact. Messages may or may not be positive and can lead to mood changes. Hurtful comments may be posted and popularity may be measured by the number of “likes”. Furthermore, teens may be exposed to content that is inappropriate for their age and development. Encourage caregivers to engage in discussion about their family rules on media usage and how to empower teens to develop their own healthy lifelong screen time habits. Keeping screens including phones away from sleeping areas and study space is one strategy. Social connectivity is an important part of teens’ development and should be encouraged through participation in school activities, sports, community, faith-​based organizations, or other safe outlets that allow face-​to-​face meetings.

12.7  SUBSTANCE USE PREVENTION Substance use avoidance or cessation is important to promote in teen years. Substance use may start as early as age 9 and should be screened for during the teen years through screening tools such as the Car, Relax, Alone, Forget, Friends, Trouble (CRAFFT) questionnaire and the Screening to Brief Intervention (S2BI) questionnaire. Three commonly used substances include alcohol, marijuana, and cigarettes14; vaping has also increased exponentially. Substance use can increase the risk of mental health issues, including depression and anxiety, and, conversely, prevents adequate treatment of mental health issues. It also affects brain development, increases risk-​ taking behaviors such as unprotected sex and impaired driving, and contributes to future heart disease, sleep deprivation and other chronic diseases.

12.8  CONCLUSION Adolescence is a critical time to encourage lifestyle change in order to promote lifelong healthy habits that can impact morbidity, mortality, and future adult life.

REFERENCES 1. McNeely C, Blanchard J. The teen years explained: A guide to healthy adolescent development. www.jhsph.edu/​research/​centers-​and-​institutes/​center-​for-​adolescent-​ health/​_​docs/​TTYE-​Guide.pdf. Published 2009. Accessed January 15, 2021. 2. Uddin SG, O’Connor KS, Ashman JJ. Physician office visits by children for well and problem-​focused care: United States, 2012. NCHS Data Brief. 2016;248:1–​8. https://​ pubmed.ncbi.nlm.nih.gov/​27227817/​. 3. Greer FR, Krebs NF, American Academy of Pediatrics Committee on Nutrition. Optimizing bone health and calcium intakes of infants, children, and adolescents. Pediatrics. 2006;117(2):578–​585. https://​doi.org/​10.1542/​peds.2005-​2822 4. Turner T, Hingle M. Evaluation of a mindfulness-​based mobile app aimed at promoting awareness of weight-​related behaviors in adolescents: A pilot study. JMIR Res Protoc. 2017;6(4):e67. https://​doi.org/​10.2196/​resprot.6695 5. Kenny U, O’Malley-​Keighran M-​P, Molcho M, Kelly C. Peer influences on adolescent body image: Friends or foes [published online ahead of print August 25, 2016]? J Adolesc Res. 2017;32(6):768–​799. https://​doi.org/​10.1177/​0743558416665478

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6. Wang J, Fielding-​Singh P. How food rules at home influence independent adolescent food choices. J Adolesc Health. 2018;63(2):219–​226. https://​doi.org/​10.1016/​ j.jadohealth.2018.02.010 7. Berge JM, MacLehose RF, Larson N, Laska M, Neumark-​Sztainer D. Family food preparation and its effects on adolescent dietary quality and eating patterns [published online ahead of print August 17, 2016]. J Adolesc Health. 2016;59(5):530–​536. https://​ doi.org/​10.1016/​j.jadohealth.2016.06.007 8. Weigh in: Talking to your children about weight health. www.apa.org/​obesity-​ guideline/​discussing-​weight/​talking-​to-​children.pdf. 9. Guthold R, Stevens GA, Riley LM, Bull FC. Global trends in insufficient physical activity among adolescents: a pooled analysis of 298 population-​ based surveys with 1.6 million participants [published online ahead of print November 21, 2019]. Lancet Child Adolesc Health. 2020;4(1):23–​35. https://​doi.org/​10.1016/​ S2352-​4642(19)30323-​2 10. Hirshkowitz M, Whiton K, Albert SM, et al. National Sleep Foundation’s sleep time duration recommendations: Methodology and results summary [published online ahead of print January 8, 2015]. Sleep Health. 2015;1(1):40–​43. https://​doi.org/​ 10.1016/​j.sleh.2014.12.010 11. Gooley JJ, Chamberlain K, Smith KA, et al. Exposure to room light before bedtime suppresses melatonin onset and shortens melatonin duration in humans. J Clin Endocrinol Metab. 2011;96(3):E463–​E472. https://​doi.org/​10.1210/​jc.2010-​2098 12. Wu D, Lewis ED, Pae M, Meydani SN. Nutritional modulation of immune function: Analysis of evidence, mechanisms, and clinical relevance [published online ahead of print 2018]. Front Immunol. 2019;9:3160. https://​doi.org/​10.3389/​ fimmu.2018.03160 13. Yang YC, Boen C, Gerken K, Li T, Schorpp K, Harris KM. Social relationships and physiological determinants of longevity across the human life span [published online ahead of January 4, 2016]. Proc Natl Acad Sci USA. 2016;113(3):578–​583. https://​ doi.org/​10.1073/​pnas.1511085112 14. Miech RA, Johnston LD, O’Malley PM, Bachman JG, Schulenberg JE. Monitoring the Future National Survey Results on Drug Use, 1975–​2016: Volume I, Secondary School Students. Institute for Social Research; 2017.

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Menstrual Health and Lifestyle Medicine Kranti Dasgupta, MD, DipABLM

Bloom Lifestyle Medicine, Alamo, CA, USA

Madeline Hardacre, MD, DipABLM Women’s Health Elevated, Reno, NV, USA

Michelle Tollefson, MD, FACOG, DipABLM, FACLM

Metropolitan State University of Denver, Denver, CO, USA Secretary, American College of Lifestyle Medicine 13.1 13.2

13.3

13.4 13.5

Introduction..................................................................................................216 Dysmenorrhea..............................................................................................216 13.2.1 Physical Activity............................................................................217 13.2.2 Nutrition........................................................................................217 13.2.3 Stress and Sleep.............................................................................218 13.2.4 Caffeine, Alcohol, and Tobacco.....................................................218 Premenstrual Syndrome...............................................................................218 13.3.1 Physical Activity............................................................................219 13.3.2 Nutrition........................................................................................219 13.3.3 Caffeine, Alcohol, and Tobacco.....................................................219 13.3.4 Stress and Sleep.............................................................................219 Uterine Fibroids...........................................................................................220 Conclusions..................................................................................................220

KEY POINTS • A low-​fat, high-​fiber plant-​based diet is recommended to decrease excess circulating serum estrogen, which improves menstrual symptoms in both primary dysmenorrhea and premenstrual syndrome and is associated with a reduced incidence of uterine fibroids. • Physical activity is beneficial in treating dysmenorrhea and premenstrual syndrome and should be emphasized.

DOI: 10.1201/9781003110682-14

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• Stress and sleep are linked to both dysmenorrhea and premenstrual syndrome. Stress management, relaxation techniques, and sleep optimization may play a role in management. • Caffeine and alcohol should be limited in dysmenorrhea. However, no clear association between caffeine or alcohol use and premenstrual syndrome has been found. Smokers develop worse symptoms of both dysmenorrhea and premenstrual syndrome, and tobacco cessation should be strongly encouraged. • Although some vitamins may show promise, particularly with vitamin D deficiency in fibroid disease, the suggested role of vitamin supplementation is unclear with sparse data and limited studies.

13.1  INTRODUCTION Menstrual symptoms such as pain, mood disorders, and bleeding irregularities are common concerns in women despite societal norms that prevent women from seeking care or admitting that they are a cause of impairment. In a European survey of more than 42,000 women, one in three women reported an inability to participate in daily activities due to menstrual symptoms. Even in family settings, less than half of those whose symptom severity required them to transfer a task to another family member disclosed the reason.1 Furthermore, evaluation and treatment of menstrual-​related symptoms represents substantial healthcare use and costs. There is encouraging evidence which suggests that a lifestyle-​oriented approach may yield beneficial results and can have tremendous impact on both daily functioning and healthcare expenditure.

13.2  DYSMENORRHEA Dysmenorrhea consists of recurrent painful lower abdominal cramping that occurs with menses, accompanied by symptoms such as nausea, vomiting, diarrhea, fatigue, back and/​or thigh pain, occurring just before and during menses. Primary dysmenorrhea (PD) is defined as painful menstruation occurring in the absence of pelvic pathology and will be the focus of this section. According to the American College of Obstetricians and Gynecologists (ACOG), dysmenorrhea is the most frequently reported menstrual disorder. Its prevalence is between 16% and 91% in reproductive age women, with 2–​29% describing severe pain.2 Risk factors of PD include early menarche, prolonged duration and severity of menstrual flow, having an affected first-​degree relative, as well as modifiable risk factors such as diet and stress. The mechanism underlying the pain of primary dysmenorrhea is complex and not fully understood. It is primarily thought to be due to excess endometrial production of prostaglandins,3 causing vasoconstriction, ischemia, and increased sensitivity of nerve endings,4 combined with abnormal myometrial contractility.5 Leukotrienes6 and vasopressin7 have also been implicated. Nonsteroidal anti-​inflammatory drugs (NSAIDs) are widely accepted as first-​line treatment for dysmenorrhea. One study found that 91.2% of women were taking analgesics for symptoms of PD, with 77.7% primarily self-​medicating.8 A Cochrane

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review concluded that while NSAIDs appear to be very effective treatment for dysmenorrhea, women should be aware of the risk of adverse effects.9 Particularly for women who may face many years of potential symptom management ahead, it may be prudent to prescribe lifestyle changes as initial or adjuvant therapy.

13.2.1 Physical Activity Physical activity has long been thought to help reduce the pain of PD. Although the exact mechanism for exercise-​induced analgesia remains elusive, it is believed a nonopioid mechanism such as endocannabinoids may be involved.10 In PD, it has also been proposed that the positive effect of exercise could be due to a progesterone-​ mediated reduction in prostaglandins and inflammatory cytokines.11 A systematic review and meta-​analysis of 11 randomized controlled trials utilizing physical activity interventions showed decreased pain intensity and duration in dysmenorrhea,12 while another study involving 23 trials and 2,302 women13 also concluded that exercise had a large effect. The same study demonstrated that heat had a moderate effect in reducing menstrual pain. Exercise confers many health benefits with little downside and heat application is similarly low risk; thus, both may be offered as potential alternatives and/​or adjuncts to analgesic medication.

13.2.2 Nutrition Adherence to a “snack-​pattern” diet (characterized by a high consumption of sugars, salty snacks, desserts, tea/​coffee, salt, fruit juices and added fat) is associated with an increased risk of dysmenorrhea among young women.14 Additional dietary risk factors include drinking cola beverages15,16 and eating meat has also been linked with PD.17 Barnard and colleagues18 found that a low-​fat, plant-​based diet (consisting of quantitatively unrestricted grains, vegetables, legumes, and fruits) was associated with increased sex-​hormone-​binding globulin levels and reductions in dysmenorrhea duration and intensity. The symptom effects were thought to be mediated by dietary influences on estrogen activity. As detailed in Chapter 1, the liver plays a key role in removing excess serum estrogen from the body. A clear link has been demonstrated between the high dietary fiber intake of vegetarians and decreased serum estrogen levels,17,19,20 with more widespread decreases seen in diets that are both low in fat and high in fiber.21,22 Estrogen stimulates endometrial growth, but additional research is needed to fully understand the potential clinical significance of diet’s impact on endometrial thickness and dysmenorrhea. Studies on the role of vitamin supplementation for PD are sparse. Vitamin E, an antioxidant, may have therapeutic potential as it prevents the peroxidation of phospholipids, the release of arachidonic acid, and thus conversion to prostaglandin.23,24 A single dose of vitamin D3 showed a significant reduction in pain and decreased NSAID use compared to a control group.25 Another study found a statistically significant reduction in PD pain intensity with calcium, but not with a calcium–​ vitamin D combination.26 Vitamin B1 and B6 supplementation has also been found

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to reduce pain in PD.27 A recent systematic review examining zinc supplementation28 found a reduction in PD pain severity when zinc was administered a few days before and during menstruation. Zinc exerts its effect by reducing the synthesis of both prostaglandins and inflammatory cytokines. Adolescents with dysmenorrhea showed benefit with omega-​3 fatty acid supplementation for PD,27,29 with supplementation being sufficient to decrease the NSAID rescue dose.30

13.2.3 Stress and Sleep Stress is a significant risk factor for the development of PD as stress levels directly correlate with pain intensity in PD. Stress occurring in the follicular phase of the preceding cycles had a stronger association with PD than stress occurring in the luteal phase of the preceding cycles. PD risk more than doubled in women with high stress compared to low stress in the preceding cycle.31 Women with PD were found to have increased severity of insomnia that correlated to severity of pain.32 In addition, decreased rapid eye movement (REM) sleep was seen in women with PD compared to controls,33 and menstrual pain correlated to poor sleep quality, lower alertness and daytime energy, as well as higher daytime sleepiness.34

13.2.4 Caffeine, Alcohol, and Tobacco Alcohol35 and a high-​caffeine diet are important risk factors for women with PD.36 Tobacco has also clearly been linked to PD and counseling cessation is beneficial. Smokers are more likely to have severe pain lasting longer than 2 days37 and experience chronic dysmenorrhea, with smokers who had initiated smoking by age 13 having 60% higher odds.38 Additionally, a significant dose–​response relationship between exposure to environmental tobacco smoke and an increased incidence of dysmenorrhea exists.39

13.3  PREMENSTRUAL SYNDROME Women commonly experience physical and emotional symptoms in the days preceding their menstrual cycle. In approximately 8% of women40 these symptoms result in a diagnosis of premenstrual syndrome (PMS). The diagnostic criteria for PMS, as defined by ACOG, involve one or more physical or affective symptoms that are associated with social, academic, or work dysfunction, occurring 1–​5 days prior to menses and over three consecutive menstrual cycles.41 Premenstrual dysphoric disorder, the most severe version of PMS, will be discussed in Chapter 27. The etiology of PMS likely involves variations in reproductive hormones and central neurotransmitters, but the unclear mechanism has caused difficulties defining the best therapeutic approach. Obesity,42 poor-​quality diet, tobacco use, and perceived stress have all been identified as risk factors of PMS, making lifestyle modifications a consideration in management. In fact, women provided with education on PMS and healthy lifestyle strategies

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experienced significant improvements in the emotional, behavioral, and physical components of PMS,43 demonstrating a potential opportunity for behavior change counseling.

13.3.1 Physical Activity Physical activity has long been recommended for PMS management. As with dysmenorrhea, exercise impacts circulating reproductive hormones.44 Two recent systematic reviews concluded that regular exercise, regardless of type, improved both physical and psychological symptoms.45,46 Regular yoga,47,48 Pilates,49 and swimming50 have all demonstrated benefits. Aerobic exercise produced significant reduction in physical symptoms51 and at least one study demonstrated the benefits of aerobic over anaerobic workouts.52

13.3.2 Nutrition Evidence suggests that “low-​quality” diets are associated with an increase in physical and emotional premenstrual symptoms.53,54,55 On the contrary, diets rich in whole grains56 have been found to be associated with a reduction of symptoms. Dietary carbohydrate, fiber,55,57 protein,58 and fat59 intake do not appear to play a significant role. Calcium and vitamin D seem to impact PMS symptoms. High calcium and vitamin D intake from food sources is inversely related to the development of PMS.60 Notably, this preventative effect was not seen with vitamin supplementation. Low calcium and vitamin D levels during the luteal phase were related to an exacerbation of PMS symptoms, whereas supplementation eliminated or reduced symptoms.61–​65 Various B vitamins and magnesium have been suggested to have benefit66,67 as supplements or natural food sources. A systematic review of vitamin B6 suggested that daily supplementation is beneficial.68 These studies are generally small with inconsistent findings, and while exact recommendations are scarce, the benefit of a high-​quality, nutrient-​ dense diet has many positive potential side effects.

13.3.3 Caffeine, Alcohol, and Tobacco Although limiting caffeine has been a long-​standing recommendation for PMS, no association was found between PMS and caffeine intake.69 Data on alcohol is inconsistent with a moderate increased risk reported in a systematic review,70 although a case control study71 found no strong association. Women who smoke are more likely to develop PMS. Counseling patients on tobacco cessation has numerous undisputed health benefits and should be part of all lifestyle focused strategies.

13.3.4 Stress and Sleep Both chronic stress and insufficient sleep play a role in PMS. Perceived stress is strongly associated with PMS72 and the use of relaxation methods designed to decrease sympathetic activity may be a useful adjuvant in management.73 Women with PMS

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commonly complain of sleep disturbances and describe poor-​quality sleep74 during the luteal phase. Another study demonstrated that women with severe PMS subjectively experienced poor-​quality sleep even in the absence of clear objective data on sleep studies.75 Unfortunately, studies are small and much remains unknown about the relationship between PMS and sleep.

13.4  UTERINE FIBROIDS Uterine leiomyomata (fibroids), a frequent cause of heavy bleeding, are benign tumors arising from the smooth muscle of the uterus. Cumulative incidence of fibroids by age 50 is approximately 80% and 70% in black and white women, respectively.76 Risk factors include age, premenopausal state, hypertension, family history, time since last birth, food additives, and soymilk consumption,77 as well as estrogen and progesterone exposure. Studies have shown an increased association between the development of fibroids and frequent red meat consumption, low green vegetable and fruit consumption,78 and frequent soybean or milk consumption.79 Vitamin D deficiency has been strongly associated with fibroids and supplementation appears to reduce the progression of fibroid disease.80–​87 Promising data may also extend the use of vitamin D beyond prevention to a possible therapeutic role. Given that exercise has positive effects on other hormone-​mediated tumors, it may also help prevent fibroids.88

13.5  CONCLUSIONS Lifestyle management through nutrition, physical activity, stress management, avoidance of alcohol and tobacco, and sleep optimization have been shown to be helpful in reducing symptoms of common menstrual disorders. Although high-​quality evidence is at times lacking, consideration should be given to incorporating lifestyle medicine in treatment plans for menstrual disorders. The positive side effects of a healthy lifestyle are known for benefits far beyond menstrual health.

REFERENCES 1. Schoep ME, Nieboer TE, van der Zanden M, Braat DDM, Nap AW. The impact of menstrual symptoms on everyday life: A survey among 42,879 women. Am J Obstet Gynecol. 2019;220(6):569.e1–​569.e7. https://​doi.org/​10.1016/​j.ajog.2019.02.048 2. Ju H, Jones M, Mishra G. The prevalence and risk factors of dysmenorrhea. Epidemiol Rev. 2014;36:104–​113. https://​doi.org/​10.1093/​epirev/​mxt009 3. Lundström V, Gréen K. Endogenous levels of prostaglandin F2alpha and its main metabolites in plasma and endometrium of normal and dysmenorrheic women. Am J Obstet Gynecol. 1978;130(6):640–​646. https://​doi.org/​10.1016/​ 0002-​9378(78)90320-​4 4. Barcikowska Z, Rajkowska-​Labon E, Grzybowska ME, Hansdorfer-​Korzon R, Zorena K. Inflammatory markers in dysmenorrhea and therapeutic options. Int J Environ Res Public Health. 2020;17(4):1191. Published Feb 13, 2020. https://​doi.org/​10.3390/​ ijerph17041191

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5. Hellman KM, Kuhn CS, Tu FF, et al. Cine MRI during spontaneous cramps in women with menstrual pain. Am J Obstet Gynecol. 2018;218(5):506.e1–​506.e8. https://​ doi.org/​10.1016/​j.ajog.2018.01.035 6. Dawood MY. Dysmenorrhea. Clin Obstet Gynecol. 1990;33(1):168–​178. https://​ doi.org/​10.1097/​00003081-​199003000-​00023 7. Strömberg P, Akerlund M, Forsling ML, Granström E, Kindahl H. Vasopressin and prostaglandins in premenstrual pain and primary dysmenorrhea. Acta Obstet Gynecol Scand. 1984;63(6):533–​538. https://​doi.org/​10.3109/​00016348409156715 8. Fernández-​ Martínez E, Onieva-​ Zafra MD, Parra-​ Fernández ML. Lifestyle and prevalence of dysmenorrhea among Spanish female university students. PLoS One. 2018;13(8):e0201894. Published Aug 10, 2018. https://​doi.org/​10.1371/​journal. pone.0201894 9. Marjoribanks J, Ayeleke RO, Farquhar C, Proctor M. Nonsteroidal anti-​inflammatory drugs for dysmenorrhoea. Cochrane Database Syst Rev. 2015;2015(7):CD001751. Published Jul 30, 2015. https://​doi.org/​10.1002/​14651858.CD001751.pub3 10. Koltyn KF, Brellenthin AG, Cook DB, Sehgal N, Hillard C. Mechanisms of exercise-​ induced hypoalgesia. J Pain. 2014;15(12):1294–​1304. https://​doi.org/​10.1016/​ j.jpain.2014.09.006 11. Kannan P, Cheung KK, Lau BW. Does aerobic exercise induced-​analgesia occur through hormone and inflammatory cytokine-​mediated mechanisms in primary dysmenorrhea?. Med Hypotheses. 2019;123:50–​54. https://​doi.org/​10.1016/​j.mehy.2018.12.011 12. Matthewman G, Lee A, Kaur JG, Daley AJ. Physical activity for primary dysmenorrhea: A systematic review and meta-​ analysis of randomized controlled trials. Am J Obstet Gynecol. 2018;219(3):255.e1–​255.e20. https://​doi.org/​10.1016/​ j.ajog.2018.04.001 13. Armour M, Smith CA, Steel KA, Macmillan F. The effectiveness of self-​care and lifestyle interventions in primary dysmenorrhea: A systematic review and meta-​analysis. BMC Complement Altern Med. 2019;19(1):22. Published Jan 17, 2019. https://​doi.org/​ 10.1186/​s12906-​019-​2433-​8 14. Najafi N, Khalkhali H, Moghaddam Tabrizi F, Zarrin R. Major dietary patterns in relation to menstrual pain: A nested case control study. BMC Womens Health. 2018;18(1):69. Published May 21, 2018.https://​doi.org/​10.1186/​s12905-​018-​0558-​4 15. Fernández-​ Martínez E, Onieva-​ Zafra MD, Parra-​ Fernández ML. Lifestyle and prevalence of dysmenorrhea among Spanish female university students. PLoS One. 2018;13(8):e0201894. Published Aug 10, 2018. https://​doi.org/​10.1371/​journal. pone.0201894 16. Hailemeskel S, Demissie A, Assefa N. Primary dysmenorrhea magnitude, associated risk factors, and its effect on academic performance: Evidence from female university students in Ethiopia. Int J Womens Health. 2016;8:489–​496. Published Sep 19, 2016. https://​doi.org/​10.2147/​IJWH.S112768 17. Shultz TD, Leklem JE. Nutrient intake and hormonal status of premenopausal vegetarian Seventh-​ day Adventists and premenopausal nonvegetarians. Nutr Cancer. 1983;4(4):247–​259. https://​doi.org/​10.1080/​01635588209513765 18. Barnard ND, Scialli AR, Hurlock D, Bertron P. Diet and sex-​hormone binding globulin, dysmenorrhea, and premenstrual symptoms. Obstet Gynecol. 2000;95(2):245–​250. https://​doi.org/​10.1016/​S0029-​7844(99)00525-​6 19. Goldin BR, Adlercreutz H, Dwyer JT, Swenson L, Warram JH, Gorbach SL. Effect of diet on excretion of estrogens in pre-​and postmenopausal women. Cancer Res. 1981;41(9 Pt 2):3771–​3773.

222

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20. Goldin BR, Adlercreutz H, Gorbach SL, et al. Estrogen excretion patterns and plasma levels in vegetarian and omnivorous women. N Engl J Med. 1982;307(25):1542–​1547. https://​doi.org/​10.1056/​NEJM198212163072502 21. Goldin BR, Woods MN, Spiegelman DL, et al. The effect of dietary fat and fiber on serum estrogen concentrations in premenopausal women under controlled dietary conditions. Cancer. 1994;74(3 Suppl):1125–​ 1131. https://​doi.org/​10.1002/​ 1097-​0142(19940801)74:3+3.0.CO;2-​5 22. Woods MN, Gorbach SL, Longcope C, Goldin BR, Dwyer JT, Morrill-​LaBrode A. Low-​fat, high-​fiber diet and serum estrone sulfate in premenopausal women. Am J Clin Nutr. 1989;49(6):1179–​1183. https://​doi.org/​10.1093/​ajcn/​49.6.1179 23. Ziaei S, Faghihzadeh S, Sohrabvand F, Lamyian M, Emamgholy T. A randomised placebo-​controlled trial to determine the effect of vitamin E in treatment of primary dysmenorrhoea. BJOG. 2001;108(11):1181–​1183. https://​doi.org/​10.1111/​ j.1471-​0528.2003.00279.x 24. Ziaei S, Zakeri M, Kazemnejad A. A randomised controlled trial of vitamin E in the treatment of primary dysmenorrhoea. BJOG. 2005;112(4):466–​469. https://​doi.org/​ 10.1111/​j.1471-​0528.2004.00495.x 25. Lasco A, Catalano A, Benvenga S. Improvement of primary dysmenorrhea caused by a single oral dose of vitamin D: Results of a randomized, double-​blind, placebo-​ controlled study. Arch Intern Med. 2012;172(4):366–​367. https://​doi.org/​10.1001/​ archinternmed.2011.715 26. Zarei S, Mohammad-​ Alizadeh-​ Charandabi S, Mirghafourvand M, Javadzadeh Y, Effati-​Daryani F. Effects of calcium-​vitamin D and calcium-​alone on pain intensity and menstrual blood loss in women with primary dysmenorrhea: A randomized controlled trial. Pain Med. 2017;18(1):3–​13. https://​doi.org/​10.1093/​pm/​pnw121 27. Proctor ML, Murphy PA. Herbal and dietary therapies for primary and secondary dysmenorrhoea. Cochrane Database Syst Rev. 2001;(3):CD002124. https://​doi.org/​ 10.1002/​14651858.CD002124 28. Nasiadek M, Stragierowicz J, Klimczak M, Kilanowicz A. the role of zinc in selected female reproductive system disorders. Nutrients. 2020;12(8):2464. Published Aug 16, 2020. https://​doi.org/​10.3390/​nu12082464 29. Harel Z, Biro FM, Kottenhahn RK, Rosenthal SL. Supplementation with omega-​ 3 polyunsaturated fatty acids in the management of dysmenorrhea in adolescents. Am J Obstet Gynecol. 1996;174(4):1335–​1338. https://​doi.org/​10.1016/​S00029378(96)70681-​6 30. Rahbar N, Asgharzadeh N, Ghorbani R. Effect of omega-​3 fatty acids on intensity of primary dysmenorrhea. Int J Gynaecol Obstet. 2012;117(1):45–​47. https://​doi.org/​ 10.1016/​j.ijgo.2011.11.019 31. Wang L, Wang X, Wang W, et al. Stress and dysmenorrhoea: A population based prospective study. Occup Environ Med. 2004;61(12):1021–​1026. https://​doi.org/​10.1136/​ oem.2003.012302 32. Woosley JA, Lichstein KL. Dysmenorrhea, the menstrual cycle, and sleep. Behav Med. 2014;40(1):14–​21. https://​doi.org/​10.1080/​08964289.2013.829020 33. Baker FC, Driver HS, Rogers GG, Paiker J, Mitchell D. High nocturnal body temperatures and disturbed sleep in women with primary dysmenorrhea. Am J Physiol. 1999;277(6):E1013–​E1021. https://​doi.org/​10.1152/​ajpendo.1999.277.6.E1013 34. Liu X, Chen H, Liu ZZ, Fan F, Jia CX. Early menarche and menstrual problems are associated with sleep disturbance in a large sample of Chinese adolescent girls. Sleep. 2017;40(9):10.1093/​sleep/​zsx107. https://​doi.org/​10.1093/​sleep/​zsx107

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35. Parazzini F, Tozzi L, Mezzopane R, Luchini L, Marchini M, Fedele L. Cigarette smoking, alcohol consumption, and risk of primary dysmenorrhea. Epidemiology. 1994;5(4):469–​472. https://​doi.org/​10.1097/​00001648-​199407000-​00016 36. Faramarzi M, Salmalian H. Association of psychologic and nonpsychologic factors with primary dysmenorrhea. Iran Red Crescent Med J. 2014;16(8):e16307. https://​ doi.org/​10.5812/​ircmj.16307 37. Harlow SD, Park M. A longitudinal study of risk factors for the occurrence, duration and severity of menstrual cramps in a cohort of college women [published correction appears in Br J Obstet Gynaecol 1997 Mar;104(3):386]. Br J Obstet Gynaecol. 1996;103(11):1134–​1142. https://​doi.org/​10.1111/​j.1471-​0528.1996.tb09597.x 38. Ju H, Jones M, Mishra GD. Smoking and trajectories of dysmenorrhoea among young Australian women. Tob Control. 2016;25(2):195–​202. https://​doi.org/​10.1136/​ tobaccocontrol-​2014-​051920 39. Chen C, Cho SI, Damokosh AI, et al. Prospective study of exposure to environmental tobacco smoke and dysmenorrhea. Environ Health Perspect. 2000;108(11):1019–​ 1022. https://​doi.org/​10.1289/​ehp.001081019 40. Deuster PA, Adera T, South-​Paul J. Biological, social, and behavioral factors associated with premenstrual syndrome. Arch Fam Med. 1999;8(2):122–​128. https://​doi.org/​ 10.1001/​archfami.8.2.122 41. ACOG Committee on Practice Bulletins—​ Gynecology. ACOG Practice Bulletin: No 15: Premenstrual syndrome. Obstet Gynecol. 2000 Apr;95(4): suppl 1–​9. PMID: 24829972. 42. Bertone-​Johnson ER, Hankinson SE, Willett WC, Johnson SR, Manson JE. Adiposity and the development of premenstrual syndrome. J Womens Health (Larchmt). 2010;19(11):1955–​1962. https://​doi.org/​10.1089/​jwh.2010.2128 43. Bastani F, Hashemi S. Effects of a web based lifestyle education on general health and severity of the symptoms of premenstrual syndrome (PMS) among female students: A randomized controlled trial. Procedia Soc Behav Sci. 2012;46:3356–​3362. https://​ doi.org/​10.1016/​j.sbspro.2012.06.066 44. Santoro N, Filicori M, Crowley WF Jr. Hypogonadotropic disorders in men and women: Diagnosis and therapy with pulsatile gonadotropin-​ releasing hormone. Endocr Rev. 1986;7(1):11–​23. https://​doi.org/​10.1210/​edrv-​7-​1-​11 45. Yesildere Saglam H, Orsal O. Effect of exercise on premenstrual symptoms: A systematic review. Complement Ther Med. 2020;48:102272. https://​doi.org/​10.1016/​ j.ctim.2019.102272 46. Pearce E, Jolly K, Jones LL, Matthewman G, Zanganeh M, Daley A. Exercise for premenstrual syndrome: A systematic review and meta-​analysis of randomised controlled trials. BJGP Open. 2020;4(3):bjgpopen20X101032. Published Aug 25, 2020. https://​ doi.org/​10.3399/​bjgpopen20X101032 47. Tsai SY. Effect of yoga exercise on premenstrual symptoms among female employees in Taiwan. Int J Environ Res Public Health. 2016;13(7):721. Published 2016 Jul 16. https://​doi.org/​10.3390/​ijerph13070721 48. Ghaffarilaleh G, Ghaffarilaleh V, Sanamno Z, Kamalifard M. Yoga positively affected depression and blood pressure in women with premenstrual syndrome in a randomized controlled clinical trial. Complement Ther Clin Pract. 2019;34:87–​92. https://​doi.org/​ 10.1016/​j.ctcp.2018.11.007 49. Çitil ET, Kaya N. Effect of pilates exercises on premenstrual syndrome symptoms: A quasi-​experimental study [published online ahead of print, 2020 Nov 24]. Complement Ther Med. 2020;57:102623. https://​doi.org/​10.1016/​j.ctim.2020.102623

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50. Maged AM, Abbassy AH, Sakr HRS, et al. Effect of swimming exercise on premenstrual syndrome. Arch Gynecol Obstet. 2018;297(4):951–​959. https://​doi.org/​10.1007/​ s00404-​018-​4664-​1 51. Mohebbi Dehnavi Z, Jafarnejad F, Sadeghi Goghary S. The effect of 8 weeks aerobic exercise on severity of physical symptoms of premenstrual syndrome: A clinical trial study. BMC Womens Health. 2018;18(1):80. Published May 31, 2018. https://​doi.org/​ 10.1186/​s12905-​018-​0565-​5 52. Umar U. The effect of anaerobic and aerobic exercise on endurance and non-​endurance athletes on premenstrual syndrome (PMS). IOP Conference Series: Materials Science and Engineering. 2017;180: 012183. https://​doi.org/​10.1088/​1757-​899X/​180/​ 1/​012183 53. Hashim MS, Obaideen AA, Jahrami HA, et al. Premenstrual syndrome is associated with dietary and lifestyle behaviors among university students: A cross-​sectional study from Sharjah, UAE. Nutrients. 2019;11(8):1939. Published Aug 17, 2019. https://​ doi.org/​10.3390/​nu11081939 54. Isgin-​Atici K, Kanbur N, Akgül S, Buyuktuncer Z. Diet quality in adolescents with premenstrual syndrome: A cross-​ sectional study. Nutr Diet. 2020;77(3):351–​358. https://​doi.org/​10.1111/​1747-​0080.12515 55. Houghton SC, Manson JE, Whitcomb BW, et al. Carbohydrate and fiber intake and the risk of premenstrual syndrome. Eur J Clin Nutr. 2018;72(6):861–​870. https://​doi.org/​ 10.1038/​s41430-​017-​0076-​8 56. Esmaeilpour M, Ghasemian S, Alizadeh M. Diets enriched with whole grains reduce premenstrual syndrome scores in nurses: an open-​label parallel randomised controlled trial. Br J Nutr. 2019;121(9):992–​1001. https://​doi.org/​10.1017/​S000711 4519000333 57. Gold EB, Bair Y, Block G, et al. Diet and lifestyle factors associated with premenstrual symptoms in a racially diverse community sample: Study of women’s health across the nation (SWAN) [published correction appears in J Womens Health (Larchmt). 2007 Jul-​Aug;16(6):934]. J Womens Health (Larchmt). 2007;16(5):641–​656. https://​ doi.org/​10.1089/​jwh.2006.0202 58. Houghton SC, Manson JE, Whitcomb BW, et al. Protein intake and the risk of premenstrual syndrome. Public Health Nutr. 2019;22(10):1762–​1769. https://​doi.org/​ 10.1017/​S1368980018004019 59. Houghton SC, Manson JE, Whitcomb BW, et al. Intake of dietary fat and fat subtypes and risk of premenstrual syndrome in the nurses. Health Study II. Br J Nutr. 2017;118(10):849–​857. https://​doi.org/​10.1017/​S0007114517002690 60. Bertone-​Johnson ER, Hankinson SE, Bendich A, Johnson SR, Willett WC, Manson JE. Calcium and vitamin D intake and risk of incident premenstrual syndrome. Arch Intern Med. 2005;165(11):1246–​1252. https://​doi.org/​10.1001/​archinte.165.11.1246 61. Abdi F, Ozgoli G, Rahnemaie FS. A systematic review of the role of vitamin D and calcium in premenstrual syndrome [published correction appears in Obstet Gynecol Sci. 2020 Mar;63(2):213]. Obstet Gynecol Sci. 2019;62(2):73–​86. https://​doi.org/​10.5468/​ ogs.2019.62.2.73 62. Shobeiri F, Araste FE, Ebrahimi R, Jenabi E, Nazari M. Effect of calcium on premenstrual syndrome: A double-​blind randomized clinical trial. Obstet Gynecol Sci. 2017;60(1):100–​105. https://​doi.org/​10.5468/​ogs.2017.60.1.100 63. Thys-​Jacobs S, Starkey P, Bernstein D, Tian J. Calcium carbonate and the premenstrual syndrome: Effects on premenstrual and menstrual symptoms. Premenstrual Syndrome Study Group. Am J Obstet Gynecol. 1998;179(2):444–​452. https://​doi.org/​ 10.1016/​S0002-​9378(98)70377-​1

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64. Bahrami A, Avan A, Sadeghnia HR, et al. High dose vitamin D supplementation can improve menstrual problems, dysmenorrhea, and premenstrual syndrome in adolescents. Gynecol Endocrinol. 2018;34(8):659–​663. https://​doi.org/​10.1080/​ 09513590.2017.1423466 65. Tartagni M, Cicinelli MV, Tartagni MV, et al. Vitamin D supplementation for premenstrual syndrome-​related mood disorders in adolescents with severe hypovitaminosis D. J Pediatr Adolesc Gynecol. 2016;29(4):357–​361. https://​doi.org/​10.1016/​j.jpag. 2015.12.006 66. Ebrahimi E, Khayati Motlagh S, Nemati S, Tavakoli Z. Effects of magnesium and vitamin b6 on the severity of premenstrual syndrome symptoms. J Caring Sci. 2012;1(4):183–​189. Published Nov 22, 2012. doi:10.5681/​jcs.2012.026 67. Retallick-​ Brown H, Blampied N, Rucklidge JJ. A pilot randomized treatment-​ controlled trial comparing vitamin B6 with broad-​spectrum micronutrients for premenstrual syndrome. J Altern Complement Med. 2020;26(2):88–​97. https://​doi.org/​ 10.1089/​acm.2019.0305 68. Wyatt KM, Dimmock PW, Jones PW, Shaughn O’Brien PM. Efficacy of vitamin B-​ 6 in the treatment of premenstrual syndrome: Systematic review. BMJ. 1999;318(7195):1375–​1381. https://​doi.org/​10.1136/​bmj.318.7195.1375 69. Purdue-​Smithe AC, Manson JE, Hankinson SE, Bertone-​Johnson ER. A prospective study of caffeine and coffee intake and premenstrual syndrome. Am J Clin Nutr. 2016;104(2):499–​507. https://​doi.org/​10.3945/​ajcn.115.127027 70. Fernández MDM, Saulyte J, Inskip HM, Takkouche B. Premenstrual syndrome and alcohol consumption: A systematic review and meta-​ analysis. BMJ Open. 2018;8(3):e019490. Published Apr 16, 2018. https://​doi.org/​10.1136/​bmjopen2017-​019490 71. Bertone-​Johnson ER, Hankinson SE, Johnson SR, Manson JE. Timing of alcohol use and the incidence of premenstrual syndrome and probable premenstrual dysphoric disorder. J Womens Health (Larchmt). 2009;18(12):1945–​1953. https://​doi.org/​10.1089/​ jwh.2009.1468 72. Del Mar Fernández M, Regueira-​Méndez C, Takkouche B. Psychological factors and premenstrual syndrome: A Spanish case-​control study. PLoS One. 2019;14(3):e0212557. Published Mar 6, 2019 https://​doi.org/​10.1371/​journal.pone.0212557 73. Dvivedi J, Kaur H, Dvivedi S. Effect of 1 week ‘61-​points relaxation training’ on cold pressor test induced stress in premenstrual syndrome. Indian J Physiol Pharmacol. 2008;52(3):262–​266. 74. Nicolau ZFM, Bezerra AG, Polesel DN, et al. Premenstrual syndrome and sleep disturbances: Results from the Sao Paulo Epidemiologic Sleep Study. Psychiatry Res. 2018;264:427–​431. https://​doi.org/​10.1016/​j.psychres.2018.04.008 75. Baker FC, Kahan TL, Trinder J, Colrain IM. Sleep quality and the sleep electroencephalogram in women with severe premenstrual syndrome. Sleep. 2007;30(10):1283–​ 1291. https://​doi.org/​10.1093/​sleep/​30.10.1283 76. Baird DD, Dunson DB, Hill MC, Cousins D, Schectman JM. High cumulative incidence of uterine leiomyoma in black and white women: ultrasound evidence. Am J Obstet Gynecol. 2003;188(1):100–​107. https://​doi.org/​10.1067/​mob.2003.99 77. Stewart EA, Cookson CL, Gandolfo RA, Schulze-​Rath R. Epidemiology of uterine fibroids: A systematic review. BJOG. 2017;124(10):1501–​1512. https://​doi.org/​ 10.1111/​1471-​0528.14640 78. Chiaffarino F, Parazzini F, La Vecchia C, Chatenoud L, Di Cintio E, Marsico S. Diet and uterine myomas. Obstet Gynecol. 1999;94(3):395–​398. https://​doi.org/​10.1016/​ S0029-​7844(99)00305-​1

226

226

Kranti Dasgupta et al.

79. Gao M, Wang H. Frequent milk and soybean consumption are high risks for uterine leiomyoma: A prospective cohort study. Medicine (Baltimore). 2018;97(41):e12009. https://​doi.org/​10.1097/​MD.0000000000012009 80. Parazzini F, Di Martino M, Candiani M, Viganò P. Dietary components and uterine leiomyomas: A review of published data. Nutr Cancer. 2015;67(4):569–​579. https://​ doi.org/​10.1080/​01635581.2015.1015746 81. Baird DD, Hill MC, Schectman JM, Hollis BW. Vitamin d and the risk of uterine fibroids. Epidemiology. 2013 May;24(3):447–​ 53. PMID: 23493030; PMCID: PMC5330388.https://​doi.org/​10.1097/​EDE.0b013e31828acca0 82. Ciebiera M, Włodarczyk M, Ciebiera M, Zaręba K, Łukaszuk K, Jakiel G. Vitamin D and uterine fibroids-​review of the literature and novel concepts. Int J Mol Sci. 2018;19(7):2051. Published Jul 14, 2018. https://​doi.org/​10.3390/​ijms19072051 83. Ciavattini A, Delli Carpini G, Serri M, et al. Hypovitaminosis D and “small burden” uterine fibroids: Opportunity for a vitamin D supplementation. Medicine (Baltimore). 2016;95(52):e5698. https://​doi.org/​10.1097/​MD.0000000000005698 84. Arjeh S, Darsareh F, Asl ZA, Azizi Kutenaei M. Effect of oral consumption of vitamin D on uterine fibroids: A randomized clinical trial. Complement Ther Clin Pract. 2020;39:101159. https://​doi.org/​10.1016/​j.ctcp.2020.101159 85. Ciebiera M, Ali M, Prince L, et al. The evolving role of natural compounds in the medical treatment of uterine fibroids. J Clin Med. 2020;9(5):1479. Published May 14, 2020. https://​doi.org/​10.3390/​jcm9051479 86. Corachán A, Ferrero H, Escrig J, et al. Long-​term vitamin D treatment decreases human uterine leiomyoma size in a xenograft animal model. Fertil Steril. 2020;113(1):205. e1–​216.e4. https://​doi.org/​10.1016/​j.fertnstert.2019.09.018 87. Ciebiera M, Ali M, Zgliczyńska M, Skrzypczak M, Al-​Hendy A. Vitamins and uterine fibroids: Current data on pathophysiology and possible clinical relevance. Int J Mol Sci. 2020;21(15):5528. Published Aug 1, 2020. https://​doi.org/​10.3390/​ijms21155528 88. Baird DD, Dunson DB, Hill MC, Cousins D, Schectman JM. Association of physical activity with development of uterine leiomyoma. Am J Epidemiol. 2007;165(2):157–​ 163. https://​doi.org/​10.1093/​aje/​kwj363

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Women’s Sexual Health and Lifestyle Medicine Megan Alexander, MS

Boston University School of Medicine, Boston, MA, USA

Shannon Worthman, BS

American College of Lifestyle Medicine, Chesterfield, MO, USA

Rashmi Kudesia, MD, MSc, FACOG, DipABLM CCRM Fertility Houston/​Houston Methodist Hospital, Houston, TX, USA

Michelle Tollefson, MD, FACOG, DipABLM, FACLM, Professor

Metropolitan State University of Denver, Denver, CO, USA American College of Lifestyle Medicine Secretary 14.1 14.2

14.3

Introduction..................................................................................................228 Lifestyle Medicine and Sexual Health.........................................................230 14.2.1 Nutrition........................................................................................230 14.2.2 Physical Activity............................................................................230 14.2.3 Sleep..............................................................................................231 14.2.4 Stress..............................................................................................231 14.2.5 Positive Social Connections..........................................................232 14.2.6 Substance Use................................................................................233 14.2.6.1 Alcohol.........................................................................233 14.2.6.2 Cigarettes......................................................................233 14.2.6.3 Cannabis/​Marijuana......................................................233 Conclusion...................................................................................................233

KEY POINTS • Sexual health is linked to overall health, with sexual dysfunction being common. A Lifestyle Medicine approach can support sexual health through various mechanisms, including improved vascular health and psychological well-​being. DOI: 10.1201/9781003110682-15

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• A plant-​ predominant, antioxidant-​ rich dietary pattern and regular exercise support key measures of sexual health. • Acute and chronic stress, as well as depression, can negatively impact sexual health. Mindfulness-​based stress reduction strategies hold particular promise for treatment. • Sleep quality, social support, intimacy, affection and substance use are intricately linked to sexual desire, satisfaction, and function. • Clinicians should discuss sexual health with patients in a highly individualized way. A multidisciplinary team may be best positioned to help patients address the complex relationship between lifestyle and sexual health.

14.1  INTRODUCTION Sexual health is defined by the World Health Organization as: a state of physical, emotional, mental and social well-​being in relation to sexuality; it is not merely the absence of disease, dysfunction or infirmity. Sexual health requires a positive and respectful approach to sexuality and sexual relationships, as well as the possibility of having pleasurable and safe sexual experiences, free of coercion, discrimination and violence.1

Thus, the factors impacting sexual health and sexuality are vast, and best conceptualized in a biopsychosocial model.2 Variables as diverse as access to health care, mental and physical health, medication use, gender identity and expression, partner availability and relationship quality, lived experiences, cultural norms, religion, and more may all play a role. The sexual experience itself is more complex than the classic four-​step, linear model of progression through the physical stages of excitement, plateau, orgasm, and resolution.3 A more complete model includes desire, emotional and physical satisfaction, emotional intimacy, and biologic and psychological factors, while recognizing many nonlinear paths to arousal.2,4 Because women place varying values on each domain, discussions around healthy sexuality are necessarily highly individualized. Despite this complexity, research evaluating women’s perceived sexual functioning notably almost entirely employs the Female Sexual Function Index (FSFI), which assesses the domains of desire, arousal, lubrication, orgasm, pain, and satisfaction.5 Like most such instruments, it is helpful but imperfect; it does not directly assess emotional intimacy or sex-​related distress, and cannot speak about larger psychosocial forces at play. Sexual dysfunction is common, and frequently related to general health. An estimated 43% of women, irrespective of age, report trouble in at least one FSFI domain.6–​9 Dysfunction is more common in women with chronic health problems, including metabolic syndrome, hypertension, dyslipidemia, coronary heart disease, diabetes, overweight and obese body mass indices (BMI), anxiety, and depression. 10–​19 At all ages, individuals with higher self-​reported health are more likely to report an interest in sex.15,20,21 General health influences sexual function in myriad ways. Vascular compromise, for example, is well known to cause erectile dysfunction in men,22,23 but women can

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also experience decreased vaginal lubrication24 and engorgement of the vagina and clitoris.25 Metabolic syndrome, obesity, and atherosclerosis have all been associated with inflammatory and pro-​oxidant markers, decreased nitric oxide bioavailability, and subsequent narrowing of blood vessels or insufficient dilation despite arousal, blunting the sexual response24,26–​28 (Figure 14.1). From a psychological standpoint, positive mood and body image have been associated with improved sexual health29 and body shame with decreased arousal and orgasm.30 Interestingly, the link between body image and sexual desire has been found to be unrelated to BMI, with body size itself being less important than how one feels about their body,31 though healthy lifestyle choices can positively impact both mood and body image.32–​36 Taken together, these mechanisms suggest that all women, and perhaps especially those with chronic cardiometabolic and psychological conditions,10–​17,19 may experience improved sexual health through positive lifestyle behavior modifications. Although an in-​depth discussion of sexual dysfunction is beyond the scope of this

FIGURE 14.1  Healthy lifestyle behaviors can support female sexual function. Healthy lifestyle behaviors can improve vascular health, promoting physiologic genital arousal and vaginal lubrication, through the outlined mechanisms. Lifestyle behaviors can also influence other domains of female sexual function, such as desire, orgasm, lack of pain, and satisfaction (mechanisms not specified). Additionally, adoption of healthy lifestyle behaviors may prevent and reverse many cardiometabolic diseases, further contributing to improved female sexual function. Other key influences on sexual health include mood and body image (not pictured). SNS = Sympathetic nervous system.

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chapter, the following sections will focus on an evidence-​based lifestyle approach to sexual health, detailing relevant benefits from Lifestyle Medicine interventions.

14.2  LIFESTYLE MEDICINE AND SEXUAL HEALTH 14.2.1 Nutrition Dietary composition impacts sexual health indirectly through the aforementioned association between cardiometabolic disease and sexual dysfunction, but also directly as evidenced by research on dietary patterns, specific foods, and individual nutrients. The Mediterranean diet (MD) is the most widely studied in this context, with its emphasis on vegetables, fruits, nuts, whole grains, legumes, olive oil, and fish, making it high in antioxidants and low in saturated fat and refined carbohydrates. Adherence to a MD results in better sexual function in a dose-​dependent manner, regardless of menopausal and metabolic syndrome status. 10,37,38 Other dietary approaches are less well-​studied. Diets high in plants and whole foods, or that reverse cardiometabolic disease, could provide comparable benefits as seen with the MD, but research is needed. In contrast, the standard American diet is indirectly linked to sexual dysfunction, as its predominant components –​processed foods, refined carbohydrates, sodium, and saturated fat-​containing animal products –​are extensively associated with metabolic syndrome, cardiovascular disease, and elevated BMI.39–​41 Specific dietary components have also been investigated. Low sodium intake enhances the ability of vessels to dilate as needed for vaginal lubrication.26 Consumption of soy, a phytoestrogen, has been associated with increased vaginal blood flow and lubrication and decreased dyspareunia in postmenopausal women.42–​45 Apples, watermelon, and cocoa have also been linked to enhanced vascular and sexual health. 42,45–​50 Meanwhile, vitamin D and iron deficiencies are risk factors of sexual dysfunction through hormonal and fatigue-​mediated mechanisms, respectively, and resolution of these deficiencies may well be therapeutic.51–​54 In summary, a diet rich in plants and whole foods holds potential for improving sexual health.

14.2.2 Physical Activity Exercise promotes sexual health over the short and long terms. Exercise-​mediated activation of the sympathetic nervous system promotes prompt physiological arousal. Erotic stimulus after exercise results in enhanced vaginal blood flow.31 Exercise also directly improves mood via endorphin and serotonin release, with effects outlasting the duration of intervention.32,33 In a more intermediate-​term fashion, exercise positively impacts a variety of other hormones with links to sexual function, such as estrogen, testosterone, prolactin, oxytocin, and cortisol.55 For example, studies in premenopausal women have shown exercise to increase serum estradiol and testosterone, with subsequent sexual benefits.56–​58 However, it is important to note that excessive exercise, especially if associated with low body weight, can result in hypogonadotropic hypogonadism and diminished circulating estrogen levels.59 Over time, as with dietary interventions, physical activity can enhance sexual response via improving vascular and psychological health. Regular physical activity

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decreases the risk of hypertension, atherosclerosis, and arterial stiffening, and supports nitric oxide bioavailability.57,60–​62 Body image is also generally more positive in those who exercise regularly.34 Self-​reported outcomes similarly support the benefits of physical activity, with greater likelihood of being sexually active,63,64 increased coital frequency,65 and decreased sexual dysfunction.65–​68 While all women stand to benefit from the effects of physical activity on sexual health, there are particular studied benefits for certain populations, including those with elevated BMI and a goal of weight loss, women with obesity and infertility, women in the postpartum and postmenopausal periods, and those on anti-​depressants (see Supplementary Material). In summary, physical activity holds promise as a treatment modality for sexual dysfunction. Suggested aerobic activity levels follow recommendations from the World Health Organization (150–​ 300 minutes weekly of moderate-​ intensity, or 75–​150 minutes of vigorous-​intensity activity, or an equivalent combination),15,69–​72 though older women might see benefits with as little as walking at least 1–​2 times weekly.15 Pelvic floor muscle training, particularly for those with pelvic floor dysfunction, can improve sexual function in women across the life course.73–​75 Although data is limited to inform the choice of how to exercise, interventional studies support structured mind-​body programs based on the Pilates or yoga traditions as beneficial to sexual health.76–​79

14.2.3 Sleep Both quantity and quality of sleep contribute to sexual desire, satisfaction, and function, although research into this interplay has primarily focused on postmenopausal and postpartum women. Both of these life stages feature complex and simultaneous sudden changes in sleep patterns, stress levels, mood and mental health, body image, genital physiology, and energy levels, and are therefore difficult to study. However, the Women’s Health Initiative demonstrated that in postmenopausal women, short sleep duration (10 mL (without a cyst or dominant follicle) in either ovary.12

15.2.3 Management of PCOS Conventional pharmacotherapeutic management of PCOS involves hormonal contraception, metformin, anti-​androgen therapy, clomiphene citrate or letrozole based on goals of therapy. A full discussion of these agents is not the focus of this chapter, and readers are directed to current major clinical guidelines for the diagnostic testing and pharmaceutical management guidelines.1,2,9,10,13

15.2.4 Lifestyle Management of PCOS Therapeutic lifestyle modification is a mainstay of PCOS management. Most guidelines describe weight loss as the primary therapy in PCOS, especially given that elevated body mass index (BMI) is seen in 50–​80% of women with PCOS. As little as 5% body weight reduction can restore regular menses and improve response to ovulation-​inducing and fertility medications.14 Healthy lifestyle, even in the absence of weight loss, still benefits PCOS patients (especially those with normal BMI) improving the quality of life and overall health.10 In a systematic review of six studies15 (three studies used exercise alone and another three used multicomponent therapy including diet, exercise, and behavioral management), lifestyle intervention was significantly better than conventional treatment for total testosterone, hirsutism score, weight, waist circumference, waist-​hip-​ratio (WHR), fasting insulin, oral glucose tolerance test, insulin, and percent weight change. Another review of 15 studies comparing either exercise alone or combined therapies found statistically significant improvements in free androgen index (FAI), weight, and BMI in women with PCOS compared with no or minimal intervention.16

15.2.5 Nutrition A recent meta-​analysis of 19 studies showed that a high-quality diet was significantly related to improvements in homeostasis model assessment of insulin resistance (HOMA-​IR), fasting insulin, fasting plasma glucose, BMI, weight, and waist circumference in PCOS patients.17 In this review, Mediterranean and calorie-​restricted diets were found to be particularly effective in reducing BMI and body weight. The dietary approaches to stop hypertension (DASH) diet was found effective in decreasing fasting plasma glucose, insulin, and HOMA-​IR. Calorie-​restricted diets were effective for decreasing waist circumference. Dietary interventions resulted in a greater decrease in BMI than metformin. Both low-​carbohydrate and low-​fat diets were more effective than metformin in reducing BMI. Additionally, diet worked more quickly than metformin, with obvious advantages within 12 weeks.17 15.2.5.1 Macronutrients Gonzalez et al. demonstrated higher oxidative stress (leukocyte reactive oxygen species generation) and higher inflammation (activated tumor necrosis factor-​alpha

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[TNFα], and C-​reactive protein [CRP]) in response to saturated fat ingestion (dairy heavy whipped cream) in women with PCOS independent of BMI, indicating that inflammation and oxidative stress were linked to IR in these patients.18,19 In another study of women with PCOS, the serum leptin concentration positively correlated with the intake of total fat, total cholesterol, saturated fatty acids, and monounsaturated fatty acids (MUFA), whereas the serum ghrelin concentration correlated in an inverse manner with the intake of total fat, and higher HOMA-​IR with total dietary fat intake.20 In another study of women with PCOS, 21 those with IR consumed less fiber, less magnesium, and had a greater glycemic load than those without IR. Fiber intake of women with PCOS was negatively correlated with IR, fasting insulin, glucose tolerance, testosterone, and dehydroepiandrosterone sulfate. Magnesium intake was negatively correlated with IR, CRP, and testosterone, but positively correlated with high-​density lipoprotein (HDL) cholesterol. Fiber intake accounted for a large proportion of the variance observed in IR. 15.2.5.2 Food Types A prospective 8-​week ad libitum low-​starch/​low-​dairy dietary intervention resulted in weight loss, improved insulin sensitivity, and reduced testosterone in overweight/​ obese women with PCOS.22 There was statistically significant improvement in waist circumference, waist to height ratio, fasting insulin, 2-​hour insulin, HOMA-​IR, total testosterone, free testosterone, and hirsutism scores. In a small randomized controlled trial (RCT), a low glycemic index, nutritionally balanced pulse-​based diet containing lentils, beans, split peas, and chickpeas without a calorie-​restricted protocol was studied for 16 weeks.23 All women participated in aerobic exercise (minimum 5 days/​ week, 45 minutes/​day) and received monthly health counseling about PCOS and the benefits of lifestyle modification. Follicle numbers per ovary, ovarian volume, free androgen index, intermenstrual intervals, and BMI all decreased, and insulin sensitivity increased at 16 weeks. These benefits were maintained at 6 months post-​ intervention despite weight regain, but not at 12 months.

15.2.6 Exercise A meta-​analysis of 19 studies on PCOS found an increase in oxygen use during exercise, decrease in HOMA-​IR, and decrease in waist circumference as a result of vigorous-​intensity exercise.24 Another meta-​analysis found that exercise improved lipid profiles and decreased waist circumference, systolic blood pressure, and fasting insulin.25 The impact of exercise interventions on reproductive function remains unclear, although this small RCT did find modestly improved menstrual cycle pattern with exercise, the effect of which was enhanced by adding metformin.26

15.2.7 Sleep Sleep disturbances, including obstructive sleep apnea (OSA), occur more frequently among women with PCOS compared to controls.27 Current clinical guidelines recommend screening for OSA symptoms in overweight/​obese women with PCOS.10 Sleep problems are also reported to occur more commonly in lean PCOS patients compared

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with healthy non-​PCOS controls. The association of PCOS with sleep disturbances is possibly bidirectional. Hyperandrogenemia and possible changes in cortisol and melatonin secretion might be implicated in poor sleep patterns in PCOS.

15.2.8 Social Connection Multiple studies have explored the effects of PCOS on patients’ social relationships and interactions. Patients frequently report perceiving lack of self-​esteem. Reports describe patients feeling a sense of “not normal” or “unfeminine” due to lack of periods.28 Also, hirsutism, overweight, or sense of “too much masculine hormones” reportedly negatively affects their perceptions of attractiveness, sexual relationships, and ability to make social contacts.29,30 There are also myriad reports of marital relationships being negatively affected by fertility struggles.31 Conversely, support group intervention, peer-​led programs that provide opportunities to share and identify with other women going through similar hurdles, and community-​based resources help women with PCOS feel empowered and impact positive self-​ management behaviors.32

15.2.9 Cessation of Risky Substances In one small study, incidence of MetS was significantly higher in tobacco smokers with PCOS compared to nonsmokers and non-​PCOS smokers, even when adjusted for BMI.33 In another prospective observational study of lean PCOS women, diastolic blood pressure, white blood cell count, homocysteine, insulin, and glucose levels were all higher in people who smoked tobacco compared with nonsmokers.34 Smoking is associated with higher free androgen levels in PCOS patients.35 Smoking cessation counseling and interventions are paramount for PCOS patients to minimize their cardiometabolic risks and also to optimize their fertility. Similarly, PCOS patients, even if they don’t have MetS, may still have a high risk for hepatic steatosis,36 and, thus, should be counseled to limit alcohol, especially if this is part of a multicomponent weight loss intervention. Illicit drugs including heroin and marijuana have both been clinically associated with hypothalamic amenorrhea and hypogonadism in humans. Cocaine and methamphetamine have been studied in animal models to affect ovulatory function. For these and other reasons, it is prudent to counsel PCOS patients to refrain from use of these substances.

15.2.10 Stress Management A small RCT studied an 8-​week mindfulness stress management program and found statistically significant reductions in stress, depressive and anxiety symptoms, and in salivary cortisol concentrations, along with an increase in life satisfaction and quality of life scores in the intervention group.37 In another small RCT women with BMI ≥ 25 kg/​m2 were randomized to 8 weeks of mindfulness-​based stress reduction (MBSR) or health education and followed for 16 weeks. The MBSR group demonstrated significantly decreased perceived stress at 16 weeks, and significant reductions in fasting glucose at 8 weeks and 16 weeks compared to baseline.38

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15.2.11 Conclusion Lifestyle therapy, described above in the context of the pillars of Lifestyle Medicine, is a mainstay of PCOS management.

15.3  ENDOMETRIOSIS 15.3.1 Introduction Endometriosis is a complex, chronic, inflammatory, estrogen-​ dependent disease that develops when endometrial tissue grows outside of the uterine cavity. These implants or nodules of tissue can be found throughout the pelvis, affecting multiple organs. The lesions become inflamed and can cause chronic, severe, and debilitating pain: cyclical or noncyclical in nature. Studies have shown that it may take some women up to a decade to be diagnosed with endometriosis.39,40 The American College of Obstetrics and Gynecology (ACOG) and the American Society of Reproductive Medicine (ASRM) now endorse clinical diagnosis based on symptomatology. Endometriosis affects 10–​14% of women of reproductive age. The average age of diagnosis is 28 years.43 For this reason, not only gynecologists but also pediatricians, emergency department physicians, internists, gastroenterologists, colorectal surgeons, urologists, and psychiatrists should be familiar with this potentially debilitating disease. Although there are several theories with regard to the pathophysiology of endometriosis, the most accepted theory is that of retrograde menstruation. The overall process is multifactorial, including complex genetic, immunologic, environmental, and hormonal components.

15.3.2 Clinical Presentation and Diagnostic Testing Classically women with endometriosis present with dysmenorrhea, dyspareunia, dyschezia, and/​or unexplained infertility. However, patients with endometriosis can present with a variety of symptoms that affect multiple organ systems. While the female reproductive organs are the most commonly affected organs, endometriosis can also affect the gastrointestinal tract, urinary bladder, and lungs, and it can also be found in cesarean section or laparoscopy scars. Patients can present with cyclic or noncyclic pain, diarrhea, constipation, bloating, dysuria, and even pneumothorax if the lungs are involved. Chronic pain in general is complex and can be inflammatory, neuropathic, and/​or nociceptive in nature. This chronic pain can affect patients in many aspects of their lives and is challenging to treat. Ultrasound and magnetic resonance imaging can be used to diagnose endometriomas (ovarian cysts filled with endometriotic fluid) or rectovaginal endometriotic nodules; however, peritoneal endometriotic implants cannot be seen on imaging. While tumor markers such as CA-​125 and other serum markers of inflammation may be elevated, they are nonspecific. Traditionally, endometriosis has been diagnosed surgically, preferably via laparoscopy with histologic confirmation obtained through biopsy. However, in more recent years, there has been a push to endorse clinical diagnosis based on symptomatology. Aggressive early diagnosis and medical management

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aim to limit the number of surgeries a woman with endometriosis will have in her lifetime.41,42 Traditional treatments for endometriosis include surgical excision or ablation of endometriotic lesions often combined with medications aimed at lowering or stabilizing estrogen levels and inflammation.

15.3.3 Lifestyle and Endometriosis  15.3.3.1 Nutrition While endometriosis is a chronic, inflammatory, estrogen-​ dependent disease, rationale suggests that elimination of processed, pro-​inflammatory, and/​or estrogen promoting foods may improve symptoms. However, the studies that examine diet and endometriosis have been small, inconsistent, and inconclusive. Many of the studies have been conducted outside of the United States, where food production may vary.44,45,46,47 Studies have looked at correlations between endometriosis risk and consumption of meat, dairy, soy, fiber, green vegetables, vitamin D, and omega 3 fatty acids.48,49 Analysis of any studies on dietary modifications must also take into consideration how the consumed food was produced. The use of pesticides in much of conventional American agriculture and hormones used in meat and dairy production could be confounding factors that potentially affect study outcomes and patient experience. Studies on the elimination of gluten and low fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) diets may improve gastrointestinal distress in patients with endometriosis.50,51 Ultimately, healthcare professionals should work with their patients to find the dietary modifications that help reduce their individual symptoms. A food diary and consideration of an elimination diet and/​or food allergy testing may help patients identify specific foods that they should avoid as they work to manage their endometriosis symptoms. Ongoing studies exploring gut microbiome involvement in the inflammatory and immunologic pathogenesis of endometriosis may provide future therapeutic options.52,53 15.3.3.2 Exercise While quality studies are needed, it is suggested that the anti-​inflammatory and antioxidant properties offered by regular exercise as well as overall reduction of estrogen levels may be beneficial for inflammatory processes, like endometriosis.54 Yoga has been associated with reduction in levels of chronic pain and improvement in quality of life in women with endometriosis.55 Paradoxically, there is an inverse relationship between obesity and severity of endometriosis with lower BMI more likely to be associated with severe endometriosis.56 It is unclear whether this is a cause or effect relationship of the disease. 15.3.3.3 Sleep Women with endometriosis have poorer quality of sleep, which is itself associated with lower quality of life.57 Poor quality of sleep, excessive daytime sleepiness, frequent fatigue, and insomnia have been found in patients with endometriosis.58–​60 As

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such, it stands to argue that improvement in the disease process would improve the overall quality of life in women with endometriosis. 15.3.3.4 Stress As expected, women with chronic pain experience higher levels of stress, depression, anxiety, and poor quality of life.61 Catastrophizing and fear of pain can be particularly common in patients with endometriosis. Therefore, it is important for patients to find behavioral, cognitive, and emotional strategies to cope with the chronic stress that comes with having chronic pain. Psychotherapy with acupuncture, mindfulness, and meditation have all been successfully employed to help improve chronic pain and quality of life symptoms in women with endometriosis.62–​65 15.3.3.5 Relationships Psychosocial impairment including strained interpersonal relationships, sexuality, partnership, work, and education are all hallmarks of women who suffer from endometriosis.66,67 Dyspareunia and chronic pain put particular strain on relationships. Healthcare providers should be alerted about the diagnosis of endometriosis if women report missing school, work, and social events due to the severity of their pain. 15.3.3.6 Substance Use The opioid epidemic in the United States has magnified the overuse and risk of opioid abuse in women with endometriosis and chronic pelvic pain. In a study of 178 gynecologists surveyed, two out of five admitted to typically prescribing opioids to patients with endometriosis or chronic pelvic pain of unknown cause. Another study revealed that women with endometriosis had 71% more emergency department visits compared with controls in the first year after diagnosis.68 A third study showed that 48.1% of patients were still taking narcotic analgesics 1 year after endometriosis surgery.69 It is clear that women with endometriosis are at particular risk of being prescribed and exposed to excessive opioid medications. Opioids should be used sparingly and should not be considered as primary treatment for endometriosis pain. A linear positive association was found between indoor passive exposure to tobacco smoke during childhood and the risk of endometriosis.70 Women reporting current, but not former, alcohol consumption in adulthood were found to have slightly higher risk of endometriosis, in fertile but not infertile women; alcohol consumption was found to be associated with an increased risk of deep endometriotic nodules but not peritoneal endometriosis in this review.71 15.3.3.7 Conclusion Endometriosis has been called the “great imitator” as its symptoms can mimic other diseases, making it difficult to diagnose. A woman’s overall health is often adversely affected by endometriosis. It is important to advise patients with endometriosis on their diet, exercise, sleep, social connectedness, stress reduction techniques, and avoidance of risky substances in order to improve their health outcomes and decrease pain.

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15.4  UNEXPLAINED INFERTILITY For unexplained infertility, see Supplemental Material online.

15.5  CONCLUSION Implementing Lifestyle Medicine guidelines is an advisable suggestion for patients presenting with unexplained infertility. Preconception care should aim to include dietary and nutrition advice, encouragement of regular physical activity, sleep hygiene recommendations, stress reduction education, cessation of risky substance use, and fostering positive social connections. Addressing these lifestyle factors can help women make positive changes that may improve their chances of achieving pregnancy.

REFERENCES 1. Goodman NF, Cobin RH, Futterweit W, et al. American Association of Clinical Endocrinologists, American College of Endocrinology and Androgen Excess and PCOS Society. Disease state clinical review: Guide to the best practices in the evaluation and treatment of polycystic ovary syndrome—​Part 1. Endocr Pract. 2015;21(11):1291–​ 1300. https://​doi.org/​10.4158/​EP15748.DSC 2. Legro RS, Arslanian SA, Ehrmann DA, et al. Diagnosis and treatment of polycystic ovary syndrome: An Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2013;98(12):4565–​4592. https://​doi.org/​10.1210/​jc.2013-​2350 3. Goodarzi MO, Quiñones MJ, Azziz R, Rotter JI, Hsueh WA, Yang H. Polycystic ovary syndrome in Mexican-​Americans: Prevalence and association with the severity of insulin resistance. Fertil Steril. 2005;84(3):766–​769. https://​doi.org/​10.1016/​ j.fertnstert.2005.03.051 4. Boyle JA, Cunningham J, O’Dea K, Dunbar T, Norman RJ. Prevalence of polycystic ovary syndrome in a sample of indigenous women in Darwin, Australia. Med J Aust. 2012;196(1):62–​66. https://​doi.org/​10.5694/​mja11.10553 5. Wijeyaratne CN, Balen AH, Barth JH, Belchetz PE. Clinical manifestations and insulin resistance (IR) in polycystic ovary syndrome (PCOS) among South Asians and Caucasians: Is there a difference? Clin Endocrinol (Oxf). 2002;57(3):343–​350. https://​ doi.org/​10.1046/​j.1365-​2265.2002.01603.x 6. Vink JM, Sadrzadeh S, Lambalk CB, Boomsma DI. Heritability of polycystic ovary syndrome in a Dutch twin-​family study. J Clin Endocrinol Metab. 2006;91(6):2100–​ 2104. https://​doi.org/​10.1210/​jc.2005-​1494 7. Kahsar-​Miller MD, Nixon C, Boots LR, Go RC, Azziz R. Prevalence of polycystic ovary syndrome (PCOS) in first-​degree relatives of patients with PCOS. Fertil Steril. 2001;75(1):53–​58. https://​doi.org/​10.1016/​S0015-​0282(00)01662-​9 8. Dumesic DA, Oberfield SE, Stener-​Victorin E, Marshall JC, Laven JS, Legro RS. Scientific statement on the diagnostic criteria, epidemiology, pathophysiology, and molecular genetics of polycystic ovary syndrome. Endocr Rev. 2015;36(5):487–​525. https://​doi.org/​10.1210/​er.2015-​1018 9. McCartney CR, Marshall JC. Clinical practice. Polycystic ovary syndrome. N Engl J Med. 2016;375(1):54–​64. https://​doi.org/​10.1056/​NEJMcp1514916 10. Teede HJ, Misso ML, Costello MF, et al. Recommendations from the international evidence-​based guideline for the assessment and management of polycystic ovary syndrome [published correction appears in Hum Reprod. 2019 Feb 1;34(2):388]. Hum Reprod. 2018;33(9):1602–​1618. https://​doi.org/​10.1093/​humrep/​dey256

251

Polycystic Ovary Syndrome

251

11. Gambineri A, Patton L, Altieri P, et al. Polycystic ovary syndrome is a risk factor for type 2 diabetes: Results from a long-​term prospective study. Diabetes. 2012;61(9):2369–​2374. https://​doi.org/​10.2337/​db11-​1360 12. Balen AH, Laven JS, Tan SL, Dewailly D. Ultrasound assessment of the polycystic ovary: International consensus definitions. Hum Reprod Update. 2003;9(6):505–​514. https://​doi.org/​10.1093/​humupd/​dmg044 13. Goodman NF, Cobin RH, Futterweit W, et al. American Association of Clinical Endocrinologists, American College of Endocrinology and Androgen Excess and PCOS Society. Disease state clinical review: Guide to the best practices in the evaluation and treatment of polycystic ovary syndrome -​Part 2. Endocr Pract. 2015;21(12):1415–​ 1426. https://​doi.org/​10.4158/​EP15748.DSCPT2 14. Moran LJ, Pasquali R, Teede HJ, Hoeger KM, Norman RJ. Treatment of obesity in polycystic ovary syndrome: A position statement of the Androgen Excess and Polycystic Ovary Syndrome Society. Fertil Steril. 2009;92(6):1966–​1982. https://​ doi.org/​10.1016/​j.fertnstert.2008.09.018 15. Moran LJ, Hutchison SK, Norman RJ, Teede HJ. Lifestyle changes in women with polycystic ovary syndrome. Cochrane Database Syst Rev. 2011;(7):CD007506. Published Jul 6, 2011. https://​doi.org/​10.1002/​14651858.CD007506.pub3 16. Lim SS, Hutchison SK, Van Ryswyk E, Norman RJ, Teede HJ, Moran LJ. Lifestyle changes in women with polycystic ovary syndrome. Cochrane Database Syst Rev. 2019;3(3):CD007506. Published Mar 28, 2019. https://​doi.org/​10.1002/​ 14651858.CD007506.pub4 17. Shang Y, Zhou H, Hu M, Feng H. Effect of diet on insulin resistance in polycystic ovary syndrome. J Clin Endocrinol Metab. 2020;105(10):dgaa425. https://​doi.org/​ 10.1210/​clinem/​dgaa425 18. González F, Considine RV, Abdelhadi OA, Acton AJ. Oxidative stress in response to saturated fat ingestion is linked to insulin resistance and hyperandrogenism in polycystic ovary syndrome. J Clin Endocrinol Metab. 2019;104(11):5360–​5371. https://​ doi.org/​10.1210/​jc.2019-​00987 19. González F, Considine RV, Abdelhadi OA, Acton AJ. Inflammation triggered by saturated fat ingestion is linked to insulin resistance and hyperandrogenism in polycystic ovary syndrome. J Clin Endocrinol Metab. 2020;105(6):e2152–​e2167. https://​ doi.org/​10.1210/​clinem/​dgaa108 20. Polak AM, Krentowska A, Łebkowska A, et al. The association of serum levels of leptin and ghrelin with the dietary fat content in non-​obese women with polycystic ovary syndrome. Nutrients. 2020;12(9):2753. https://​doi.org/​10.3390/​nu12092753 21. Cutler DA, Pride SM, Cheung AP. Low intakes of dietary fiber and magnesium are associated with insulin resistance and hyperandrogenism in polycystic ovary syndrome: A cohort study. Food Sci Nutr. 2019;7(4):1426–​1437. Published Feb 27, 2019. https://​doi.org/​10.1002/​fsn3.977 22. Phy JL, Pohlmeier AM, Cooper JA, et al. Low starch/​low dairy diet results in successful treatment of obesity and co-​ morbidities linked to polycystic ovary syndrome (PCOS). J Obes Weight Loss Ther. 2015;5(2):259. https://​doi.org/​10.4172/​ 2165-​7904.1000259 23. Kazemi M, McBreairty LE, Zello GA, et al. A pulse-based diet and the Therapeutic Lifestyle Changes diet in combination with health counseling and exercise improve health-related quality of life in women with polycystic ovary syndrome: secondary analysis of a randomized controlled trial. J Psychosomatic Obstetrics & Gynecology. 2020 Apr 2;41(2):144–53. https://doi.org/10.1080/0167482X.2019. 1666820

252

252

Mahima Gulati et al.

24. Patten RK, Boyle RA, Moholdt T, et al. Exercise interventions in polycystic ovary syndrome: A systematic review and meta-​ analysis. Front Physiol. 2020;11:606. Published Jul 7, 2020. https://​doi.org/​10.3389/​fphys.2020.00606 25. Benham JL, Yamamoto JM, Friedenreich CM, Rabi DM, Sigal RJ. Role of exercise training in polycystic ovary syndrome: A systematic review and meta-​analysis. Clin Obes. 2018;8(4):275–​284. https://​doi.org/​10.1111/​cob.12258 26. Tiwari N, Pasrija S, Jain S. Randomised controlled trial to study the efficacy of exercise with and without metformin on women with polycystic ovary syndrome. Eur J Obstet Gynecol Reprod Biol. 2019;234:149–​154. https://​doi.org/​10.1016/​j.ejogrb.2018.12.021 27. Fernandez RC, Moore VM, Van Ryswyk EM, et al. Sleep disturbances in women with polycystic ovary syndrome: Prevalence, pathophysiology, impact and management strategies. Nat Sci Sleep. 2018;10:45–​64. https://​doi.org/​10.2147/​NSS.S127475 28. Kitzinger C, Willmott J. “The thief of womanhood”: Women’s experience of polycystic ovarian syndrome. Soc Sci Med. 2002;54(3):349–​361. https://​doi.org/​10.1016/​ S0277-​9536(01)00034-​X 29. Hahn S, Janssen OE, Tan S, et al. Clinical and psychological correlates of quality-​of-​ life in polycystic ovary syndrome. Eur J Endocrinol. 2005;153(6):853–​860. https://​ doi.org/​10.1530/​eje.1.02024 30. Elsenbruch S, Hahn S, Kowalsky D, et al. Quality of life, psychosocial well-​being, and sexual satisfaction in women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2003;88(12):5801–​5807. https://​doi.org/​10.1210/​jc.2003-​030562 31. Drosdzol A, Skrzypulec V, Mazur B, Pawlińska-​Chmara R. Quality of life and marital sexual satisfaction in women with polycystic ovary syndrome. Folia Histochem Cytobiol. 2007;45 Suppl 1:S93–​S97. 32. Percy CA, Gibbs T, Potter L, Boardman S. Nurse-​led peer support group: Experiences of women with polycystic ovary syndrome. J Adv Nurs. 2009;65(10):2046–​2055. https://​doi.org/​10.1111/​j.1365-​2648.2009.05061.x 33. Pau CT, Keefe CC, Welt CK. Cigarette smoking, nicotine levels and increased risk for metabolic syndrome in women with polycystic ovary syndrome. Gynecol Endocrinol. 2013;29(6):551–​555. https://​doi.org/​10.3109/​09513590.2013.788634 34. Morotti E, Battaglia B, Fabbri R, Paradisi R, Venturoli S, Battaglia C. Cigarette smoking and cardiovascular risk in young women with polycystic ovary syndrome. Int J Fertil Steril. 2014;7(4):301–​312. 35. Xirofotos D, Trakakis E, Peppa M, et al. The amount and duration of smoking is associated with aggravation of hormone and biochemical profile in women with PCOS. Gynecol Endocrinol. 2016;32(2):143–​146. https://​doi.org/​10.3109/​ 09513590.2015.1101440 36. Polyzos SA, Goulis DG, Kountouras J, et al. Non-​alcoholic fatty liver disease in women with polycystic ovary syndrome: Assessment of non-​invasive indices predicting hepatic steatosis and fibrosis. Hormones (Athens). 2014;13(4):519–​531. https://​doi.org/​ 10.14310/​horm.2002.1493 37. Stefanaki C, Bacopoulou F, Livadas S, et al. Impact of a mindfulness stress management program on stress, anxiety, depression and quality of life in women with polycystic ovary syndrome: A randomized controlled trial. Stress. 2015;18(1):57–​66. https://​doi.org/​10.3109/​10253890.2014.974030 38. Raja-​Khan N, Agito K, Shah J, et al. Mindfulness-​based stress reduction in women with overweight or obesity: A randomized clinical trial. Obesity (Silver Spring). 2017;25(8):1349–​1359. https://​doi.org/​10.1002/​oby.21910 39. Nnoaham, KE., Hummelshoj L, Webster P, World Endometriosis Research Foundation Global Study. Impact of endometriosis on quality of life and work productivity: A

253

Polycystic Ovary Syndrome

253

multicenter study across ten countries. Fertil Steril. 2011 Aug;96(2):366–​373.e8. https://​ doi.org/​10.1016/​j.fertnstert.2011.05.090 40. Giudice LC. Clinical practice. Endometriosis. N Engl J Med. 2010 Jun 24;362(25):2389–​ 2398. https://​doi.org/​10.1056/​NEJMcp1000274 41. American College of Obstetricians and Gynecologists. Practice bulletin no. 114: Management of endometriosis. Obstet Gynecol. 2010 Jul;116(1):223–​236. https://​doi.org/​10.1097/​AOG.0b013e3181e8b073 42. Practice Committee of the American Society for Reproductive Medicine. Treatment of pelvic pain associated with endometriosis: a committee opinion. Fertil Steril. 2014 Apr;101(4):927–​935. Erratum in: Fertil Steril. 2015 Aug;104(2):498.https://​doi.org/​ 10.1016/​j.fertnstert.2014.02.012 43. Falcone T, Flyckt R. Clinical management of endometriosis. Obstet Gynecol. 2018 Mar;131(3):557–​571. https://​doi.org/​10.1097/​AOG.0000000000002469 44. Parazzini F, Viganò P, Candiani M, Fedele L. Diet and endometriosis risk: A literature review. Reprod Biomed Online. 2013 Apr;26(4):323–​336. https://​doi.org/​10.1016/​ j.rbmo.2012.12.011 45. Hansen SO, Knudsen UB. Endometriosis, dysmenorrhoea and diet. Eur J Obstet Gynecol Reprod Biol. 2013 Jul;169(2):162–​ 171. https://​doi.org/​10.1016/​ j.ejogrb.2013.03.028 46. Jurkiewicz-​Przondziono J, Lemm M, Kwiatkowska-​Pamuła A, et al. Influence of diet on the risk of developing endometriosis. Ginekol Pol. 2017;88(2):96–​102. https://​ doi.org/​10.5603/​GP.a2017.0017 47. Fjerbaek A, Knudsen UB. Endometriosis, dysmenorrhea and diet—​What is the evidence? Eur J Obstet Gynecol Reprod Biol. 2007 Jun;132(2):140–​147. https://​doi.org/​ 10.1016/​j.ejogrb.2006.12.006 48. Parazzini F, Chiaffarino F, Surace M, et al. Selected food intake and risk of endometriosis. Hum Reprod. 2004 Aug;19(8):1755–​1759. https://​doi.org/​10.1093/​humrep/​ deh395 49. Trabert B, Peters U, De Roos AJ, Scholes D, Holt VL. Diet and risk of endometriosis in a population-​based case-​control study. Br J Nutr. 2011 Feb;105(3):459–​67. https://​ doi.org/​10.1017/​S0007114510003661 50. Marziali M, Venza M, Lazzaro S, Lazzaro A, Micossi C, Stolfi VM. Gluten-​free diet: A new strategy for management of painful endometriosis related symptoms? Minerva Chir. 2012 Dec;67(6):499–​504. 51. Moore JS, Gibson PR, Perry RE, Burgell RE. Endometriosis in patients with irritable bowel syndrome: Specific symptomatic and demographic profile, and response to the low FODMAP diet. Aust N Z J Obstet Gynaecol. 2017 Apr;57(2):201–​205. https://​ doi.org/​10.1111/​ajo.12594 52. Laschke MW, Menger MD. The gut microbiota: A puppet master in the pathogenesis of endometriosis? Am J Obstet Gynecol. 2016 Jul;215(1):68.e1–​68.e4. https://​doi.org/​ 10.1016/​j.ajog.2016.02.036 53. Leonardi M, Hicks C, El-​Assaad F, El-​Omar E, Condous G. Endometriosis and the microbiome: A systematic review. BJOG. 2020 Jan;127(2):239–​249. https://​doi.org/​ 10.1111/​1471-​0528.15916 54. Bonocher CM, Montenegro ML, Rosa E Silva JC, Ferriani RA, Meola J. Endometriosis and physical exercises: A systematic review. Reprod Biol Endocrinol. 2014 Jan 6;12:4. https://​doi.org/​10.1186/​1477-​7827-​12-​4 55. Gonçalves AV, Barros NF, Bahamondes L. The practice of hatha yoga for the treatment of pain associated with endometriosis. J Altern Complement Med. 2017 Jan;23(1):45–​ 52. https://​doi.org/​10.1089/​acm.2015.0343

254

254

Mahima Gulati et al.

56. Holdsworth-​Carson SJ, Dior UP, Colgrave EM, et al. The association of body mass index with endometriosis and disease severity in women with pain. J Endometr Pelvic Pain Disord. 2018;10(2):79–​87. https://​doi.org/​10.1177/​2284026518773939 57. Arion K, Orr NL, Noga H, et al. A quantitative analysis of sleep quality in women with endometriosis. J Womens Health (Larchmt). 2020 Sep;29(9):1209–​1215. https://​ doi.org/​10.1089/​jwh.2019.8008 58. Leone Roberti Maggiore U, Bizzarri N, Scala C, et al. Symptomatic endometriosis of the posterior cul-​de-​sac is associated with impaired sleep quality, excessive daytime sleepiness and insomnia: A case-​control study. Eur J Obstet Gynecol Reprod Biol. 2017 Feb;209:39–​43. https://​doi.org/​10.1016/​j.ejogrb.2015.11.026 59. Nunes FR, Ferreira JM, Bahamondes L. Pain threshold and sleep quality in women with endometriosis. Eur J Pain. 2015 Jan;19(1):15–​20. https://​doi.org/​10.1002/​ejp.514 60. Ramin-​Wright A, Schwartz ASK, Geraedts K, et al. Fatigue -​A symptom in endometriosis. Hum Reprod. 2018 Aug 1;33(8):1459–​1465. https://​doi.org/​10.1093/​humrep/​ dey115 61. Zarbo C, Brugnera A, Frigerio L, et al. Behavioral, cognitive, and emotional coping strategies of women with endometriosis: A critical narrative review. Arch Womens Ment Health. 2018 Feb;21(1):1–​13. https://​doi.org/​10.1007/​s00737-​017-​0779-​9 62. Meissner K, Schweizer-​ Arau A, Limmer A, et al. Psychotherapy with somatosensory stimulation for endometriosis-​ associated pain: A randomized controlled trial. Obstet Gynecol. 2016 Nov;128(5):1134–​ 1142. https://​doi.org/​10.1097/​AOG. 0000000000001691 63. Fox SD, Flynn E, Allen RH. Mindfulness meditation for women with chronic pelvic pain: A pilot study. J Reprod Med. 2011 Mar–​Apr;56(3–​4):158–​162. 64. Ball EF, Nur Shafina Muhammad Sharizan E, Franklin G, Rogozińska E. Does mindfulness meditation improve chronic pain? A systematic review. Curr Opin Obstet Gynecol. 2017 Dec;29(6):359–​ 366. https://​doi.org/​10.1097/​GCO.0000 000000000417 65. Kold M, Hansen T, Vedsted-​Hansen H, Forman A. Mindfulness-​based psychological intervention for coping with pain in endometriosis. Nord Psychol. 2012 Mar 1;64(1):2–​ 16. https://​doi.org/​10.1080/​19012276.2012.693727 66. Aerts L, Grangier L, Streuli I, et al. Psychosocial impact of endometriosis: From co-​ morbidity to intervention. Best Pract Res Clin Obstet Gynaecol. 2018 Jul;50:2–​10. https://​doi.org/​10.1016/​j.bpobgyn.2018.01.008 67. Gilmour JA, Huntington A, Wilson HV. The impact of endometriosis on work and social participation. Int J Nurs Pract. 2008 Dec;14(6):443–​ 448. https://​doi.org/​ 10.1111/​j.1440-​172X.2008.00718.x 68. Fuldeore M, Yang H, Du EX, Soliman AM, Wu EQ, Winkel C. Healthcare utilization and costs in women diagnosed with endometriosis before and after diagnosis: A longitudinal analysis of claims databases. Fertil Steril. 2015 Jan;103(1):163–​171. https://​ doi.org/​10.1016/​j.fertnstert.2014.10.011 69. Soliman AM, Du EX, Yang H, Wu EQ, Haley JC. Retreatment rates among endometriosis patients undergoing hysterectomy or laparoscopy. J Womens Health (Larchmt). 2017 Jun;26(6):644–​654. https://​doi.org/​10.1089/​jwh.2016.6043 70. Kvaskoff M, Bijon A, Clavel-​Chapelon F, Mesrine S, Boutron-​Ruault MC. Childhood and adolescent exposures and the risk of endometriosis. Epidemiology. 2013 Mar;24(2):261–​269. https://​doi.org/​10.1097/​EDE.0b013e3182806445 71. Parazzini F, Cipriani S, Bravi F, et al. A meta-​analysis on alcohol consumption and risk of endometriosis. Am J Obstet Gynecol. 2013 Aug;209(2):106.e1–​106.e10. https://​ doi.org/​10.1016/​j.ajog.2013.05.039

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Lifestyle Medicine in Menopause and Bone Health Amanda McKinney, MD, FACLM, FACOG Doane University, Crete, NE, USA

16.1 16.2

16.3

16.4 16.5

Introduction..................................................................................................256 Impacts of Lifestyle on Menopause.............................................................257 16.2.1 Abnormal Uterine Bleeding..........................................................257 16.2.2 Vasomotor Symptoms....................................................................257 16.2.3 Mood Disorders/​Psychological Symptoms...................................257 Using Lifestyle Medicine to Manage Menopausal Symptoms....................258 16.3.1 Healthful Eating.............................................................................258 16.3.2 Phytoestrogens...............................................................................258 16.3.3 Physical Activity............................................................................260 16.3.4 Stress..............................................................................................260 16.3.5 Social Connectedness....................................................................260 16.3.6 Sleep..............................................................................................261 16.3.7 Avoiding Risky Substances...........................................................261 Pathophysiology of Bone Health.................................................................261 Lifestyle Recommendations for Prevention and Treatment of Osteoporosis.................................................................................................262 16.5.1 Healthful Eating.............................................................................262 16.5.2 Physical Activity............................................................................264 16.5.3 Stress Management, Social Connectedness, Relationships, and Sleep.......................................................................................264 16.5.4 Substances.....................................................................................264

KEY POINTS • Lifestyle behaviors can impact the timing of menopause, menopausal symptoms, and bone health. • Lifestyle behavior modification can improve menopausal symptoms and prevent chronic diseases prevalent in menopausal women, including osteoporosis.

DOI: 10.1201/9781003110682-17

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16.1  INTRODUCTION Menopause, or the “climacteric” (meaning a critical period or event), is the end of the monthly menstrual cycle.1 Menopause can mean significant changes for women mentally, emotionally, and physically, but healthy lifestyle behaviors can help. Diet, physical activity, and other lifestyle behaviors can improve menopausal symptoms and prevent or reverse potential pathologic outcomes. However, relevant patient education and counseling requires special provider knowledge and attention. The medical definition of “natural menopause” is typically defined as absence of vaginal bleeding for 1 year. Physiologically, there is a decrease in ovarian hormone production, resulting in permanent cessation of ovulation and menstruation.2 Although menopause is associated with fluctuating hypothalamic and pituitary hormones that regulate the menstrual cycle, menopause is not a central event, but rather natural ovarian failure. The ovary becomes unresponsive to the pituitary hormones, follicle-​ stimulating hormone (FSH) and luteinizing hormone (LH), and follicles deplete leading to cessation of estrogen and progesterone production in the ovary (but with continued androgen production). Androgens (whether ovarian or adrenal) are converted in the peripheral tissues, primarily adipose, to estrogen. As a result, obese postmenopausal women have higher circulating estrogen levels increasing the risk of other menopause-​associated diseases, such as breast cancer.2 Age of menopause varies widely; for most women, it occurs between ages of 48–​ 55 years, with the perimenopausal transition lasting for about 4 years.1 Menopause is reached when follicles are depleted from approximately 2 million at birth to around 1,000.3 Gold, et al. found the median, adjusted age at natural menopause is 51.4 years.4

FIGURE 16.1  Healthy menopause.

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16.2  IMPACTS OF LIFESTYLE ON MENOPAUSE Although menopause is a universal phenomenon, onset age, transition duration, and final menstrual period timing are not. Menopausal onset varies by race and ethnicity, largely in the context of demographic, genetic, and lifestyle factors. Family and twin studies suggest that heritability may be responsible for menopausal timing 30–​ 85% of the time.3 Lifestyle factors leading to a later menopause include living in developed countries and urban areas, while factors that result in earlier menopause include smoking, malnourishment, and lower socioeconomic status.3 Symptomatology is also quite variable. The most common symptoms associated with the menopause and perimenopause are disrupted uterine bleeding patterns and vasomotor and urogenital symptoms. Women also experience somatic symptoms such as fatigue and body aches and psychological symptoms such as irritability, anxiety, depression, decreased libido, and difficulty sleeping.5 Lifestyle behaviors such as diet, exercise, and smoking can impact the presence and/​or severity of some of these symptoms.

16.2.1 Abnormal Uterine Bleeding Irregular cycles are common but weight changes, chronic stress, and excessive exercise can exacerbate existing hormonal imbalances. There is a higher risk of pre-​and perimenopausal irregular menstrual cycles with obesity, smoking, or reporting a higher level of perceived stress.6 Postmenopausal bleeding is considered abnormal and should be evaluated. Approximately 10% of women with postmenpausal bleeding have endometrial cancer. Unopposed estrogen leads to hypertrophy of the endometrial lining followed by hyperplastic changes and, ultimately, cancer; therefore, obese women are at higher risk. Likewise, women with type 2 diabetes are twice as likely to develop postmenopausal endometrial cancer. A high-​fat diet, even in the absence of obesity, increases the risk of other types of cancer.7

16.2.2 Vasomotor Symptoms Vasomotor symptoms are very common in the perimenopause and menopause, with 60% of women experiencing hot flashes, 48% enduring night sweats, and 41% reporting insomnia. Typically, vasomotor symptoms develop 1–​2 years before periods cease except in cases of surgery, chemotherapy, or radiation therapy-​induced menopause, in which vasomotor symptom onset is abrupt. Estrogen deficit is the culprit, but there also appears to be thermoregulatory involvement. It is somewhat counterintuitive that women with higher levels of body fat report more severe hot flashes yet the association remains. Weight loss has been associated with a decrease in number and severity of hot flashes.2

16.2.3 Mood Disorders/​Psychological Symptoms Limited information is available for the impact of lifestyle factors on perimenopause-​ related mood disturbances. However, a study of Chinese women revealed that

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depressive symptoms were associated with discordant family relationships, irregular periods, constipation, and severity of other perimenopausal symptoms. Constipation was also found to be a risk factor for anxiety.8 Most commonly diet-​ induced, constipation impacts as many as 60 million Americans. Diets high in fiber, that is, whole plants, are commonly curative and nearly universally preventative.10, 11 Another smaller study of peri-​and early-​menopausal women found depression was more likely with increased severity of perimenopausal somatic symptoms, although exercise tended to be protective.9

16.3  USING LIFESTYLE MEDICINE TO MANAGE MENOPAUSAL SYMPTOMS Because severity and duration of menopausal symptoms are often dependent on lifestyle factors, lifestyle measures can be used in their treatment. Traditionally symptom relief has largely been reliant on hormone replacement therapy (HRT). Due to associated risks of HRT, Lifestyle Medicine symptom management can bring relief and reduce HRT-​related risks, while simultaneously reducing the risks of other lifestyle-​related chronic diseases. Lifestyle Medicine strategies, primarily diet, accomplish this mainly through modulation of systemic circulating estrogen levels.12

16.3.1 Healthful Eating Food is medicine. Excluding prevention, there are two strategies by which healthful eating can be used in the management of menopausal symptoms. One is the use of plant-​derived phytoestrogens to replace ovarian estrogen. The other is utilizing a whole-​food, plant-​based diet for weight loss and metabolic optimization, improving menopausal symptoms and preventing and reversing common post-​ menopause chronic disease processes. The focus here will be on the former.

16.3.2 Phytoestrogens Because synthetic and “bioidentical” hormone therapies are associated with an increased risk of breast cancer, phytoestrogens like soy are often utilized to reduce vasomotor menopause symptoms. It is incorrect to associate that same risk with the use of soy. Whole soy foods interact with estrogen receptors uniquely, which decouples breast cancer risk from soy consumption and offers patients relief from menopausal symptoms, without the fear of increasing breast cancer risk.13 The two primary types of estrogen receptors are alpha and beta receptors. Endogenous and synthetic estrogens act as nonselective agonists at both receptor types. Drugs that are considered “anti-​estrogen” such as fulvestrant, used to treat metastatic breast cancer, are nonselective antagonists at all estrogen receptors. Mixed agonist-​antagonists such as synthetic selective estrogen receptor modifiers (SERMs), like tamoxifen, and phytoestrogens act selectively and primarily on beta-​receptors.14

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Beta-​receptors are found primarily in ovarian granulosa cells, kidney, brain, bone, heart, lungs, intestinal mucosa, and endothelial cells. Alpha-​receptors are found mainly in the endometrium, breast cancer cells, ovarian stromal cells, and the hypothalamus.14 Because endogenous and synthetic estrogens act indiscriminately, they impact all these tissues simultaneously. Consequently, exogenous estrogens work well to prevent menopause-​related osteopenia and treat vasomotor symptoms but stimulate proliferation of the mammary cells that can lead to breast cancer development by binding to estrogen receptors in the breast.13 This mechanism is responsible for the increased risk of postmenopausal breast cancer and other cancers in obese women. Conversely, phytoestrogens act like synthetic SERMs. They bind both alpha-​and beta-​estrogen receptors but have a higher affinity for beta-​receptors. Phytoestrogens have both agonistic and antagonistic effects; they are strong beta-​receptor agonists but weak alpha-​receptor agonists. Structural similarities between phytoestrogens and mammalian estradiol allow for estradiol displacement. Because their activation of the breast beta-​receptors inhibits mammary cell growth and counteracts effects associated with activated alpha-​receptors, phytoestrogens help protect against breast cancer.15 The primary soy phytoestrogen is genistein. Genistein binds beta-​receptors with 7–​30-​fold greater affinity than alpha-​receptors.16 While soy foods are not a panacea for menopausal symptoms, and the placebo effect might be partially responsible for their effects,17 two recent meta-​analyses reported that isoflavone supplementation, a legume-​based phytochemical, was associated with a 34% reduction in hot flashes. Consumption of at least 15 mg of genistein, equivalent to approximately 3 ounces of tofu or 1 cup of soy milk daily, reduces hot flashes by up to 50%.18 This total reduction includes that provided by the placebo effect.19 While a study of Chinese women revealed decreased hot flashes with an omnivorous diet,20 a study of Japanese women found that consumption of soy and isoflavones was inversely associated with hot flashes.21 Overall, clinical studies utilizing soy have revealed either a positive or neutral impact on vaginal health indices that reflect vaginal moisture, elasticity, and pH, and a positive or neutral impact on hot flashes.22–​30 Unlike oral estrogens, soy isoflavones neither negatively impact serum lipids nor provoke the prothrombotic effects. There is a favorable influence of soy isoflavones on vascular function and no induction of endometrial trophic effects. Therefore, they do not increase the risk of endometrial hyperplasia and cancer. This reflects the fact that the alpha receptor is the exclusive mediator of estrogen’s endometrial impact.16 In fact, a prospective analysis of over 46,000 postmenopausal women revealed that those in the highest quintile of soy consumption had a 26.7% reduced risk of endometrial cancer.31 A 2008 meta-​analysis confirmed this and revealed a 48% lower risk for ovarian cancer in women consuming the most soy. 32 Beta estrogen receptor expression in the kidney affords premenopausal women relative protection from kidney failure. Soy isoflavones may have nephroprotective potential as well. Likewise, estrogen appears to protect women from left ventricular hypertrophy via the beta-​receptor in heart tissue, leading to the theory that soy can also be cardioprotective.16 It is important to note that while studies utilize soy isolates in order to blind participants’ consumption of whole food, minimally processed soy products with their accompanying fiber and other phytonutrients are a more efficacious approach.

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Not all phytoestrogens are safe and beneficial. Hops, used in beer brewing, contains a potent phytoestrogen called 8-​prenylnaringenin (8-​PN). Because 8-​ PN binds to both alpha-​and beta-​estrogen receptors, it provides some relief from menopausal vasomotor symptoms.33–​37 However, 8-​PN has a much weaker affinity for the beta-​receptor than for the alpha-​receptor, which is a concern for potential increased breast cancer risk with use of hops-​containing supplements and beer consumption.38,39

16.3.3 Physical Activity During menopausal transition, many women experience weight gain and changes in body fat composition and distribution. Studies reveal that women in midlife often gain an average of 0.5 kg or more annually. Physical activity has not been shown to prevent age-​related weight gain altogether but can protect against the development of obesity and accumulation of metabolically harmful intra-​abdominal fat.40 Exercise recommendations consistent with the Health and Human Services physical activity guidelines for significant health benefits for Americans provide results including weight loss, which can be helpful in dealing with vasomotor symptoms.41 It should be noted that exercise alone does not alleviate vasomotor symptoms but may provide improvements in sleep quality, insomnia, and depression during the menopausal transition.42 Group physical activity, by providing a social support network, is helpful for managing vasomotor symptoms.44 Many somatic symptoms that women encounter during menopausal transition, such as joint pain and stiffness, fatigue, difficulty concentrating, poor sleep, irritability, and depression, can also be partially or completely resolved with regular physical activity. Exercise has been well documented to enhance mental well-​ being and protect against depression and anxiety through increased levels of dopamine, serotonin, and endorphins.42

16.3.4 Stress Stress appears to be a precipitating, or at least potentiating, factor in hot flashes given that stress hormones like cortisol and catecholamines also impact thermoregulation. Using exercise to manage stress responses could reduce the occurrence of vasomotor symptoms.42 Yoga has been shown to be fairly effective in managing menopausal symptoms through stress reduction, while simultaneously reducing physical and psychological risk factors for cardiovascular disease.44

16.3.5 Social Connectedness Menopause-​ related symptoms can disrupt interpersonal relationships. Many postmenopausal women are no longer sexually active and 12–​ 13% of the time menopause-​related symptoms are the cause.45 Despite this, overall life satisfaction is unrelated to menopausal status but rather determined by the presence of premenopausal mood disturbances. Supportive partners and positive workplace relationships can help ease the transition.46, 47

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16.3.6 Sleep Sleep is critical for good health, yet a significant number of women experience sleep difficulties during menopausal transition. As many as 26% of women experience severe symptoms that meet the diagnostic criteria for insomnia and can result in impaired daytime functioning. Most sleep disturbances in the perimenopause are related to hot flashes. Vasomotor symptoms also exacerbate age-​related and other sleep-​disturbing comorbidities, such as sleep apnea and restless leg syndrome, negatively impacting quality of life and health status. Nonpharmacological sleep management strategies such as cognitive behavioral therapy and lifestyle-​based strategies to address vasomotor symptoms should be utilized as first-​line therapies.48

16.3.7 Avoiding Risky Substances Based on current estimates, the number of older female consumers of alcohol is expected to rise over the next two decades. Because of gender differences in alcohol metabolism, women are at increased risk of negative consequences associated with excessive consumption. While older women may benefit from low levels of alcohol consumption with regard to cardiovascular disease and osteoporosis, these benefits are often nullified with higher consumption levels. Additionally, all alcohol consumption increases the risk of breast cancer.49 The menopausal transition can be a critical time for women with regard to alcohol consumption and smoking. The Study of Women across the Nation (SWAN) found that women who self-​identified as excessive drinkers commonly transition to non-​excessive drinking during the menopausal transition. However, women that transitioned from non-​excessive to excessive drinking did so during the early stages of menopausal transition. While depression and circulating estrogen levels did not impact drinking status, those with higher testosterone levels were less likely to transition to non-​excessive drinking.50 Likewise, SWAN found no associations between menopausal transition and smoking; however, those with higher levels of circulating estrogen were more likely to quit smoking, while those with higher testosterone levels or depression were more likely to continue smoking or relapse.51 These results highlight the need to assess alcohol and tobacco use in perimenopausal and postmenopausal women. It is recommended that women consume no more than one alcoholic beverage daily and never more than two standard drinks in one sitting.52 If risky behaviors are identified, patients should be referred for interventions that target smoking or alcohol cessation.

16.4  PATHOPHYSIOLOGY OF BONE HEALTH Peak bone mass and mineral density is achieved during the reproductive years. Osteopenia is natural bone loss that occurs after age 30, is not pathologic, and does not warrant treatment. Osetopenia is defined as a bone density T-​score of −1 to −2.5.53 A T-​score less than −2.5 is considered osteoporosis.

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To determine who is most at risk, the fracture-​risk algorithm, FRAX®, can be used. FRAX® uses global models of population-​based cohorts and clinical risk factors to calculate an individual’s 10-​year risk of major osteoporotic and hip fracture. Treatment is recommended when the risk of hip fracture is at least 3%, or 20% for major osteoporotic fracture. No guidelines have been issued regarding screening intervals or cessation of screening due to insufficient data; however, the U.S. Preventive Services Task Force suggests a minimum of 2 years between screenings.54 Bones can become fragile as a result of (a) failure to produce optimal bone mass and strength during growth; (b) excessive bone resorption; and (c) lack of a sufficient rebuilding response to resorption. Menopausal estrogen deficiency is a factor in the development of osteoporosis due to increased bone resorption and an impaired response to it. As such, there is continuous bone loss that occurs for several years after the menopausal transition. Increased bone formation, normally seen in response to weight-​bearing exercise, is also diminished when estrogen is deficient.55 Ultimately, postmenopausal osteoporosis results from an imbalance between bone resorption by osteoclasts and bone formation via osteoblasts. It appears that oxidative stress, or chronic inflammation, plays a role.56 Osteoclasts chisel away at older bone, opening up spaces to be refilled by osteoblasts.57 In a prooxidant or inflammatory setting, increased osteoclastic activity and decreased osteoblastic activity may be seen, providing conditions for the development of postmenopausal osteoporosis.58 Additionally, elderly osteoporotic women have consistently lower natural antioxidant levels compared to comparably aged women without osteoporosis.59

16.5  LIFESTYLE RECOMMENDATIONS FOR PREVENTION AND TREATMENT OF OSTEOPOROSIS 16.5.1 Healthful Eating In order to combat prooxidant conditions, consumption of foods with high levels of antioxidants is essential. Evidence from a combination of study types strongly points to a positive link between fruit and vegetable consumption and bone health.60 Whole plant foods upregulate osteoblastogenesis and downregulate osteoclastogenesis.61 A fruit and vegetable approach may provide a very sensible alternative therapy for osteoporosis treatment, one that is likely to have numerous additional health-​related benefits.60 Higher fruit and vegetable intakes are shown to have positive effects on bone mineral status in all age groups.62 Doubling fruit intake would result in a 5.6% increase in bone mineral density (BMD) of the spine in older women, translating to reduced fracture risk.63 Likewise, femoral neck BMD is higher in women who consume high amounts of fruit in childhood, as fruits contain several key nutrients important to bone health, namely, potassium, magnesium, fiber, B-​carotene, and vitamin C.64 A large study of Chinese men and women compared a vegetarian dietary pattern with an omnivorous dietary pattern and found that individuals closer to a vegetarian dietary pattern had lower risk of hip fracture. Compared with omnivores, participants who most closely followed a vegetarian diet had a 34% reduction in fracture risk.65

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Individual plant foods have also been assessed. Almond consumption inhibits osteoclast activity for a positive effect on bone health.78 Likewise, prunes increase serum concentrations of insulin-​like growth factor-​1 (IGF-​1) and bone-​specific alkaline phosphatase, both associated with greater bone formation rates.66 Genistein stimulates osteoblastic bone formation, inhibits osteoclastic bone resorption, and prevents bone loss in animal models.67 A study of Japanese women confirmed that consumption of soy can also increase BMD, reducing fracture risk.68 Other studies have shown a reduction of whole-​body bone loss,69 a modest bone sparing effect at the femoral neck,70 or no effect.71 A large prospective cohort study found a 28–​37% lower risk of fracture for postmenopausal women who consume soy. Benefit was achieved with 5–​7 g of soy protein, or 20–​30 mg of phytoestrogens daily, which is equivalent to one daily serving of soy foods such as soy milk, tempeh or edamame.72 It is important to note that there are no fracture data on soy supplements.73 A randomized trial found that a daily intake of two glasses of soy milk prevents lumbar spine bone loss in postmenopausal women as well as transdermal progesterone.74 Phytate, or IP-​6, a naturally-​occurring compound found in high concentrations in nuts, seeds, legumes, and whole grains, inhibits osteoclast activity.75 Phytates also prevent dissolution of bone in a way similar to the anti-​osteoporosis drugs, alendronate and etidronate. Accordingly, phytate consumption is associated with increased BMD in the heel, spine, and hip.76,77 Phytate consumption also corresponds to fracture risk. Postmenopausal women with lower IP-​6 levels had greater bone mass loss in the lumbar spine compared to those with high levels. The 10-​year fracture probability was also significantly higher in the low-​phytate group compared to the high-​phytate group, both in hip and major osteoporotic fracture.78 Calcium is necessary for bone remodeling and bone contains more than 90% of the body’s total calcium content. Currently, in the United States, dairy products provide 75% of the calcium available in the food supply. However, there is a long-​ standing enigma that hip fracture rates are highest in populations with the greatest milk consumption.79 Calcium supplements with and without vitamin D lack both efficacy and safety.80-​ 86 Vitamin D, however, clearly plays an important role in bone health. It increases dietary calcium absorption from 10–​15% to 30%.87 A recent meta-​analysis also revealed that as vitamin D levels in the population increase, mortality rates decline from all causes, particularly cancer.88 Healthy eating recommendations include the following: • A diet based on whole plant foods that include fruits, vegetables, legumes, and whole grains. • 500–​1000 mg per day of non-​dairy, dietary calcium should be consumed via green leafy vegetables and legumes. • Sun exposure: • Fair-​skinned individuals –​10 to 12 minutes of midday, July, summer sun OR exposing the face, arms, and hands of a fair-​skinned individual to 5 minutes of sun at noon 2–​3 times per week in the spring, summer or fall months.

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• Darker skinned individuals will require three times this exposure because very darkly pigmented skin requires 5–​10 times more solar radiation than fair skin.89 • Vitamin D3 supplementation: to achieve a target of 85% of the population achieving a blood level of 75 nmol/​L (30 ng/​mL) requires 2,000 IU of vitamin D3 daily.87

16.5.2 Physical Activity Numerous longitudinal studies have examined the effects of exercise training on bone health within all age groups. There is compelling evidence that routine physical activity, especially weight bearing and impact exercise, prevents aging-​associated bone loss. A meta-​analysis revealed that exercise training programs were found to prevent or reverse almost 1% of bone loss per year in the lumbar spine and femoral neck in both pre-​and postmenopausal women. Exercise training appears to significantly reduce the risk and number of falls and, therefore, fractures because of improved muscular strength and balance.90 Likewise, a 2011 Cochrane review investigated whether exercise could prevent bone loss and fractures in postmenopausal women and found a small but statistically significant effect. Specifically, non-​weight-​bearing, high-​force exercise such as lower-​limb, progressive-​resistance strength training was the most effective exercise for femur neck BMD. Combination exercise programs were the most effective for the spine.91 Because peak bone mass is achieved by late adolescence, prevention of osteoporosis should begin then. Adopting healthy lifestyle habits such as a healthy diet, safe sun exposure, tobacco avoidance, and exercise may help prevent its development. Physical activity recommendations: • Moderate physical activity that incorporates strength, balance, weight bearing, and resistance ­exercises 2–​3 times per week should be prescribed. • Exercise regimens should be tailored to the patient’s current level of fitness.

16.5.3 Stress Management, Social Connectedness, Relationships, and Sleep As described, osteoporosis is the result of an imbalance of osteoblasts and osteoclasts driven by chronic inflammation. Stress, whether it is psychosocial in nature or due to chronically disturbed sleep, contributes to a prooxidant state. Using tactics to manage stress, build healthy resilient relationships, and create an environment conducive to regenerative sleep helps address all diseases of chronic inflammation, including osteoporosis.92,93

16.5.4 Substances Daily cola consumption, but not other carbonated soft drinks, is associated with a 3.7% lower femoral neck BMD than for those who consumed < 1 serving of cola/​

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month. This is possibly because colas contain phosphoric acid. Diets high in phosphorus and low in calcium stimulate parathyroid hormone, which increases bone resorption.94 Colas contain caffeine, but data suggest that caffeine intake in the range consumed by most women is not an important risk factor of osteoporosis. Among elderly women, however, in whom calcium balance is impaired, high caffeine intake may predispose to femoral bone loss. High caffeine consumption also tends to be positively associated with tobacco and alcohol use, which are associated with increased osteoporotic risk.95 Moderate consumption of alcohol, 1–​3 glasses of wine per day, is associated with BMD increase in ambulatory women over the age of 75, while higher alcohol intakes have detrimental effects on bone mass.96 With regard to smoking, the risk of osteoporosis in smokers in case-​control studies is increased by 33% and it is increased by 63% in prospective studies.97 Recommendations on substances: • Many conditions that arise later in life begin in childhood and adolescence. Young people should be counseled for tobacco avoidance and smokers should be counseled with the aim of cessation. • Alcohol consumption for women should be limited to one alcoholic beverage per day. Those who do not consume alcohol should not be encouraged to start. • Dairy milk and colas should be avoided.

REFERENCES 1. Wylie-​Rosett J. Menopause, micronutrients and hormone therapy. Am J Clin Nutr. 2005;81(5):1223S-​1231S. https://​doi.org/​10.1093/​ajcn/​81.5.1223 2. Dalal PK, Agarwal M. Postmenopausal syndrome. Indian J Psychiatry. 2015;57(Suppl 2):S222–​S232. https://​doi.org/​10.4103/​0019-​5545.161483 3. Gold EB. The timing of the age at which natural menopause occurs. Obstet Gynecol Clin North Am. 2011;38(3):425–​440. https://​doi.org/​10.1016/​j.ogc.2011.05.002 4. Gold EB, Bromberger J, Crawford S, et al. Factors associated with age at natural menopause in a multiethnic sample of midlife menopause. Am J Epidemiology. 2001;153(9):865–​874. https://​doi.org/​10.1093/​aje/​153.9.865 5. Levis S, Griebeler ML. The role of soy foods in the treatment of menopausal symptoms [published online ahead of print November 3, 2010]. J Nutr. 2010;140(12):2318S–​ 2321S. https://​doi.org/​10.3945/​jn.110.124388 6. Bae J, Park S, Kwon JW. Factors associated with menstrual cycle irregularity and menopause [published online ahead of print February 6, 2018]. BMC Womens Health. 2018;18(1):36. https://​doi.org/​10.1186/​s12905-​018-​0528-​x 7. American Cancer Society. Endometrial cancer risk factors. https://​www.cancer.org/​ cancer/​endometrial-​cancer/​causes-​risks-​prevention/​risk-​factors.html. Accessed Oct. 12, 2020. 8. Li RX, Ma M, Xiao XR, Xu Y, Chen XY, Li B. Perimenopausal syndrome and mood disorders in perimenopause: Prevalence, severity, relationships, and risk factors. Medicine (Baltimore). 2016;95(32):e4466. https://​doi.org/​10.1097/​MD.000000000 0004466 9. Gibbs Z, Lee S, Kulkarni J. Factors associated with depression during the perimenopausal transition. Womens Health Issues. 2013;23(5):e301–​e307. https://​doi.org/​ 10.1016/​j.whi.2013.07.001

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10. Attaluri A, Donahoe R, Valestin J, Brown K, Rao SS. Randomised clinical trial: Dried plums (prunes) vs. psyllium for constipation [published online ahead of print February 15, 2011]. Aliment Pharmacol Ther. 2011;33(7):822–​828. https://​doi.org/​10.1111/​ j.1365-​2036.2011.04594.x 11. Sanjoaquin MA, Appleby PN, Spencer EA, Key TJ. Nutrition and lifestyle in relation to bowel movement frequency: A cross-​sectional study of 20630 men and women in EPIC-​Oxford. Public Health Nutr. 2004;7(1):77–​83. https://​doi.org/​10.1079/​ PHN2003522 12. Malik E, Sheoran P, Siddiqui A. Health-​ promoting behaviors and menopausal symptoms: An interventional study in rural India. J Midlife Health. 2018;9(4):200–​ 206. https://​doi.org/​10.4103/​jmh.JMH_​96_​18 13. Auchincloss H, Haagensen CD. Cancer of the breast possibly induced by estrogenic substance. JAMA. 1940;114(16):1517–​1523. https://​doi.org/​10.1001/​jama. 1940.02810160019005 14. Couse JF, Lindzey J, Grandien K, Gustafsson JA, Korach KS. Tissue distribution and quantitative analysis of estrogen receptor-​alpha (ERalpha) and estrogen receptor-​beta (ERbeta) messenger ribonucleic acid in the wild-​type and ERalpha-​ knockout mouse. Endocrinology. 1997;138(11):4613–​4621. https://​doi.org/​10.1210/​ en.138.11.4613 15. Oseni T, Patel R, Pyle J, Jordan VC. Selective estrogen receptor modulators and phytoestrogens [published online ahead of print October 8, 2008]. Planta Med. 2008;74(13):1656–​1665. https://​doi.org/​10.1055/​s-​0028-​1088304 16. McCarty MF. Isoflavones made simple -​genistein’s agonist activity for the beta-​type estrogen receptor mediates their health benefits. Med Hypotheses. 2006;66(6):1093–​ 1114. https://​doi.org/​10.1016/​j.mehy.2004.11.046 17. Levis S, Griebeler ML. The role of soy foods in the treatment of menopausal symptoms [published online ahead of print on November 3, 2010]. J Nutr. 2010;140(12):2318S–​ 2321S. https://​doi.org/​10.3945/​jn.110.124388 18. Oregon State University. Soy Isoflavones. Linus Pauling Institute: Micronutrient Center. http:// ​ l pi.oregonstate.edu/​ i nfocenter/​ p hytochemicals/​ s oyiso/​ i ndex.html#source. Published October 2016. Accessed Oct 12, 2020. 19. Kruzer MS. Soy consumption for reduction of menopausal symptoms. Inflammopharmacology. 2008;16(5):227–​229. https://​doi.org/​10.1007/​s10787-0088021-​z 20. Zhang Q, Li F, Yu Y, Yu X, Sheng Q, Zhang X. Differential factors associated with hot flashes in Chinese perimenopausal and postmenopausal women [published online ahead of print March 25, 2009]. Maturitas. 2009;63(1):94–​98. https://​doi.org/​10.1016/​ j.maturitas.2009.02.007 21. Nagata C, Takatsuka N, Kawakami N, Shimizu H. Soy product intake and hot flashes in Japanese women: Results from a community-​ based prospective study. Am J Epidemiol. 2001;153(8):790–​793. https://​doi.org/​10.1093/​aje/​153.8.790 22. Wilcox G, Wahlqvist ML, Burger HG, Medley G. Oestrogenic effects of plant foods in postmenopausal women. BMJ. 1990;301(6757):905–​906. https://​doi.org/​10.1136/​ bmj.301.6757.905-​a 23. Baird DD, Umbach DM, Lansdell L, et al. Dietary intervention study to assess estrogenicity of dietary soy among postmenopausal women. J Clin Endocrinol Metab. 1995;80:1685–​1690. https://​doi.org/​10.1210/​jcem.80.5.7745019 24. Dalais FS, Rice GE, Wahlquist ML, et al. Effects of dietary phytoestrogens in postmenopausal women. Climacteric. 1998;1(2):124–​129. https://​doi.org/​10.3109/​ 13697139809085527

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25. Lewis JE, Nickell LA, Thompson LU, Szalai JP, Kiss A, Hilditch JR. A randomized controlled trial of the effect of dietary soy and flaxseed muffins on quality of life and hot flashes during menopause. Menopause. 2006;13(4):631–​642. https://​doi.org/​ 10.1097/​01.gme.0000191882.59799.67 26. Brzezinski A, Adlercreutz H, Shaoul R, et al. Short-​term effects of phytoestrogen-​ rich diet on postmenopausal women. Menopause. 1997;4(2):89–​94. https://​doi.org/​ 10.1097/​00042192-​199704020-​00005 27. Manonai J, Songchitsomboon S, Chanda K, Hong JH, Komindr S. The effect of a soy-​ rich diet on urogenital atrophy: A randomized, cross-​over trial [published online ahead of print on November 16, 2005]. Maturitas. 2006;54(2):135–​140. https://​doi.org/​ 10.1016/​j.maturitas.2005.09.011 28. Murkies AL, Lombard C, Strauss BJG, Wilcox G, Burger HG, Morton MS. Dietary flour supplementation decreases post-​menopausal hot flushes: Effect of soy and wheat. Maturitas. 1995;21(3):189–​195. https://​doi.org/​10.1016/​0378-​5122(95)00899-​V 29. Welty FK, Lee KS, Lew NS, Nasca M, Zhou JR. The association between soy nut consumption and decreased menopausal symptoms [published online ahead of print April 17, 2007]. J Womens Health (Larchmt). 2007;16(3):361–​369. https://​doi.org/​10.1089/​ jwh.2006.0207 30. Chiechi LM, Putignano G, Guerra V, Schiavelli MP, Cisternino AM, Carriero C. The effect of a soy rich diet on the vaginal epithelium in postmenopause: A randomized double blind trial. Maturitas. 2003;45(4):241–​246. https://​doi.org/​10.1016/​S0378-​5122 (03)00080-​X 31. Ollberding NJ, Lim U, Wilkens LR, et al. Legume, soy, tofu, and isoflavone intake and endometrial cancer risk in postmenopausal women in the multiethnic cohort study [published online ahead of print December 12, 2011]. J Natl Cancer Inst. 2012;104(1):67–​76. https://​doi.org/​10.1093/​jnci/​djr475 32. Myung SK, Ju W, Choi HJ, Kim SC. Korean Meta-​Analysis (KORMA) Study Group. Soy intake and risk of endocrine-​related gynaecological cancer: A meta-​analysis [published online ahead of print September 19, 2009]. BJOG. 2009;116(13):1697–​ 1705. https://​doi.org/​10.1111/​j.1471-​0528.2009.02322.x 33. Erkkola R, Vervarcke S, Vansteelandt S, Rompotti P, De Keukeleire D, Heyerick A. A randomized, double-​blind, placebo-​controlled, cross-​over pilot study on the use of a standardized hop extract to alleviate menopausal discomforts [published online ahead of print February 18, 2010]. Phytomedicine. 2010;17(6):389–​396. https://​doi.org/​ 10.1016/​j.phymed.2010.01.007 34. Keiler AM, Zierau O, Kretzschmar G. Hop extracts and hop substances in treatment of menopausal complaints [published online ahead of print March 9, 2013]. Planta Med. 2013;79(7):576–​579. https://​doi.org/​10.1055/​s-​0032-​1328330 35. Heyerick A, Vervarcke S, Depypere H, Bracke M, De Keukeleire D. A first prospective, randomized, double-​blind, placebo-​controlled study on the use of a standardized hop extract to alleviate menopausal discomforts [published online ahead of print March 19, 2013]. Maturitas. 2006;54(2):164–​175. https://​doi.org/​10.1055/​s-​0032-​1328330 36. Chadwick LR, Pauli GF, Farnsworth NR. The pharmacognosy of Humulus lupulus L. (hops) with an emphasis on estrogenic properties [published online ahead of print July 1, 2005]. Phytomedicine. 2006;13(1–​2):119–​131. https://​doi.org/​10.1016/​ j.phymed.2004.07.006 37. Aghamiri V, Mirghafourvand M, Mohammad-​Alizadeh-​Charandabi S, Nazemiyeh H. The effect of hop (Humulus lupulus L.) on early menopausal symptoms and hot flashes: A randomized placebo-​controlled trial. Complement Ther Clin Pract. 2016;23:130–​135. https://​doi.org/​10.1016/​j.ctcp.2015.05.001

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38. Schaefer O, Hümpel M, Fritzemeier KH, Bohlmann R, Schleuning WD. 8–​Prenyl naringenin is a potent ERalpha selective phytoestrogen present in hops and beer. J Steroid Biochem Mol Biol. 2003;84(2–​3):359–​360. https://​doi.org/​10.1016/​ S0960-​0760(03)00050-​5 39. Milligan S, Kalita J, Pocock V, et al. Oestrogenic activity of the hop phyto-​ oestrogen, 8-​prenylnaringenin. Reproduction. 2002;123(2):235–​242. https://​pubmed. ncbi.nlm.nih.gov/​11866690/​. Published February 2002. Accessed Oct 12, 2020. https://​doi.org/​10.1530/​reprod/​123.2.235 40. Sternfeld B, Dugan S. Physical activity and health during the menopausal transition. Obstet Gynecol Clin North Am. 2011;38(3):537–​566. https://​doi.org/​10.1016/​ j.ogc.2011.05.008 41. U.S. Department of Health and Human Services. President’s Council on Sports, Fitness and Nutrition. https://​health.gov/​sites/​default/​files/​2019-​09/​Physical_​Activity_​ Guidelines_​2nd_​edition.pdf 42. Sternfeld B, Guthrie KA, Ensrud KE, et al. Efficacy of exercise for menopausal symptoms: A randomized controlled trial [published online ahead of print April 2014]. Menopause. 2014;21(4):330–​338. https://​doi.org/​10.1097/​GME.0b013e31829e4089 43. Goranitis I, Bellanca L, Daley AJ, et al. Aerobic exercise for vasomotor menopausal symptoms: A cost-​utility analysis based on the Active Women trial [published online ahead of print April 26, 2017]. PLoS One. 2017;12(9):e0184328. https://​doi.org/​ 10.1371/​journal.pone.0184328 44. Vaze N, Joshi S. Yoga and menopausal transition. J Midlife Health. 2010;1(2):56–​58. https://​doi.org/​10.4103/​0976-​7800.76212 45. Harder H, Starkings RML, Fallowfield LJ, et al. Sexual functioning in 4,418 postmenopausal women participating in UKCTOCS: A qualitative free-​text analysis [published online ahead of print July 8, 2019]. Menopause. 2019; 26(10):1100–​1009. https://​doi.org/​10.1097/​GME.0000000000001377 46. Converso D, Viotti S, Sottimano I, Loera B, Molinengo G, Guidetti G. The relationship between menopausal symptoms and burnout. A cross-​sectional study among nurses. BMC Womens Health. 2019;19(1):148. https://​doi.org/​10.1186/​s12905019-​0847-​6 47. Parish SJ, Faubion SS, Weinberg M, Bernick B, Mirkin S. The MATE survey: Men’s perceptions and attitudes towards menopause and their role in partners’ menopausal transition. Menopause. 2019 Oct;26(10):1110–​1116. https://​doi.org/​10.1097/​ GME.0000000000001373 48. Baker FC, de Zambotti M, Colrain IM, Bei B. Sleep problems during the menopausal transition: Prevalence, impact, and management challenges [published online ahead of print February 9, 2018]. Nat Sci Sleep. 2018;10:73–​95. https://​doi.org/​10.2147/​ NSS.S125807 49. Epstein EE, Fischer-​Elber K, Al-​Otaiba Z. Women, aging, and alcohol use disorders. J Women Aging. 2007;19(1–​2):31–​48. https://​doi.org/​10.1300/​J074v19n01_​03 50. Peltier MR, Verplaetse TL, Roberts W, et al. Changes in excessive alcohol use among older women across the menopausal transition: A longitudinal analysis of the Study of Women’s Health across the Nation [published online ahead of print July 14, 2020]. Biol Sex Differ. 2020;11(1):37. https://​doi.org/​10.1186/​s13293-​020-​00314-​7 51. Peltier MR, Flores JM, Smith PH, et al. Smoking across the menopausal transition in a 10-​year longitudinal sample: The role of sex hormones and depressive symptoms. Nicotine Tob Res. 2020;22(6):872–​877. https://​doi.org/​10.1093/​ntr/​ntz069

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Lifestyle Medicine in Menopause

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52. Centers for Disease Control and Prevention: Alcohol and Public Health. www.cdc.gov/​alcohol/​faqs.htm#:~:text=The%20Dietary%20Guidelines%20also%20 recommend,start%20drinking%20for%20any%20reason. Published January 2020. Accessed Oct. 12, 2020. 53. Karaguzel G, Holick MF. Diagnosis and treatment of osteopenia. Rev Endocr Metab Disord. 2010;11(4):237–​251. https://​doi.org/​10.1007/​s11154-​010-​9154-​0 54. Kling JM, Clarke BL, Sandhu NP. Osteoporosis prevention, screening and treatment: A review [published online ahead of print July 10, 2014]. J Womens health (Larchmt). 2014;23(7):563–​572. https://​doi.org/​10.1089/​jwh.2013.4611 55. Raisz LG. Pathogenesis of osteoporosis: Concepts, conflicts, and prospects. J Clin Invest. 2005;115(12):3318–​3325. https://​doi.org/​10.1172/​JCI27071 56. Cervellati C, Bonaccorsi G, Cremonini E, et al. Oxidative stress and bone resorption interplay as a possible trigger for postmenopausal osteoporosis [published online ahead of print January 12, 2014]. Biomed Res Int. 2014;2014:569563. https://​doi.org/​ 10.1155/​2014/​569563 57. Sontakke AN, Tare RS. A duality in the roles of reactive oxygen species with respect to bone metabolism. Clin Chim Acta. 2002;318(1–​2):145–​148. https://​doi.org/​10.1016/​ S0009-​8981(01)00766-​5 58. Altindag O, Erel O, Soran N, Celik H, Selek S. Total oxidative/​anti-​oxidative status and relation to bone mineral density in osteoporosis [published online ahead of print September 6, 2007]. Rheumatol Int. 2008;28(4):317–​321. https://​doi.org/​10.1007/​ s00296-​007-​0452-​0 59. Maggio D, Barabani M, Pierandrei M, et al. Marked decrease in plasma antioxidants in aged osteoporotic women: Results of a cross-​sectional study. J Clin Endocrinol Metab. 2003;88(4):1523–​1527. https://​doi.org/​10.1210/​jc.2002-​021496 60. Lanham-​New SA. Fruit and vegetables: The unexpected natural answer to the question of osteoporosis prevention? Am J Clin Nutr. 2006;83(6):1254–​1255. https://​doi.org/​ 10.1093/​ajcn/​83.6.1254 61. Shen CL, von Bergen V, Chyu MC, et al. Fruits and dietary phytochemicals in bone protection [published online ahead of print October 30, 2012]. Nutr Res. 2012;32(12):897–​910. https://​doi.org/​10.1016/​j.nutres.2012.09.018 62. Prynne CJ, Mishra GD, O’Connell MA, et al. Fruit and vegetable intakes and bone mineral status: A cross sectional study in 5 age and sex cohorts. Am J Clin Nutr. 2006;83(6):1420–​1428. https://​doi.org/​10.1093/​ajcn/​83.6.1420 63. McClung MR. The relationship between bone mineral density and fracture risk. Curr Osteoporos Rep. 2005;3(2):57–​63. https://​doi.org/​10.1007/​s11914-​005-​0005-​y 64. New SA, Robins SP, Campbell MK, et al. Dietary influences on bone mass and bone metabolism: Further evidence of a positive link between fruit and vegetable consumption and bone health? Am J Clin Nutr. 2000;71(1):142–​151. https://​doi.org/​10.1093/​ ajcn/​71.1.142 65. Dai Z, Butler LM, van Dam RM, Ang LW, Yuan JM, Koh WP. Adherence to a vegetable-​ fruit-​soy dietary pattern or the Alternative Healthy Eating Index is associated with lower hip fracture risk among Singapore Chinese. J Nutr. 2014;144(4):511–​518. https://​doi.org/​10.3945/​jn.113.187955 66. Arjmandi BH, Khalil DA, Lucas EA, et al. Dried plums improve indices of bone formation in postmenopausal women. J Womens Health Gend Based Med. 2002;11(1):61–​ 68. https://​doi.org/​10.1210/​jc.2002-​021496 67. Morabito N, Crisafulli A, Vergara C, et al. Effects of genistein and hormone-​ replacement therapy on bone loss in early postmenopausal women: A randomized

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270

Amanda McKinney

double-​blind placebo-​controlled study. J Bone Miner Res. 2002;17(10):1904–​1912. https://​doi.org/​10.1359/​jbmr.2002.17.10.1904 68. Somekawa Y, Chiguchi M, Ishibashi T, Aso T. Soy intake related to menopausal symptoms, serum lipids, and bone mineral density in postmenopausal Japanese women. Obstet Gynecol. 2001;97(1):109–​115. https://​doi.org/​10.1359/​jbmr.2002. 17.10.1904 69. Wong WW, Lewis RD, Steinberg FM, et al. Soy isoflavone supplementation and bone mineral density in menopausal women: A 2-​y multicenter clinical trial [published online ahead of print September 16, 2009]. AJCN. 2009;90(5):1433–​1439. https://​ doi.org/​10.3945/​ajcn.2009.28001 70. Alekel DL, Van Loan MD, Koehler KJ, et al. The soy isoflavones for reducing bone loss (SIRBL) study: A 3-​y randomized controlled trial in postmenopausal women [published online ahead of print November 11, 2009]. AJCN. 2010;91(1): 218–​230. https://​doi.org/​10.3945/​ajcn.2009.28306 71. Tai TY, Tsai KS, Tu ST, et al. The effect of soy isoflavone on bone mineral density in postmenopausal Taiwanese women with bone loss: A 2-​ year randomized double-​blind placebo-​controlled study [published online ahead of print September 8, 2011]. Osteoporos Int. 2012;23(5):1571–​1580. https://​doi.org/​10.1007/​s00198011-​1750-​7 72. Zhang X, Shu XO, Li H, et al. Prospective cohort study of soy food consumption and risk of bone fracture among postmenopausal women. Arch Intern Med. 2005;165(16):1890–​1895. https://​doi.org/​10.1001/​archinte.165.16.1890 73. Reinwald S, Weaver CM. Soy components vs. whole soy: Are we betting our bones on a long shot [published online ahead of print Oct 27, 2010]? J Nutr. 2010;140(12):2312S–​ 2317S. https://​doi.org/​10.3945/​jn.110.124008 74. Lydeking-​Olsen E, Beck-​Jensen JE, Setchell KD, Holm-​Jensen T. Soymilk or progesterone for prevention of bone loss—​A 2 year randomized, placebo-​controlled trial [published online ahead of print Apr 14, 2004]. Eur J Nutr. 2004;43(4):246–​257. https://​doi.org/​10.1007/​s00394-​004-​0497-​8 75. del Mar Arriero M, Ramis JM, Perelló J, Monjo M. Inositol hexakisphosphate inhibits osteoclastogenesis on RAW 264.7 Cells and human primary osteoclasts [published online ahead of print Aug 14, 2012]. PLoS ONE. 2012;7(8):e43187. https://​doi.org/​ 10.1371/​journal.pone.0043187 76. López-​González AA, Grases F, Roca P, Mari B, Vicente-​Herrero MT, Costa-​Bauzá A. Phytate (myo-​inositol hexaphosphate) and risk factors for osteoporosis. J Med Food. 2008;11(4):747–​752. https://​doi.org/​10.1089/​jmf.2008.0087 77. Lopez-​Gonzalez AA, Grases F, Perello J, et al. Phytate levels and bone parameters: A retrospective pilot clinical trial. Front Biosci (Elite Ed). 2010;2:1093–​1098. https://​ doi.org/​10.2741/​e167 78. López-​González AA, Grases F, Monroy N, et al. Protective effect of myo-​inositol hexaphosphate (phytate) on bone mass loss in postmenopausal women [published online ahead of print May 22, 2012]. Eur J Nutr. 2013;52(2):717–​726. https://​doi.org/​ 10.1007/​s00394-​012-​0377-​6 79. Feskanich D, Bischoff-​Ferrari HA, Frazier AL, Willet WC. Milk consumption during teenage years and risk of hip fractures in older adults. JAMA Pediatr. 2014;168(1):54–​ 60. https://​doi.org/​10.1001/​jamapediatrics.2013.3821 80. Bischoff-​Ferrari HA, Dawson-​Hughes B, Baron JA, et al. Calcium intake and hip fracture risk in men and women: a meta-​analysis of prospective cohort studies and

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randomized controlled trials. Am J Clin Nutr. 2007;86(6):1780–​1790. https://​doi.org/​ 10.1093/​ajcn/​86.5.1780 81. Chapuy MC, Arlot ME, Duboeuf F, et al. Vitamin D3 and calcium to prevent hip fractures in the elderly women. N Engl J Med. 1992;327(23):1637–​1642. https://​ doi.org/​10.1056/​NEJM199212033272305 82. Moyer VA; U.S. Preventive Services Task Force*. Vitamin D and calcium supplementation to prevent fractures in adults: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2013;158(9):691–​696. https://​doi.org/​10.7326/​ 0003-​4819-​158-​9-​201305070-​00603 83. Reid IR, Bristow SM, Bolland MJ. Calcium supplements: Benefits and risks [published online ahead of print July 14, 2015]. J Intern Med. 2015;278(4):354–​368. https://​ doi.org/​10.1111/​joim.12394 84. Bolland MJ, Avenell A, Baron JA, et al. Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: Meta-​analysis. BMJ. 2010;341:c3691. https://​doi.org/​10.1136/​bmj.c3691 85. Reid IR. Cardiovascular effects of calcium supplements. Nutrients. 2013;5(7):2522–​ 2529. https://​doi.org/​10.3390/​nu5072522 86. Lewis JR, Zhu K, Prince RL. Adverse events from calcium supplementation: Relationship to errors in myocardial infarction self-​reporting in randomized controlled trials of calcium supplementation. J Bone Miner Res. 2012;27(3):719–​722. https://​doi.org/​10.1002/​jbmr.1484 87. Holick MF. Vitamin D: Importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis. AJCN. 2004;79(3):362–​371. https://​doi.org/​10.1093/​ajcn/​ 79.3.362 88. Theodoratou E, TzoulakI I, Zgaga L, Ioannidis JP. Vitamin D and multiple health outcomes: Umbrella review of systematic reviews and meta-​analyses of observational studies and randomised trials [published online ahead of print April 1, 2014]. BMJ. 2014;348:g2035. https://​doi.org/​10.1136/​bmj.g2035 89. Reichrath J. The challenge resulting from positive and negative effects of sunlight: How much solar UV exposure is appropriate to balance between risks of vitamin D deficiency and skin cancer [published online ahead of print February 28, 2006]? Prog Biophys Mol Biol. 2006;92(1):9–​16. https://​doi.org/​10.1016/​ j.pbiomolbio.2006.02.010 90. Warburton DER, Nicol CW, Bredin SSD. Health benefits of physical activity: The evidence. CMAJ. 2006;174(6):801–​809. https://​doi.org/​10.1503/​cmaj.051351 91. Howe TE, Shea B, Dawson LJ, et al. Exercise for preventing and treating osteoporosis in postmenopausal women. Cochrane Database Syst Rev. 2011;7:CD000333. https://​ doi.org/​10.1002/​14651858.CD000333.pub2 92. Liu YZ, Wang YX, Jiang CL. Inflammation: The common pathway of stress-​related diseases [published online ahead of print June 20, 2017]. Front Hum Neurosci. 2017;11:316. https://​doi.org/​10.3389/​fnhum.2017.00316 93. Ginaldi L, Di Benedetto MC, De Martinis M. Osteoporosis, inflammation and ageing. Immun Ageing. 2005;2:14. https://​doi.org/​10.1186/​1742-​4933-​2-​14 94. Tucker KL, Morita K, Qiao N, Hannan MT, Cupples LA, Kiel DP. Colas, but not other carbonated beverages, are associated with low bone mineral density in older women: The Framingham Osteoporosis Study. AJCN. 2006; 84(4):936–​942. https://​ doi.org/​10.1093/​ajcn/​84.4.936

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95. Cooper C, Atkinson EJ, Wahner HW, et al. Is caffeine consumption a risk factor for osteoporosis? J Bone Miner Res. 1992;7(4):465–​471. https://​doi.org/​10.1002/​ jbmr.5650070415 96. Ganry O, Baudoin C, Fardelione P. Effect of alcohol intake on bone mineral density in elderly women: The EPIDOS Study. Am J Epidem. 2000;151(8):773–​780. https://​ doi.org/​10.1093/​oxfordjournals.aje.a010277 97. Ill PO, Alexandre C. Tobacco as a risk factor of osteoporosis, myth or reality? Revue du Rhematisme. 1993 Apr;60(4):280–​286.

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Preconceptual Health Nancy L. Eriksen, MD

Associate Professor Maternal-​Fetal Medicine Department of Obstetrics and Gynecology Baylor College of Medicine Houston, TX, USA

Kristi R. VanWinden, MD

Department of Obstetrics and Gynecology Maternal-​Fetal Medicine The Permanente Medical Group Oakland, CA; San Leandro, CA, USA

John McHugh, MD

Adjunct Clinical Professor of Obstetrics and Gynecology Department of Obstetrics and Gynecology Keck School of Medicine of USC Huntington Hospital Pasadena, CA, USA 17.1 17.2 17.3

17.4

Introduction..................................................................................................274 Overview of Preconceptual Care.................................................................276 17.2.1 Benefits of and Barriers to Preconception Care............................276 17.2.2 Challenges and Opportunities........................................................277 Teratogens and Risky Substances................................................................279 17.3.1 What Is a Teratogen?.....................................................................279 17.3.2 How Do We Study the Effects of an Exposure on Fetal Development?.......................................................................279 17.3.3 Importance of Exposure Timing....................................................279 17.3.4 Medication Risks and Benefits......................................................280 17.3.5 Maternal Disease as a Teratogen...................................................282 17.3.6 Maternal Lifestyle as a Teratogen.................................................283 Preconception Nutrition...............................................................................283 17.4.1 Dietary Patterns and Vitamin and Micronutrient Deficiencies......283 17.4.2 Eliminating High-​Risk Food.........................................................285 17.4.3 Preventing Adverse Pregnancy Outcomes.....................................286 17.4.4 Reversing Chronic Disease............................................................288

DOI: 10.1201/9781003110682-18

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Physical Activity..........................................................................................288 17.5.1 Physical Conditioning for Pregnancy............................................288 17.5.2 Impact on Gestational Weight Gain...............................................289 17.5.3 Preconception Activity and Obstetric Outcomes...........................289 Sleep.............................................................................................................289 Adverse Childhood Experiences and Stress................................................291 Emotional Wellness and Mental Health.......................................................293 17.8.1 The Relationship of Mental Illness with Preconception Care and Disease....................................................................................293 17.8.2 Intimate Partner Violence and Mental Health................................293 17.8.3 The Impact of Mental Health and Mental Health Treatment on Achieving Pregnancy.....................................................................294 17.8.4 Screening for Anxiety and Depression..........................................294 17.8.5 Optimizing Treatment for Mental Health Disorders Prepregnancy.................................................................................294 Relational Connectedness............................................................................295 17.9.1 Preconception Social Support and Pregnancy Outcomes..............295

KEY POINTS • Preconception health refers to caring for women over the continuum of their life in an effort to optimize their health as well as the health of future offspring. • Micronutrient deficiencies are common in reproductive-​age women and can be avoided by focusing on healthy dietary patterns, such as plant predominant diet. • Adverse pregnancy outcomes such as gestational diabetes, preeclampsia, and preterm birth may be prevented by optimizing lifestyle behaviors preconceptually. • Medication use should be minimized when feasible prior to conception, and each medication should be individually evaluated on the basis of its potential risks and anticipated maternal benefits. • Prepregnancy physical activity is linked to appropriate gestational weight gain and physical activity levels in pregnancy and is associated with fewer pregnancy complications and pregnancy-​related symptoms. • Sleep disturbances have an impact both on the ability to become pregnant and on pregnancy outcomes. • Optimization of a woman’s mental health and emotional wellness in the preconception period is linked to improved pregnancy outcomes. • Chronic health conditions, infertility, intimate partner violence, and poor social support are related to more mental health challenges in reproductive-​age women.

17.1  INTRODUCTION A woman’s reproductive years represent a unique window of opportunity for interventions that can prevent and reduce chronic illnesses, assess mental and physical

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well-​being, and optimize her overall health. Historically, preconceptual health (PCH) has focused on reducing adverse pregnancy outcomes (APO) and improving overall reproductive outcomes, with an emphasis on reducing preterm birth and infant morbidity and mortality.1 Since the 1990s the Centers for Disease Control and Prevention (CDC) has put greater emphasis on improving women’s care. Yet despite their recommendations, the rate of chronic disease and maternal mortality in reproductive-​ age women continues to rise.2–​5 PCH is important for many reasons. First, it is essential for improving a woman’s health to enhance her fertility and to prevent and reverse chronic diseases that would have an adverse impact on her health and the health of any future pregnancy. Second, it can address maternal mortality which has more than doubled in the last 30 years. Today the most common causes of death are not related to pregnancy. Nearly half of all maternal deaths in the United States are caused by preexisting chronic diseases, such as cardiovascular disease (CVD), cardiomyopathy, non-​ cardiovascular chronic diseases and cerebrovascular accidents.4, 6,7 Addressing modifiable risk factors to prevent and reverse chronic diseases can help lower the maternal mortality rate. Third, APO such as preeclampsia, gestational diabetes, and preterm birth are largely caused by poor overall lifestyle. These also have an impact on fetal and infant morbidity and mortality, particularly when there is a potentially preventable preterm birth due to a medically indicated delivery. Additionally, these APOs are associated with an increased risk of future CVD in women. Fourth, there is emerging evidence from the Developmental Origins of Health and Disease (DOHaD) model that a variety of lifestyle factors, including diet, preexisting chronic disease, stress, smoking, alcohol, and environmental toxic substances, can result in serious health consequences extending to three or more generations.8 Evidence for the DOHaD theory exists from both animal and human studies that show changes in the epigenome that occur due to a poor lifestyle. These epigenetic changes are associated with an increased risk of noncommunicable diseases (NCDs) in the offspring, including obesity, hypertension, metabolic syndrome, and type 2 diabetes.9 In other words, modifying lifestyle factors before conception can decrease APO and improve the future health of the offspring. Finally, preconception health intersects care of the individual with public health issues. Despite all the advances in medicine in the last century we are seeing an increase in infant and maternal mortality, a decrease in the age of death, and a surge in NCDs due to unhealthy lifestyle behaviors.5 Thus, treating modifiable risk factors in the individual woman to prevent or reverse chronic disease can have a disproportionate impact on improving the population health of future generations. Preconception health is not a new concept, but we endeavor to bring a new perspective to PCH. Broadly, PCH is a term that encompasses the overall health of women during their reproductive years, generally defined as 18–​44 years of age. Enhanced PCH can improve overall health whether or not a woman chooses to have children. Therefore, PCH needs to be reframed as caring for women over the continuum of their lives.10 The goal of PCH is to have healthier women. This in turn leads to healthier pregnancies, better maternal-​fetal outcomes, decreased NCDs in their offspring, and better long-​term health for her family.11,12

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17.2  OVERVIEW OF PRECONCEPTUAL CARE Preconception care (PCC) was first introduced in the 1990s as a specialty clinic for women in England who previously had a poor pregnancy outcome.13 Since its inception, the CDC released recommendations for PCC which is defined as a set of interventions that “aim to identify and modify biomedical, behavioral, and social risks to a woman’s health or pregnancy outcome through prevention and management before pregnancy occurs.”1,14 Interpregnancy care refers to care that is given from the end of one pregnancy until the beginning of a subsequent pregnancy.10 In 2001, a joint recommendation was put in the “Guidelines for Perinatal Care” by the American College of Obstetricians and Gynecologists (ACOG), the American Academy of Pediatrics (AAP), and the March of Dimes that “all health encounters during a woman’s reproductive years, particularly those that are a part of preconception care, should include counseling on appropriate medical care and behavior to optimize pregnancy outcomes.”15 Others, including the American Academy of Family Practice,16 the American Society of Reproductive Medicine (ASRM),17 and the American College of Nurse Midwifery have released guidelines supporting the importance of PCC.18 ACOG and ASRM define the goal of PPC is “to reduce the risk of adverse health effects for the woman, fetus, and neonate by working with women to optimize health, address modifiable risk factors, and provide education about healthy pregnancy.”17 ACOG, ASRM, and the Society of Maternal-​Fetal Medicine recommend that “any patient encounter with a non-​pregnant woman with reproductive potential is an opportunity to provide counseling regarding wellness and healthy habits.”10,17 Although all women can benefit from PCC, women at greatest risk for adverse health outcomes include women who have modifiable risk factors including APO’s and chronic diseases due to unhealthy lifestyle behaviors.10

17.2.1 Benefits of and Barriers to Preconception Care The benefits of preconceptual healthcare include being able to address modifiable risk factors to prevent and reverse chronic disease, especially obesity, diabetes, and CVD to improve the overall health of women. It is also possible to prevent many of the APO’s such as gestational diabetes, preeclampsia, and preterm birth by making lifestyle changes, thereby improving fetal and neonatal outcomes. Although the United States has seen an improvement in the infant mortality rate over the last two decades, it remains highest in non-​Hispanic black infants and Native American infants.19 Currently, the United States ranks 33rd in the world for infant mortality.20 Preventing preterm birth, whether spontaneous or medically indicated, could further reduce infant mortality. The most common associated or contributing factor to maternal morbidity and mortality is underlying chronic diseases.4,6 Obesity is the most common indirect cause, accounting for 50% of maternal mortality in the United Kingdom.21 PCC also gives an opportunity to identify reversible causes of infertility and to assess women for emotional wellness, adverse childhood experiences (ACE) scores, sleep disturbances, substance abuse, and social determinants of health, which also have a significant impact on health outcomes.10,17,22

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Barriers to PCC occur both for the patient and the provider. There are 3 primary reasons why women do not seek out preconception care: perceived lack of risk, lack of knowledge, and misunderstanding of the aim of preconceptual care.23 Furthermore, a survey of women showed that even when women recognized the need to achieve health prior to conception, a majority do not recall receiving PCC services.24 The most common barriers to care listed by providers are lack of reimbursement, lack of time, lack of emphasis on preventive health in training programs, lack of efficacy of counseling to unmotivated patients, fragmented health delivery care system, and lack of treatment for high-​risk behaviors.25,26

17.2.2 Challenges and Opportunities Delivering preconceptual healthcare poses several challenges from both the provider and patient perspectives. For example, the CDC emphasizes that PCC is most effectively delivered by primary care providers (PCP), yet women often have fragmented care with multiple providers or multiple health encounters apart from their PCP.13 Family practice doctors are the most frequent provider of preventive care visits to women aged 18–​44 years.27,28 Nevertheless, one-​third of reproductive-​age women are only seen by their obstetrician gynecologist in a given year.29 And it is important to note that 80% of an obstetrician’s and gynecologist’s time is spent with women between the age of 18 and 44 years.30 Despite this, only 14% of women received PCC services from their obstetrician gynecologists or family practice physicians during their ambulatory care visit.31 An additional problem for implementing PCC is that nearly 25% of all reproductive-​ age women do not even see a doctor annually.32 One study noted that there has been a 25% decline in the use of primary care among reproductive-​age women with commercial insurance between 2008 and 2016.33 Although it is not clear as to the reason, one can speculate that with rising insurance premiums and deductibles, some women choose not to see a provider for financial reasons. Another important challenge to successful delivery of PCC is addressing the social determinants of health and environmental factors that have an adverse effect on health outcomes and contribute to health disparities. There is a need to develop a variety of models and tools that can effectively reach at-​risk and vulnerable populations with innovative solutions for addressing their health concerns. Aside from some of the challenges to providing preconception care, there are also many opportunities. One is to develop a team approach to PCC that involves multiple stakeholders. To do so requires a different perspective on who should provide PCC and where and when PCC should take place. For example, a pediatrician sees a child approximately 10 times in the first 2 years of life, providing an opportunity to talk with women about their health.34 In other words, how we view PCC depends on the lens through which we look. Since over 50% of pregnancies are unplanned, we should think of every health care visit as a potential opportunity to make a difference in the long-​term health of women.10,35 Whether a woman is seen in the emergency department or by a primary care provider, health professionals need to be conscious of any and every opportunity to ask patients about their wellness and what they are doing, or want to do, to improve their overall health.10,17

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TABLE 17.1 Preconceptual Health Checklist Lifestyle Medicine Pillar Nutrition • Fiber • Eliminate high-​risk food

Recommendation

Reference

• Folic acid • Vitamin D

25–​28 g/​day Avoid processed meat, High mercury fish 400 μg/​day 30–​50 ng/​mL

Physical activity • Total time • Weight training

150 min/​week of moderate intensity activity Strength training 2–​3 times a week

40 40

Sleep • Hours of sleep • Sleep quality • Screen OSA

7–​9 hr/​night Pittsburgh Sleep Quality Index Obstructive sleep apnea

41 42 43

Emotional wellness • Stress • ACE • Anxiety • Depression

Perceived Stress Scale ACE score General Anxiety Disorder-​2 32 ng/​mL or 80 nmol/​ L.47 Cord blood taken at the time of delivery reflected maternal blood levels with a high percentage of vitamin D insufficiency noted among Caucasian (34%) and black (7.6%) neonates.47 Despite data showing the majority of pregnant women have insufficient vitamin D levels, ACOG does not recommend supplementation48 beyond the RDA of 600 IU/​d, which is routinely included in prenatal vitamins.37 The subject of whether to supplement with higher doses of vitamin D than what is currently recommended hinges on if there are improved maternal or fetal outcomes. Studies have previously shown an association between low vitamin D levels and several adverse perinatal outcomes, although results have not been consistent among studies. Additionally, low vitamin D may increase the risk of congenital and early postnatal infection with Cytomegalovirus in human immunodeficiency virus (HIV)-​ infected women.49 A recent Cochrane review of nearly 30 studies in 2019 found that supplementing with vitamin D during pregnancy may reduce the risk of preeclampsia (relative risk (RR) 0.48), gestational diabetes (RR 0.51), and a low birthweight neonate (RR 0.55).50 These findings support vitamin D supplementation and vary from previous findings. A recent Danish randomized controlled trial (RCT) examined the question of whether supplementing with 2800 IU/​d (high dose) or 400 IU/​d (low dose) would improve bone mineralization at age 6 years.51 Their results showed that the high dose group had a significant increase in bone mineralization, with a trend toward decreased fractures, compared to the low dose group. There was no difference in anthropometrics between the groups. Whether the increased bone mineralization could potentially decrease the risk of osteoporosis in the future is not currently known. In light of more recent data suggesting both maternal and fetal benefits to vitamin D supplementation, it is prudent to check a vitamin D level at the initial prenatal visit. The optimal vitamin D level and the optimal amount of vitamin D to supplement during pregnancy are not currently known. Nevertheless, it is reasonable to provide

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supplementation if the patient is unable to get adequate sun exposure. The Endocrine Society recommends 1500–​2000 IU to prevent vitamin D insufficiency, with doses of 6000–​10,000 for women with obesity or malabsorption issues.52

18.3.2 Foods to Avoid Women who are pregnant are at increased risk of foodborne illnesses such as listeriosis and salmonellosis. Food safety guidance from the 2015–​2020 Dietary Guidelines for Americans recommend avoiding raw or undercooked meat or seafood because of the possibility of contamination with coliform bacteria, toxoplasmosis, and salmonella.53 Pregnant women should also avoid food products likely to contain listeria which can cause an infection leading to spontaneous abortion, preterm birth, fetal demise, and neonatal infection.54 These foods include processed meats that are not properly cooked, unpasteurized milk and milk products such as soft cheeses (e.g., feta, brie, and queso blanco), smoked seafoods and meat spreads from the deli counter, and salads made in the grocery store, such as egg and tuna salad,55 as well as raw or slightly cooked sprouts of any kind.54 Hispanic women are 24 times more likely to get listeriosis due to consumption of unpasteurized cheeses commonly used in Hispanic meals.54 Methylmercury exposure through consumption fish is also of concern in pregnant women because it is a neurotoxin in the developing fetus (see Chapter 17).56

18.3.3 Dietary Patterns and Adverse Pregnancy Outcomes Dietary patterns have a profound effect on the occurrence or prevention of APOs, in particular, gestational diabetes mellitus (GDM), preterm delivery (PTD), and preeclampsia. Sadly, women who live in a food desert have a 64% increased risk of at least one pregnancy-​related morbidity compared to women with ready access to healthy food.57 It is interesting to note that the Western-​type diet consisting of high meat and refined grains, while low in fiber, is associated with an increased risk of GDM,58 spontaneous PTD,64 and preeclampsia.65–​67 And women with a history of these conditions are at increased risk for future chronic disease because of their dietary lifestyle that led to the APOs. The ketogenic diet has become popular as a means of rapid weight loss and controlling blood glucose levels in diabetics. However, it is not generally regarded as safe because the principal substrate for fetal growth is glucose. Ketones do cross the placenta and consumption of a ketogenic diet increases the blood-​brain barriers permeability to ketones which are used by the fetal brain in lieu of glucose. Animal data shows that a ketogenic diet during gestation inhibits organ growth, especially in the central nervous system, heart, thymus, and liver.68 Unfortunately, there are few data on the impact of a ketogenic diet during pregnancy. One case series that used a ketogenic diet to treat epilepsy in pregnancy showed these women had vitamin deficiencies, hyperlipidemia with normal birth weight and neonatal growth at one year.69 A larger study in pregnant diabetic women found a correlation between elevated

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beta-​hydroxybutyrate and free fatty acid levels and lower intelligence.70 At present it is best to avoid a ketogenic diet during pregnancy based on the adverse effects reported in limited animal and human studies.

18.3.4 Excessive Weight Gain Excessive weight gain (EWG) is a significant risk factor for maternal and fetal morbidity and has significant health implications for the future health of both mother and infant. Currently, 35% of normal weight women and 60% of obese women exceed the IOM guidelines for weight gain.71 EWG negatively impacts maternal health, increases APO, and increases the risk of NCDs in future offspring.72 EWG leads to increased postpartum weight retention, and a greater likelihood of entering into subsequent pregnancies at a higher weight.73,74 It also leads to increased maternal and fetal complications in subsequent pregnancies.73,74 Women are also more likely to become obese or remain obese in the future.75-​77 EWG also increases the risk of GDM by 50% and hypertensive disorders are more common with EWG.78,79 And EWG negatively impacts the fetus, causing a greater number of large for gestational age (LGA) infants which subsequently leads to greater birth trauma and a 50% increased risk of Cesarean delivery.72,80,81 Finally, children of mothers with EWG are at increased risk of childhood and adult obesity.82-​83 Prospective studies that examine the impact of dietary patterns during pregnancy reveal that women are more likely to exceed the IOM guidelines for weight gain if they are on a Western diet61,84,85 than those consuming more fruits and vegetables.61,84 In light of these findings, it is important to convey to patients the importance of adopting a healthy lifestyle during pregnancy. Dietary interventions to reduce EWG during pregnancy have seen modest success. A systematic review noted an average reduction in weight gain of 3.6 kg with a significant decrease in the number of large for gestational age (LGA) infants and APO, but the overall quality of evidence was low.86 The most successful results are seen when there are more frequent group meetings in combination with the dietary approach to stop hypertension (DASH) diet,87,88 although there was no significant difference in weight 1 year postpartum.89 Further investigation is needed during pregnancy, especially with more plant predominant diets which are more efficacious in weight reduction than an omnivorous diet.90

18.3.5 Preterm Delivery Preterm birth is arguably one of the biggest public health problems faced during pregnancy. It accounts for 35% of neonatal deaths in the United States,91,92 with a recurrence rate of spontaneous preterm birth (sPTB) of approximately 50%.93 The rate of preterm birth is 11.4%, with the highest rate occurring in non-​Hispanic black women (16.3%) followed by Hispanic (11.3%) and Caucasian (10.2%) women.92 And early sPTB < 32 weeks’ gestation among non-​Hispanic blacks is more than double what is seen in Caucasian women. This leads to an estimated annual cost of more than 35 billion dollars (in 2020) and that does not take into account the long-​term morbidity seen in the very low birth weight infants.92

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Since there is no effective treatment for sPTB, most of the effort has been focused on prevention. One intervention that seems to be beneficial is supplemental omega-​3 long chain polyunsaturated fatty acids. A recent Cochrane systematic review noted a 42% reduction in PTB < 34 weeks’ gestation and 11% reduction in PTB < 37 weeks’ gestation in women who received omega-​3 compared to those who had no omega-​3 supplement.94 However, the benefit seems to apply to women with low omega-​3 status. Adequate omega-​3 free fatty acids can be achieved through consumption of fatty fish as well as flax seed, chia seed, walnuts, soybeans, and leafy green vegetables. Very few studies have addressed the role of dietary patterns in the occurrence of PTB. A recent large prospective cohort study from the United States examined the role of the DASH diet in the incidence of preterm birth. Greater adherence to the DASH diet was associated with a 41% reduction in PTB (odds ratio [OR] 0.59), with a similar reduction in the occurrence of sPTB (OR 0.58).91 In contrast, the group consuming a higher percentage of processed meat, dairy, fried food, and fast food had a 50% increase in the incidence of PTB (OR 1.53).91 Similar reduction in PTB has also been noted in prospective studies of pregnant women most adherent to a Mediterranean diet (OR 0.61) in Denmark95 and a vegetable, fruit, and rice diet in China (OR 0.55).96 The most impressive results to date are from an RCT of Norwegian women using a Mediterranean-​like diet.97 Patients were enrolled during the second trimester and were randomized to a control diet or a diet consisting of fish, low-​fat dairy, legumes, whole grains, low in saturated fat (< 32% overall fat), limited cholesterol to < 150 mg/​day, with six servings per day of fruits and vegetables. Women with a history of PTB, medical complications, or smoking were excluded. Using intent-​to-​treat analysis there was a 90% reduction in preterm birth in the study group (0.7%) compared to controls (7.4%). Overall, there was a 70% adherence rate to the diet. These rates are very impressive considering it was a very low risk group for PTB and the intervention occurred during the second trimester. And these results are substantially better than our current means of prevention of sPTB using weekly 17-​hydroxyprogesterone caproate (17-​OH P) which only lowers the risk of subsequent sPTB by 29%.98 Given these encouraging results, more studies are needed especially in women at highest risk of PTB.

18.3.6 Gestational Diabetes Gestational diabetes mellitus affects approximately 6% of women and increases the risk of maternal and fetal morbidity.13 Poorly controlled GDM increases the risk of preeclampsia and Cesarean in the mother and macrosomia, birth trauma, neonatal hypoglycemia, and hyperbilirubinemia in the infant. Offspring are also at increased risk of childhood and adult obesity and diabetes.13 Dietary patterns during pregnancy can either increase or decrease the risk of GDM. Prospective cohort studies indicated a much higher risk of diabetes with a Western-​type diet.61 Women with the highest protein intake during pregnancy have a more than 80% increased risk of GDM (adjusted odds ratio [aOR] 1.783), whereas women eating more whole foods can reduce their risk into half (aOR 0.54).63 Adherence to a Mediterranean diet can also decrease the risk of GDM in both a prospective99 and RCT (RR 0.73).100

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Diet is also the mainstay of treatment of GDM and has been shown to lower the risk of maternal and fetal complications. Fasting blood glucose (FBG) levels are most predictive of increased neonatal fat mass and subsequent development of childhood obesity and diabetes.13 The American Diabetes Association (ADA) recommends a diet composed of 33–​ 40% carbohydrates, 20% protein, and 40% fat.13 However, there is legitimate concern that a higher dietary fat in humans and animals promotes insulin resistance as well as offspring adiposity and metabolic syndrome. Recently, a small pilot study randomized woman to a low carbohydrate conventional diet (40% carbs/​45% fat/​ 15% protein) or choosing healthy options in carbohydrate energy (CHOICE) diet (60% carbs/​25% fat/​15% protein) in the third trimester and compared the metabolic profile in these women.101 After 7 weeks in the trial, the FBG and free fatty acids were significantly reduced in the CHOICE group. Multiple proinflammatory genes were lower on CHOICE and infant adiposity trended lower with CHOICE.101 Another trial randomized women with GDM to either a DASH diet or a control diet. Women on the DASH diet had a significant reduction in the need for treatment with insulin, as well as the incidence of polyhydramnios and macrosomia.102 Given these findings, treatment of GDM should emphasize more whole foods containing complex carbohydrates along with a lower fat content. More studies are needed to determine the optimal diet to treat GDM during pregnancy.

18.3.7 Gestational Hypertension and Preeclampsia Hypertensive disorders affect 3.8% of all US pregnancies and up to 9% of pregnancies globally.103 Together they are responsible for a significant amount of preterm birth and maternal death.104 Preeclampsia also is associated with a fourfold risk of end-​stage renal disease105 and threefold risk of future CVD.106 Gestational hypertension is also concerning as 50% eventually develop preeclampsia and it also leads to other APOs.104 Furthermore, both confer a significant risk for hypertension postpartum.107 Dietary patterns greatly influence the development of hypertensive disease in pregnancy. The Western diet significantly increases the risk of preeclampsia,65,108 whereas dietary patterns that are higher in vegetables, fruit, whole grains, nuts, legumes, and fish (a Mediterranean style diet) are associated with a reduced risk of hypertensive disease in pregnancy.66,108 In fact, there is a dose-​dependent correlation between the amount of dietary fiber consumed during pregnancy and subsequent preeclampsia. Women who consume > 21 g/​day of fiber have a 67% reduction in preeclampsia compared to women consuming < 12 g/​day, which is common in a Western diet.109 And for each 5 g/​day increase in fiber, there is a subsequent 14% reduction in preeclampsia risk.109 There is only one study that examined the effect of a vegan diet and risk for preeclampsia. In a group of 775 vegan mothers only one developed preeclampsia.110 Although this was a retrospective study, it examined a community that was very homogeneous in that they ate organic produce, were physically active, nonsmokers, and had close relationships. Their results are profound and bear repeating in a prospective trial.

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Patients with a history of preeclampsia or those at risk of preeclampsia should be counseled about the benefits of a plant predominate diet to reduce their risk. The available studies show a greater likelihood of avoiding preeclampsia with a high-​fiber diet than low-​dose aspirin (81 mg) which only reduces the incidence of preeclampsia by 24–​30%.111,112

18.3.8 Reversing Chronic Disease Over the last 3–​4 decades there has been a steady increase in the number of pregnant women presenting with one or more NCDs.113,114 The most common chronic disease that obstetric providers encounter is obesity, which now occurs in over one-​ third of pregnant women. Mood or anxiety disorders are seen in approximately 14% of pregnant women.115 Of these, 9% are due to a major depressive disorder, with the remainder mostly being generalized anxiety disorder.115,116 The remainder include hypertension, diabetes, respiratory diseases, thyroid disorders, autoimmune disorders, and CVD.113,114,117 Significant health disparities exist in the prevalence of chronic disease, with low income and women of color being disproportionately affected. Women of lower income are significantly more likely to have a chronic disease than women with higher income and are three times more likely to have three or more chronic diseases.118 These women tend to be less educated, unmarried, and Hispanic or non-​ Hispanic black compared to higher income women.116 This study also demonstrated that non-​Hispanic black women are twice as likely as white women to have a chronic disease.118 The increased incidence of chronic diseases can be attributed in large part to poor lifestyle behaviors including smoking, obesity, and binge drinking before pregnancy.118 Given the widespread impact of chronic disease on both the mother and fetus, it is prudent to consider addressing lifestyle behaviors during pregnancy. There are no contraindications to a plant predominant diet which has been used effectively to treat and even reverse obesity, hypertension, diabetes, and heart disease. It is important to maintain adequate caloric intake and focus on increasing the fiber and micronutrient content of food. The goal is not to lose weight, rather to improve their metabolic health.

18.4  PHYSICAL ACTIVITY 18.4.1 Introduction Pregnancy is an important opportunity for providers to promote exercise because it has been shown to benefit both the mother and fetus. In April 2020, the ACOG updated their guidelines for physical activity in pregnancy in line with recommendations from the American College of Sports Medicine (ACSM) and Physical Activity Guidelines for Americans.119 Canada,120 Australia, Denmark, France, Japan, Norway, Spain, and Australia also have released similar recommendations.121 These guidelines support moderate-​intensity physical activity during pregnancy and encourage initiating an exercise program during pregnancy.

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With only 27.3% of pregnant women meeting the minimum standard of physical activity (150 minutes/​week) as of 2018,122 it has become imperative to intentionally prescribe exercise in pregnancy. It is suggested that women should seek advice from their healthcare provider before starting or continuing an exercise program, yet obstetricians are not consistently or accurately counseling their pregnant patients.123,124 Women also perceive that their provider’s knowledge is limited125 and their support is lacking.126

18.4.2 Safety of Exercise in Pregnancy The majority of women can safely exercise in pregnancy even if they have been sedentary in the past. Exceptions are those with maternal or pregnancy-​related conditions that are contraindications to exercise. Maternal diseases considered to be a contraindication to exercise include moderate to severe heart disease, unstable maternal arrhythmia, severe restrictive lung disease, and severe undernutrition.119,120,127,128 Obstetrical contraindications to exercise include vaginal bleeding, placental abruption, cervical insufficiency (including those with a cerclage), preterm premature rupture of the membranes, preterm contractions/​labor, fetal growth restriction, vasa previa, and severe preeclampsia.119,120,127,128 Consultation with relevant specialists is recommended if there are concerns for maternal safety. The physical activity readiness tool PARmed -​X FOR PREGNANCY is a health screening checklist and conversation starter for participation in prenatal exercise programs.129 Some women express concerns regarding the potential of exercise to increase the risk of miscarriage, preterm labor, or harmful effects to their baby. Yet, the literature overwhelmingly demonstrates no increase in the odds of miscarriage, congenital anomalies, perinatal mortality, or hyperthermia.130,131

18.4.3 Benefits of Exercise in Pregnancy There are numerous benefits of exercise during pregnancy, including reducing EWG, reduction in APO, reduction in anxiety and depression, and improved delivery outcomes. Weight management during pregnancy is one of the predictable challenges for both mother and her healthcare provider. EWG during pregnancy is associated with increased risk for LGA babies, macrosomia, gestational diabetes, increased risk for operative delivery, and increased risk of postpartum weight retention.132 Moderate and vigorous physical activity is inversely associated with excessive gestational weight gain.133 and decreases the odds of postpartum weight retention.134,135

18.4.4 Hypertensive Disease Hypertensive disorders of pregnancy include the spectrum of gestational hypertension and preeclampsia. Pregnant women who do not exercise, regardless of BMI, are three times more likely to develop hypertension.136 In contrast, higher levels of prepconceptual or early pregnancy physical activity reduce the risk of developing preeclampsia by 20–​35% and are inversely associated with preeclampsia in a dose-​ dependent manner.137

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18.4.5 Metabolic Disease During pregnancy insulin resistance increases due to physiologic changes in pregnancy, increasing the risk of GDM. Prenatal exercise reduces maternal circulating blood glucose concentrations138 and reduces the risk of GDM.119 Exercise during pregnancy is associated with a significant reduction in the frequency of gestational diabetes in overweight/​obese pregnant women.139 It is also used to treat GDM13 and pregestational diabetes140 in an effort to achieve euglycemia.

18.4.6 Labor and Delivery Pregnant women are often anxious about childbirth, even to the point of requesting a Cesarean delivery.141 Even so, structured physical activity during pregnancy can reduce the risk of Cesarean142 and instrumental delivery.143 In contrast, a low level of physical activity increases the risk of operative delivery.142 Recent data from smaller studies demonstrate shortening of the first stage of labor by over 100 minutes,144 and a decrease in the duration of the total first and second stages of labor by 57 minutes.145

18.4.7 Depression and Anxiety during Pregnancy and Postpartum Depression and anxiety during pregnancy increase the risk of postpartum depression.146 Moderate quality evidence from RCTs reveals that exercise-​only interventions reduce the severity of prenatal depressive symptoms and the odds of prenatal depression by 67% when compared to no exercise. There was also a dose response, with a greater volume of exercise associated with a greater reduction in the severity of prenatal depressive symptoms.147 However, the impact of prenatal exercise on postpartum depression is not as clear. Women who met the physical activity recommendations of more than 150 minutes of moderate to vigorous physical activity per week did have a lower risk of postpartum depressive symptoms when compared to women who were not active during pregnancy. These results persisted in the sample of ethnic minority women.148 Others have not demonstrated a reduction in postpartum depression although noncompliance may have contributed to these results.149 Further study is needed to investigate this relationship.

18.4.8 Impact of Pelvic Floor Muscle Training The 2019 Canadian guidelines for physical activity include pelvic floor muscle training (PFMT), such as Kegel exercises, to be performed on a daily basis to reduce the risk of urinary incontinence.120,150 PFMT is effective in the primary prevention of urinary incontinence in primiparous women.151 And prenatal PFMT significantly shortens the first and second stages of labor in primigravidas.152 A large Cochrane review demonstrated that PFMT decreases the risk of urinary incontinence postpartum.153 And the addition of aerobic exercise in conjunction with PFMT reduces the odds of urinary incontinence by 50% compared to only 37% of women who did PFMT alone.154 Among women who were incontinent during pregnancy, exercise training was not therapeutic; however, PFMT with or without exercise

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did reduce symptom severity of urinary incontinence both during pregnancy and in the postnatal period.154

18.4.9 A Prescription for Exercise 18.4.9.1 Frequency The recently updated ACOG Committee Opinion and Canadian Guidelines suggest no less than 150 minutes of moderate intensity exercise weekly spread over 5–​7 days per week from the first trimester until delivery. For women who have been previously sedentary, they may begin exercising three times per week and increasing gradually.119,120,155 18.4.9.2 Intensity Intensity should be tailored to the individual’s fitness.150 Moderate intensity exercise using heart rate described by ACOG guidelines is considered less than 60 to 80% of age predicted maximum internal heart rate and usually does not exceed 140 bpm.119 Data is insufficient to counsel pregnant women regarding strenuous or vigorous exercise, particularly athletes who desire to continue their training during pregnancy and are not under the guidance of coaches or organizations. Vigorous aerobic exercise at 55–​75% maximum heart rate for 60 minutes three times per week for 12 weeks was found to be safe.156 The impact on neonatal outcomes is not known and further studies are needed. 18.4.9.3 Type Those activities that have been studied in RCTs and found to be safe include walking, stationary cycling, aerobic exercises, dancing, resistance training including weights and elastic bands, stretching exercises, and water aerobics.157 Activities that risk falling and/​or abdominal trauma and contact sports in general are not recommended and would be considered unsafe especially during the second and third trimesters.127 In general, women are also cautioned to avoid scuba diving during pregnancy. Animal data suggest possible adverse fetal effects due to fetal decompression illness and hyperbaric oxygen exposure;158 however, there is limited published data in humans. There are limited studies with few subjects on exercise and pregnancy at high altitude. Available studies show that acute exposure up to 2500 meters with moderate duration exercise poses little risk to mother and fetus during the third trimester of a normal pregnancy.159 General recommendations for exercise at high altitude include adequate hydration, allowing acclimatization to altitudes more than 2,500 m for the first 4–​5 days of exposure, limiting intensity to the “talk test”, and being well informed regarding the symptoms of acute mountain sickness. Preexisting conditions such as hypertensive diseases of pregnancy and/​or fetal growth restriction are considered contraindications for traveling to or exercising at high altitude after 20 weeks’ gestation.159,160 In general, there are few studies that address resistance and strength training programs in pregnancy; however, no adverse outcomes have been reported.120,161 Data is lacking specifically about heavy resistance weight training during pregnancy.162

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18.4.9.4 Time There is minimal data on the safe upper limit for the duration of exercise and pregnancy, and intensity should be considered as a variable. As the RCTs have shown, exercise in pregnancy is safe and beneficial with sessions lasting approximately 30–​ 60 minutes.157 When starting an exercise program, previously sedentary women may begin exercising with as little as 10–​15 minutes of continuous exercise with the goal of gradually increasing to 30–​60-​minute sessions.150 In summary, exercise in pregnancy is safe and beneficial for both the mother and fetus. Pregnancy is an ideal time to counsel a woman as she is often motivated to ask questions, heed advice, and modify her habits. Women deserve providers who are knowledgeable and supportive about this important impact they can have on their pregnancies. Exercise is an uncomplicated prescription for the benefits of two generations.

18.5  SLEEP One in three Americans does not get the Centers for Disease Control and Prevention (CDC) recommended 7–​9 hours of sleep per night163, and over the last century the amount of sleep the average American gets has decreased by an hour and a half.164 Women entering prenatal care reflect the baseline poor sleep health of the general population, and sleep worsens further in pregnancy.165,166 Physiologic changes during pregnancy, including increased intra-​abdominal pressure, increased airway edema, and more frequent needs for nighttime urination, can worsen sleep disturbances. Poor sleep quantity and quality have been linked to a number of APOs. Screening for impaired sleep coupled with intervention and possible referral for sleep disorders has the potential to improve care for women and newborns. Sleep disturbances studied in over 2,000 women across the duration of their pregnancy found that 76% of pregnant women reported poor sleep quality, with all reporting frequent nighttime awakenings, 19% reporting sleep-​disordered breathing (SDB), and 24% reporting awakenings from restless leg syndrome. Other common issues contributing to poor-​quality sleep included frequent urination (83%) and difficulty finding a comfortable position for sleep (76%).166 Despite the fact that many of the causes of poor sleep can be diagnosed and corrected during pregnancy, few prenatal care providers have been trained to take an accurate sleep history and education on sleep is not a formal part of residency training for Obstetrician Gynecologists (OB-​GYNs).167 Furthermore, sleep is not a component of history on the ACOG prenatal record. One option for screening sleep is the Pittsburgh Sleep Quality Index (PSQI), which asks patients to recall several components of healthy sleep.168 The form is scored to give a single composite score, with a composite score of 6 on the PSQI, indicating a baseline of impaired sleep.169 When screening for poor sleep in pregnancy, prenatal care providers should be aware of the varied risk factors for sleep impairment in pregnancy, including multiparity,170 African-​American ethnicity,170 evening and variable shift work,171 age greater than 30,172and obesity.173

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18.5.1 Obstructive Sleep Apnea and Pregnancy Outcomes SDB refers to sleep disruption caused by impaired airflow, and the most common and severe manifestation is obstructive sleep apnea (OSA). The physiologic changes of pregnancy can lead to impaired air movement, ultimately resulting in recurrent episodes of OSA. Pregnancy-​associated edema can narrow the lumen of the airway, and weight gain can increase pressure on the airway, decreasing airflow. Healthy sleep is associated with a decrease in catecholamine levels and sympathetic tone; however, hypoxemia and sleep fragmentation associated with SDB lead to an increase in sympathetic tone, blunting of the blood pressure decrease of pregnancy, and an increase in morning blood pressure.174 OSA is prevalent in women of reproductive age and increases with gestational age. In nonpregnant women, SDB may be as high as 9%, similar to the 10% seen in the first trimester and rising to 27% by the third trimester.175 The weight gain, airway and respiratory changes of pregnancy may worsen pre-​existing OSA or create new onset OSA in a previously healthy woman. It is not clear if these two groups manifest different pregnancy outcomes. In the nonpregnant population, chronic hypertension and diabetes are linked to OSA. Both conditions increase the risk of the hypertensive disorders of pregnancy including preeclampsia and it is likely that a similar mechanism links OSA to preeclampsia. Airflow limitation followed by arousal and awakening leads to repetitive cycles of hypoxemia. These cycles of oxygenation cause oxidative stress and stimulate the sympathetic nervous system. This stimulation leads to endothelial dysfunction, altering vascular resistance and impairing placental tissue perfusion and oxygenation. Ultimately, this placental hypoxia activates pathways leading to preeclampsia. Sleep deprivation also interferes with glucose metabolism by reducing glucose clearance by 40%.176 And during pregnancy there is a linear correlation between the severity of OSA and the incidence of gestational diabetes. One study found increasing rates of GDM in patients without OSA (25%), 43% for mild OSA, and 63% for moderate/​severe OSA.177 Studies are ongoing to assess if the reversal of OSA with continuous positive airway pressure (CPAP) has an impact on the risk of gestational diabetes.178 CPAP improves airflow in SDB and has been studied as a treatment for pregnancy-​ related changes of SDB. It has been shown to increase fetal movement, and in preeclamptic women CPAP decreases systemic resistance and increases cardiac output.179 Autotitrating CPAP adjusts for the airway pressure needed as the pregnancy progresses and can be used in pregnancy.180 Prenatal providers should be aware that referral to sleep specialists for further studies and management should be done in pregnancy in women suspected of having OSA.

18.5.2 Labor Outcomes The impact of sleep on labor outcomes is poorly understood. Decreased sleep the night before the onset of labor significantly increases the perception of pain in spontaneous labor.181 Primiparous women who average 40, or >35 kg/​m2 with at least one serious morbidity. However, bariatric surgery is a major intervention with short-​and long-​term risks. A lifestyle-​focused approach favors at least 6 months of lifestyle interventions prior to considering bariatric surgery, and lifestyle modification should not be considered to have failed without the patient trying or declining an intensive lifestyle immersion program. Women undergoing bariatric surgery should delay pregnancy for at least 12–​24 months.7

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19.4.2 Physical Activity Physical activity interventions are not themselves effective in reducing PPWR but enhance the effectiveness of dietary interventions.37,39,40 Postpartum physical activity also has beneficial effects on cardiovascular fitness, quality of life, stress, sleep patterns, physical symptoms, and postpartum depression (PPD).37,39,41 Women should gradually increase their activity level in the postpartum period and in most cases can return to pre-​pregnancy activities by 4–​6 weeks postpartum.37,42 Beyond 6 weeks, women should aim to meet adult guidelines of at least 150 minutes of moderate physical activity or 75 minutes of vigorous activity per week, as well as resistance training. Physical activity interventions involving structured, measurable programs, such as those incorporating heart rate monitors or pedometers, have been found to be beneficial in the postpartum period.39 Home exercise programs using video-​based instruction are beneficial and have excellent compliance given their flexibility.41 Exercise classes tailored to new mothers may provide a positive mother–​infant activity and incorporate a component of peer support.

19.4.3 Sleep Maternal sleep duration and quality are affected by infant sleep patterns and nighttime care needs, particularly in the first 3 months postpartum. Frequent sleep disruptions lead to short sleep duration and unrestful sleep, especially in women who have difficulty with sleep initiation.43–​45 Fragmented sleep continues in 20–​30% of infants through 12 months of age or beyond.43,44 PPWR at 6 months postpartum is threefold higher in women who sleep less than 5 hours per night compared with those sleeping 5 or more hours per night.34,43 Impaired sleep is also associated with postpartum mood symptoms, relationship strain, and less effective parenting.43,44 Behaviorally, sleep deprivation leads to less self-​care, physical activity, planning, and preparation of healthy meals.34,46–​48 The most effective intervention to improve postpartum sleep is cognitive behavioral therapy (CBT) focused on sleep hygiene.46 Stress reduction techniques, exercise, and sufficient intake of polyunsaturated and omega-​3 fatty acids may promote sleep quality and regulate melatonin levels.41,44,46 High prolactin levels are associated with more deep, restorative sleep in healthy breastfeeding mothers.45,49 Family interventions should focus on infant sleep routines and creating a conducive sleep environment, often in a different room from the infant.44–​46,50 Pharmacologic therapy may be considered in refractory cases but is less effective than CBT.46

19.4.4 Emotional Wellness Postpartum blues is a self-​limited condition that affects up to 80% of women in the first few days postpartum and typically resolves within 2 weeks, without impairing the mother’s ability to function and care for the infant.51 Treatment centers around emotional and social support while awaiting spontaneous resolution. PPD is a major depressive episode seen in 10–​20% of women in the postpartum period and lasting 2 weeks or more. PPD may manifest with depression, anxiety, or

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a combination. Symptoms may be severe and disabling and often require both supportive and pharmacologic treatment.51 PPD has been linked to negative offspring outcomes including attachment insecurity, infantile colic, and behavioral and emotional challenges.51 Although PPD often resolves in the postpartum period, up to one-​fourth of affected women continue to have elevated depression scores 3 years postpartum.52 All women should be screened for PPD and anxiety using a validated screening tool. There should be a planned response protocol for management of a positive result, as well as an emergency referral protocol for suicidal ideation, homicidal ideation, or acute psychosis.53,54 Screening in conjunction with newborn pediatric visits is useful when there is a system for efficient collaboration with obstetric providers.7 Postpartum psychosis is the rarest but most potentially dangerous of the recognized postpartum mood disorders. It occurs in only 0.1% of postpartum women but is considered a psychiatric emergency and almost always requires hospitalization.51 A less recognized postpartum psychological complication is post-​traumatic stress disorder (PTSD), which occurs in 1.5–​7% of women as a result of perceived trauma during the labor and delivery process. The perception of trauma is often driven more by a woman’s experience of feeling vulnerable, unprotected, and unheard than by the actual situation or outcome.55–​58 Postpartum PTSD can have long-​term impacts, including relationship strain, sexual dysfunction, depression, fear of future childbirth, and impaired infant bonding.56–​59 Anniversary reactions timed to a previous PTSD experience can be particularly bothersome for women who feel they should be celebrating their child’s birthday, an incongruously joyous event.56 Many experts now recommend universal screening for PTSD symptoms related to delivery. It is important to recognize that an outside appraisal of the birth experience may not be predictive of the patient’s perceptions of the experience.55,57 Screening, alone, has clinical benefits for postpartum mood disorders.54 Although data are mixed, evidence suggests fewer PPD symptoms with healthy dietary patterns, multivitamin supplementation, increased intake of polyunsaturated fatty acids, and increased intake of certain micronutrients (e.g., calcium, vitamin D, zinc, and possibly selenium).33 CBT is beneficial for women with PPD, although psychotropic medications are indicated for severe symptoms and those impacting maternal quality of life.59 The mainstay of treatment for postpartum PTSD is trauma-​informed psychotherapy.56,57 Depression often coexists with PTSD and should be treated, but symptoms of trauma should not be attributed solely to PPD.57 In a future pregnancy, a woman with PTSD will benefit from heightened antepartum and peripartum support with attempts to help her feel empowered, well-​informed, and involved in all decision-​making.57

19.4.5 Avoiding Risky Substances Nearly 50% of smokers and 70–​90% of alcohol and illicit substance users become abstinent in pregnancy,60 in some cases permanently. However, the postpartum period is a high-​risk time for relapse due to increased stress levels, hormonal changes, sleep deprivation, and mood disorders.61 Nearly 50% of smokers who had quit in pregnancy

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relapse within 2 weeks of delivery, and 80% within 6 months.60 By 3 months postpartum, 51% of abstinent drinkers, 41% of abstinent marijuana users, and 27% of abstinent cocaine users have resumed use.60 Depending on the nature of the exposure, postpartum substance use may be associated with increased offspring risks, including SIDS, respiratory and ear infections, asthma, obesity, neurodevelopmental changes, psychiatric illness, cancers, and increased substance use later in life.62,63 Substance use disorders are also associated with more maternal health consequences, postpartum psychiatric disorders, unintended pregnancy, and lower rates of contraceptive use.7 Early postpartum follow-​up may be beneficial for women with a history of substance abuse, and the provider should ask directly about drug cravings and potential for relapse.61 Counseling should be provided to support continued abstinence. Women who have resumed substance use postpartum should be offered behavioral interventions and pharmacotherapy as indicated.

19.4.6 Positive Psychology and Connectedness Postpartum social support is associated with less stress and depression, better adaptation to parenthood, and more breastfeeding.64,65 Poor social support is linked to more pain symptoms, fatigue, hypertension, and a fivefold increase in PPD.65 Postpartum complications are increased in women with healthcare disparities or concerns about safety in their home or community. Intimate partner violence (IPV) affects 17% of women in their first year postpartum and is associated with maternal mood disorders, PTSD, physical injury, homicide, suicide, and reproductive coercion.7,66 For women without a stable support network, peer support groups can be beneficial.65 Women with barriers to adequate healthcare, including low health literacy, limited English proficiency, or other communication barriers, may benefit from involvement of patient navigators, interpreters, health educators, or lay community healthcare workers.7 IPV survivors should be referred for targeted social interventions.67

19.5  REPRODUCTIVE LIFE PLANNING The ideal interpregnancy interval (IPI), which is defined as the time between a birth or pregnancy loss and conception of the next pregnancy, is between 18 and 60 months. A modest increase in obstetric risks is seen with an IPI outside of this range, and more significant risks with an IPI less than 6 months or more than 10 years. A short IPI is associated with maternal obesity, anemia, preterm birth, preeclampsia, poor fetal growth, fetal or neonatal loss, and neonatal morbidity; these risks are further increased in women with a history of prior adverse pregnancy outcomes. A short IPI following a Cesarean delivery increases risks of uterine rupture and maternal blood transfusion in a subsequent pregnancy. There are also data suggesting increased risks of schizophrenia, attention deficit hyperactivity disorder, and autism-​spectrum disorders in the offspring of short-​interval pregnancies. A long IPI increases risks of preeclampsia and labor dystocia.7,68 In the United States, half of pregnancies are unplanned and one in three women become pregnant less than 18 months postpartum.7 Providers should address a

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patient’s desire for future childbearing before delivery and help her create an appropriate contraceptive plan, as indicated. If a woman does not desire future childbearing, the postpartum period offers an opportunity to discuss the transition to well-​woman care and options for pregnancy prevention.

19.6  ADVERSE PREGNANCY OUTCOMES AND FUTURE HEALTH Pregnancy provides a glimpse into a woman’s future health, as adverse pregnancy outcomes are predictive of future health complications.7,36,69

19.6.1 Cardiovascular Disease Traditional cardiovascular risk factors, such as hypertension, elevated BMI, diabetes, and abnormal lipid levels, are associated with an increased risk of adverse pregnancy outcomes. In turn, adverse pregnancy outcomes are considered pregnancy-​related cardiovascular risk indicators, with the highest risk being among women with more severe or recurrent complications.35,70,71 Women with a history of preeclampsia have an increased risk of hypertension, ischemic heart disease, stroke, peripheral vascular disease, metabolic disease, renal disease, premature cardiac death, and all-​cause mortality when compared with women without a history of preeclampsia.35,36,69,70,72–​77 The risk of cardiovascular disease is increased 8–​10-​fold for cases of preeclampsia that are severe, preterm, associated with iatrogenic preterm delivery, or associated with fetal growth restriction.35,72,77 Gestational hypertension, gestational diabetes, placental abruption, preterm birth, and stillbirth are also associated with cardiovascular disease and premature mortality, particularly when they exist in combination.35,36,75–​78 Fetal undergrowth and overgrowth are both related to increased cardiovascular disease risk, with the highest risk being among women delivering babies that are both small-​for-​gestational age and preterm.75,78 Adverse pregnancy outcomes are biologically interrelated disorders caused by placental dysfunction, vasospasm, inflammation, and endothelial activation.70,79 The unifying vascular pathology that underlies adverse pregnancy outcomes is strikingly similar to that underlying cardiovascular diseases, which explains why they share common risk factors and are strongly predictive of each other.69,70,79 Pregnancy is a type of cardiovascular stress test, in which the physiologic demands of pregnancy unmask and amplify preexisting vascular or metabolic dysfunction35,72 (Figure 19.1). To what degree adverse pregnancy outcomes directly cause cardiovascular disease or simply uncover a latent predisposition for cardiovascular dysfunction is not entirely clear.69,70,72,73,79

19.6.2 Renal Disease Preeclampsia is associated with an increased risk of microalbuminuria and chronic kidney disease.70,72,74 The risk of end-​stage renal disease is increased 3–​10-​fold in women with a history of preeclampsia, even after controlling for coexistent hypertension and diabetes.74 Preeclampsia may initiate a cascade of events in the kidney

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Range of baseline function

VASCULAR FUNCTION

Lifestyle modification

Baseline function

Age-rel

ated va

scular de

cline

Baseline function Pregnancy function Threshold for clinicallyevident vascular dysfunctio

Pregnancy function

First pregnancy

Second pregnancy

FIGURE 19.1  Pregnancy acts as a stress test that can unmask underlying vascular dysfunction. Lifestyle intervention after a complicated pregnancy may improve baseline vascular function, mitigating the risk of recurrent vascular dysfunction in a subsequent pregnancy and later in life.

that leads to progressive renal insufficiency. Women with proteinuric hypertension in pregnancy have been found to shed viable renal podocytes in the urine, a process shown in animal models to lead to irreversible glomerulosclerosis once a certain threshold of lost cells is reached.74 However, the link between preeclampsia and renal disease may be related to common risk factors and not to the impact of a single hypertensive pregnancy on the kidney.74

19.6.3 Type 2 Diabetes Mellitus Women with a history of GDM have a lifetime risk for Type 2 diabetes at least eightfold higher than unaffected women.1,36,80 Immediately postpartum 5–​10% of women with GDM will meet the criteria for Type 2 diabetes, and by 10 years after delivery 50% will develop Type 2 diabetes.1,80 Delivery of a macrosomic infant and a history of preterm birth are also related to future Type 2 diabetes, independent of a diagnosis of GDM.36,75,76 GDM is also a strong cardiovascular risk factor, although much of this risk relates to the likelihood of developing Type 2 diabetes. The risk of cardiovascular disease is increased fourfold if Type 2 diabetes develops, compared with 1.4-​fold in women with a history of GDM who never develop Type 2 diabetes.81 Prevention of progression to Type 2 diabetes may mitigate much of the excess cardiovascular risk.

19.6.4 Offspring Effects The theory of developmental origins of health and disease suggests that early-​life environmental exposures influence long-​term health through epigenetic mechanisms that may propagate through several generations.82 Tissues are particularly sensitive to environmental influences during critical developmental periods in pregnancy and early childhood. Exposure to maternal health conditions, obesity, or pregnancy complications during early development are thought to condition or “program” the

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offspring, predisposing to increased obesity and cardiometabolic disease susceptibility later in life.82 Indeed, maternal obesity and diabetes during pregnancy are associated with lifelong perturbations in metabolic tissues of the offspring.82 In addition, adults born of a preeclamptic pregnancy have been found to have higher BMI, higher mean blood pressure, and earlier onset of hypertension.74

19.6.5 Screening and Interventions The American College of Obstetrics and Gynecology (ACOG) and American Heart Association (AHA) recommend that women with a history of preeclampsia, gestational hypertension, gestational diabetes, or preterm birth should be referred for cardiovascular risk screening within the first year postpartum, including an assessment of blood pressure, BMI, waist circumference, fasting blood glucose, lipid profile, metabolic panel, renal function, and electrocardiogram. Then the patient should have a minimum annual evaluation of blood pressure, lipid profile, and fasting blood glucose.7,35,72,78 Since 2011, the AHA has identified both preeclampsia and gestational diabetes as historical risk factors for cardiovascular disease. However, cardiovascular risk calculators still fail to account for the impact of adverse pregnancy outcomes, and other pregnancy outcomes are not yet recognized as independent AHA risk factors. As discussed previously, women with a history of GDM should be screened for overt diabetes 4–​12 weeks postpartum.1,35 If consistent with diabetes, the patient should be referred for lifestyle and medical management. Testing should be repeated yearly if there is evidence of impaired glucose tolerance (IGT), and at least every 3 years if normal.35 Lifestyle interventions are recommended for all women with a history of GDM, as they have been shown to be effective in reducing progression from IGT to Type 2 diabetes83 and to reduce PPWR and PPD in women with a history of GDM.84 Adverse pregnancy outcomes are largely rooted in abnormal placental vasculature including an imbalance of prostacyclin and thromboxane.70 Low-​dose aspirin therapy diminishes this imbalance, and its use in pregnancy reduces the risk of preeclampsia by 10–​20% in women at elevated risk based on prior history or risk factors.70,85,86 The fact that aspirin may also be beneficial for cardiovascular risk reduction further supports a shared pathophysiology for cardiovascular disease and hypertensive disorders of pregnancy. Pregnancy certainly provides a window into a woman’s future health, but all the risks predicted by pregnancy outcomes are modifiable. Aggressive lifestyle interventions including a whole-​food, minimally processed, plant-​based diet; physical activity; weight loss; and other positive lifestyle modifications can reverse the underlying risk factors and dramatically lower the risk of progression to chronic disease. Interventions started before a future pregnancy can lower the risk of obstetric complications and have long-​term beneficial effects on the child related to metabolic programming.87

19.7  CONCLUSION The postpartum period presents a unique opportunity to intervene positively in a woman’s life. Adverse pregnancy outcomes may be a sobering preview of future health

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risks and acting as a strong motivator of change. Lifestyle intervention following pregnancy may reduce the risk of not only recurrent pregnancy complications in the future, but also health risks throughout the lifespan. Development of a targeted model of Lifestyle Medicine care for reproductive-​age women may be an ideal strategy, as it could provide focused intervention for women’s health, pregnancy, breastfeeding, and newborn care, ideally in a setting that fosters social support through a network of women at a similar stage of life. For additional reading, see supplementary material.

REFERENCES 1. Paladine HL, Blenning CE, Strangas Y. Postpartum care: An approach to the fourth trimester. Am Fam Physician. 2019;100(8):485–​491. www.aafp.org/​afp/​2019/​1015/​ p485.html 2. Hamilton N, Stevens N, Lillis T, Adams N. The fourth trimester: Toward improved postpartum health and healthcare of mothers and their families in the United States. J Behav Med. 2018;41:571–​576. https://doi.org/​10.1007/​s10865-​018-​9969-​9 3. Spelke B, Werner E. The fourth trimester of pregnancy: Committing to maternal health and well-​being postpartum. R I Med J. 2018; Oct:30–​33. www.rimed.org/​ rimedicaljournal/​2018/​10/​2018-​10-​30-​obgyn-​spelke.pdf 4. Bryant AS, Haas JS, McElrath TF, McCormick MC. Predictors of compliance with the postpartum visit among women living in healthy start project areas. Matern Child Health J. 2006;10(6). https://​escholarship.org/​uc/​item/​87t7k7zp 5. Tully KP, Stuebe AM, Verbiest SB. The fourth trimester: A critical transition period with unmet maternal health needs. Am J Obstet Gynecol. 2017;217(1):37–​41. https://​ doi.org/​10.1016/​j.ajog.2017.03.032 6. Presidential Task Force on Redefining the Postpartum Visit, Committee on Obstetric Practice. ACOG Committee Opinion Number 736: Optimizing postpartum care. Obs Gynecol. 2018;131(5):e140–​e150. https://doi.org/​10.1097/​AOG.0000000000002633 7. American College of Obstetrics and Gynecologists. Obstetric Care Consensus Number 8: Interpregnancy care. Obs Gynecol. 2019;133(1):e51–​e72. https://doi.org/​10.1097/​ AOG.0000000000003025 8. Centers for Disease Control and Prevention. Breastfeeding: Frequently asked questions. www.cdc.gov/​breastfeeding/​faq/​index.htm. Published 2020. Accessed October 18, 2020. 9. U.S. Department of Agriculture and U.S. Department of Health and Human Services. Dietary Guidelines for Americans, 2020–​2025. 9th edition. December 2020. Accessed December 29, 2020. https://doi.org/​10.3945/​an.111.000430 10. Holick MF, Binkley NC, Heike ABF, et al. Evaluation, treatment, and prevention of vitamin D deficiency: An Endocrine Society Clinical Practice guideline. J Clin Endocrinol Metab. 2011;96:1911–​1930. https://doi.org/​10.1210/​jc.2011-​0385 11. U.S. Surgeon General. Breastfeeding: Surgeon General’s call to action factsheet. www.hhs.gov/​ s urgeongeneral/​ r eports-​ a nd-​ p ublications/​ b reastfeeding/​ factsheet/​ index.html. Published 2011. Accessed October 18, 2020. 12. Ip S, Chung M, Raman G, et al. Breastfeeding and maternal and infant health outcomes in developed countries. Evid Report/​Technology Assess No 153 AHRQ Publ No 07–​ E007 Rockville, MD Agency Healthc Res Qual. 2007. www.ncbi.nlm.nih.gov/​books/​ NBK38337/​ 13. Duijts L, Jaddoe VWV, Hofman A, Moll HA. Prolonged and exclusive breastfeeding reduces the risk of infectious diseases in infancy. Pediatrics. 2010;126(1): e18–​e25. https://​doi.org/​10.1542/​peds.2008-​3256

360

360

Kristi R. VanWinden and Elizabeth Collins

14. Shulman RJ, Schanler RJ, Lau C, Heitkemper M, Ou C-​N, O’Brian Smith E. Early feeding, feeding tolerance, and lactase activity in preterm infants. J Pediatr. 1998; 133:645–​649. https:/​doi.org/​10.1016/​s0022-​3476(98)70105-​2 15. Shulman RJ, Schanler RJ, Lau C, Heitkemper M, Ou C-​ N, Smith B. Early feeding, antenatal glucocorticoids, and human milk decrease intestinal permeability in preterm infants. Pediatr Res. 1998; 44:519–​523. https://doi.org/​10.1203/​ 00006450-​199810000-​00009 16. Gridneva Z, Kugananthan S, Hepworth AR, et al. Effect of human milk appetite hormones, macronutrients, and infant characteristics on gastric emptying and breastfeeding patterns of term fully breastfed infants. Nutrients. 2017;9(15). https://​ doi.org/​10.3390/​nu9010015 17. Fanaro S, Chierici R, Guerrini P, Vigi V. Intestinal microflora in early infancy: Composition and development. Acta Paediatr. 2003; Suppl 441:48–​ 55. https://​doi.org/​10.1111/​j.1651-​2227.2003.tb00646.x 18. Ip S, Chung M, Raman G, Trikalinos TA, Lau J. A summary of the Agency for Healthcare Research and Quality’s evidence report on breastfeeding in developed countries. Breastfeed Med. 2009;4(Suppl 1):S17–​ S30. https://​doi.org/​10.1089/​ bfm.2009.0050 19. Quigley MA, Kelly YJ, Sacker A. Breastfeeding and hospitalization for diarrheal and respiratory infection in the United Kingdom millennium cohort study. Pediatrics. 2007;119(4):e837–​e842. https://doi.org/​10.1542/​peds.2006-​2256 20. Li R, Fein SB, Grummer-​Strawn LM. Association of breastfeeding intensity and bottle-​ emptying behaviors at early infancy with infants’ risk for excess weight at late infancy. Pediatrics. 2008;122(Suppl. 2):S77–​S84. https://​doi.org/​10.1542/​peds.2008-​1315j 21. Li R, Fein SB, Grummer-​Strawn LM. Do infants fed from bottles lack self-​regulation of milk intake compared with directly breastfed infants? Pediatrics. 2010;125(6): e1386–​ e1393. https://doi.org/​10.1542/​peds.2009-​2549 22. Owen CG, Martin RM, Whincup PH, Smith GD, Cook DG. Effect of infant feeding on the risk of obesity across the life course: A quantitative review of published evidence. Pediatrics. 2005;115(5):1367–​1377. https://doi.org/​10.1542/​peds.2004-​1176 23. Das UN. Breastfeeding prevents type 2 diabetes mellitus: But, how and why? Am J Clin Nutr. 2007;85(5):1436–​1437. https://doi.org/​10.1093/​ajcn/​85.5.1436 24. Kwan ML, Buffler PA, Abrams B, Kiley VA. Breastfeeding and the risk of childhood leukemia: A meta-​analysis. Public Health Rep. 2004;119:521–​535. https://doi.org/​ 10.1016/​j.phr.2004.09.002 25. Vest AN, Zhou L, Huang X, et al. Design and testing of a transcutaneous RF recharging system for a fetal micropacemaker. IEEE Trans Biomed Circuits Syst. 2017. https://​doi.org/​10.1109/​TBCAS.2016.2620805 26. Horta BL, Loret De Mola C, Victora CG. Breastfeeding and intelligence: A systematic review and meta-​analysis. Acta Paediatr. 2015;104:14–​19. https://doi.org/​10.1111/​ apa.13139 27. Horta BL, De Sousa BA, De Mola CL. Breastfeeding and neurodevelopmental outcomes. Curr Opin Clin Nutr Metab Care. 2018;21(3):174–​178. https://doi.org/​ 10.1097/​MCO.0000000000000453 28. Cohen SS, Alexander DD, Krebs NF, et al. Factors associated with breastfeeding initiation and continuation: A meta-​analysis. J Pediatr. 2018; 203:190–​196. https://doi.org/​ 10.1016/​j.jpeds 29. Turcksin R, Bel S, Galjaard S, Devlieger R. Maternal obesity and breastfeeding intention, initiation, intensity and duration: A systematic review. Matern Child Nutr. 2014;10(2):166–​183. https://doi.org/​10.1111/​j.1740-​8709.2012.00439.x

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Postpartum Health and Lactation

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30. Baby Friendly USA. www.babyfriendlyusa.org/​ 31. Su X, Zhang Z, Qu X, Tian Y, Zhang G. Hemoglobin A1c for diagnosis of postpartum abnormal glucose tolerance among women with gestational diabetes mellitus: Diagnostic meta-​ analysis. PLoS One. 2014;9(7):e102144. https://doi.org/​ 10.1371/​journal.pone.0102144 32. Gould JF, Best K, Makrides M. Perinatal nutrition interventions and post-​partum depressive symptoms. J Affect Disord. 2017; 224:2–​ 9. https://doi.org/​10.1016/​ j.jad.2016.12.014 33. Sparling TM, Henschke N, Nesbitt RC, Gabrysch S. The role of diet and nutritional supplementation in perinatal depression: A systematic review. Matern Child Nutr. 2017;13(e12235). https://doi.org/​10.1111/​mcn.12235 34. McKinley MC, Allen-​Walker V, McGirr C, Rooney C, Woodside J V. Weight loss after pregnancy: Challenges and opportunities. Nutr Res Rev. 2018;31(2):225–​238. https://doi.org/​10.1017/​S0954422418000070 35. Smith GN, Louis JM, Saade GR. Pregnancy and the postpartum period as an opportunity for cardiovascular risk identification and management. Obstet Gynecol. 2019;134(4):851–​862. https://doi.org/​10.1097/​AOG.0000000000003363 36. Hoover EA, Louis JM. Optimizing health: Weight, exercise, and nutrition in pregnancy and beyond. Obstet Gynecol Clin North Am. 2019;46(3):431–​440. https://doi.org/​ 10.1016/​j.ogc.2019.04.003 37. Farpour-​Lambert NJ, Ells LJ, Martinez de Tejada B, Scott C. Obesity and weight gain in pregnancy and postpartum: An evidence review of lifestyle interventions to inform maternal and child health policies. Front Endocrinol (Lausanne). 2018;9(546). https://doi.org/​10.3389/​fendo.2018.00546 38. Haire-​Joshu D, Cahill AG, Stein RI, et al. Randomized controlled trial of home-​ based lifestyle therapy on postpartum weight in underserved women with overweight/​obesity. Obes (Silver Spring). 2019;27(4):535–​541. https://doi.org/​10.1002/​ oby.22413 39. Harrison CL, Brown WJ, Hayman M, Moran LJ, Redman LM. The role of physical activity in preconception, pregnancy and postpartum health. Semin Reprod Med. 2016;34(2):e28–​e37. https://doi.org/​10.1055/​s-​0036-​1583530 40. Amorim AA, Linne YM, Lourenco PMC. Diet or Exercise, or Both, for Weight Reduction in Women after Childbirth. John Wiley & Sons Ltd; 2007. https://doi.org/​ 10.1002/​14651858.CD005627.pub2 41. Yang CL, Chen CH. Effectiveness of aerobic gymnastic exercise on stress, fatigue, and sleep quality during postpartum: A pilot randomized controlled trial. Int J Nurs Stud. 2018; 77:1–​7. https://doi.org/​10.1016/​j.ijnurstu.2017.09.009 42. Committee on Obstetric Practice. ACOG Committee Opinion Number 804: Physical activity and exercise during pregnancy and the postpartum period. Obs Gynecol. 2020;135(4):e178–​e188. https://doi.org/​10.1097/​AOG.0000000000003772 43. Christian LM, Carroll JE, Teti DM, Hall MH. Maternal sleep in pregnancy and postpartum Part I: Mental, physical, and interpersonal consequences. Curr Psychiatry Rep. 2019;21(20). https://doi.org/​10.1007/​s11920-​019-​0999-​y 44. Owais S, Chow CHT, Furtado M, Frey BN, Van Lieshout RJ. Non-​pharmacological interventions for improving postpartum maternal sleep: A systematic review and meta-​analysis. Sleep Med Rev. 2018; 41:87–​ 100. https://doi.org/​10.1016/​ j.smrv.2018.01.005 45. Wilkerson AK, Uhde TW. Perinatal sleep problems: Causes, complications, and management. Obstet Gynecol Clin North Am. 2018;45(3):483–​494. https://doi.org/​ 10.1016/​j.ogc.2018.04.003

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46. Christian LM, Carroll JE, Porter K, Hall MH. Sleep quality across pregnancy and postpartum: Effects of parity and race. Sleep Heal. 2019;5(4):327–​334. https://doi.org/​ 10.1016/​j.sleh.2019.03.005 47. Christian LM, Kowalsky JM, Mitchell AM, Porter K. Associations of postpartum sleep, stress, and depressive symptoms with LPS-​stimulated cytokine production among African American and White women. J Neuroimmunol. 2018; 316:98–​106. https://doi.org/​10.1016/​j.jneuroim.2017.12.020 48. Irwin MR, Olmstead R, Carroll JE. Sleep disturbance, sleep duration, and inflammation: A systematic review and meta-​analysis of cohort studies and experimental sleep deprivation. Biol Psychiatry. 2016;80(1):40–​52. https://doi.org/​10.1016/​ j.biopsych.2015.05.014 49. Figueiredo B, Dias CC, Brandão S, Canário C, Nunes-​Costa R. Breastfeeding and postpartum depression: State of the art review. J Pediatr (Rio J). 2013;89(4):332–​338. https://doi.org/​10.1016/​j.jped.2012.12.002 50. Carroll JE, Teti DM, Hall MH, Christian LM. Maternal sleep in pregnancy and postpartum Part II: Biomechanisms and intervention strategies. Curr Psychiatry Rep. 2019;21(19). https://doi.org/​10.1007/​s11920-​019-​1000-​9 51. Osborne LM, Payne JL. Mood and anxiety disorders. In Clinical Updates in Women’s Health Care. ACOG; 2017. Summary in Obstet Gynecol. 2017;130(13)674. https://doi.org/​10.1097/​AOG.0000000000002295 52. Putnick DL, Sundaram R, Bell EM, et al. Trajectories of maternal postpartum depressive symptoms. Pediatrics. 2020;146(5):e20200857. https://doi.org/​10.1542/​ peds.2020-​0857 53. Kendig S, Keats JP, Camille Hoffman M, et al. Consensus bundle on maternal mental health perinatal depression and anxiety. Obstet Gynecol. 2017; 129(3):422–​ 430. https://doi.org/​10.1097/​AOG.0000000000001902 54. Committee on Obstetric Practice. ACOG Committee Opinion Number 757: Screening for perinatal depression. Obstet Gynecol. 2018;132(5):e208–​e212. https://doi.org/​ 10.1097/​AOG.0000000000002927 55. Beck CT. Birth trauma in the eye of the beholder. Nurs Res. 2004;53(1):28–​35. https://doi.org/​10.1097/​00006199-​200401000-​00005 56. Beck CT. Birth trauma and its sequelae. J Trauma Dissociation. 2009;10(2):189–​203. https://doi.org/​10.1080/​15299730802624528 57. Anderson CA. The trauma of birth. Health Care Women Int. 2017;38(10):999–​1010. https://doi.org/​10.1080/​07399332.2017.1363208 58. Dikmen-​Yildiz P, Ayers S, Phillips L. Longitudinal trajectories of post-​traumatic stress disorder (PTSD) after birth and associated risk factors. J Affect Disord. 2018; 229:377–​385. https://doi.org/​10.1016/​j.jad.2017.12.074 59. Kronenfeld N, Berlin M, Shaniv D, Berkovitch M. Use of psychotropic medications in breastfeeding women. Birth Defects Res. 2017;109:957–​997. https://doi.org/​10.1002/​ bdr2.1077 60. Forray A, Merry B, Lin H, Ruger JP, Yonkers KA. Perinatal substance use: A prospective evaluation of abstinence and relapse. Drug Alcohol Depend. 2015;150:147–​ 155. https://​doi.org/​10.1016/​j.drugalcdep.2015.02.027 61. Gopman S. Prenatal and postpartum care of women with substance use disorders. Obstet Gynecol Clin North Am. 2014;41(2):213–​228. https://doi.org/​10.1016/​ j.ogc.2014.02.004 62. Holbrook BD. The effects of nicotine on human fetal development. Birth Defects Res Part C -​Embryo Today Rev. 2016;108(2):181–​192. https://doi.org/​10.1002/​ bdrc.21128

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63. Committee on Obstetric Practice. ACOG Committee Opinion Number 807: Tobacco and nicotine cessation during pregnancy. Obstet Gynecol. 2020;135(5):e221–​e229. https://​doi.org/​10.1097/​AOG.0000000000003822 64. Tani F, Castagna V. Maternal social support, quality of birth experience, and post-​ partum depression in primiparous women. J Matern Neonatal Med. 2017;30(6):689–​ 692. https://​doi.org/​10.1080/​14767058.2016.1182980 65. Cornish DL, Dobie SR. Social support in the “fourth trimester”: A qualitative analysis of women at 1 month and 3 months postpartum. J Perinat Educ. 2018;27(4):233–​242. https://​doi.org/​10.1891/​ 1058-​1243.27.4.233 66. Sarkar NN. The impact of intimate partner violence on women’s reproductive health and pregnancy outcome. J Obstet Gynaecol (Lahore). 2008;28(3):266–​271. https://​ doi.org/​10.1080/​01443610802042415 67. Alhusen JL, Ray E, Sharps P, Bullock L. Intimate partner violence during pregnancy: Maternal and neonatal outcomes. J Women’s Heal. 2015;24(1):100–​106. https://​doi.org/​10.1089/​jwh.2014.4872 68. Conde-​Agudelo A, Belizan JM. Maternal morbidity and mortality associated with interpregnancy interval: Cross sectional study. BMJ. 2000;321:1255–​1259. https://​ doi.org/​10.1136/​bmj.321.7271.1255 69. Rich-​Edwards JW, Fraser A, Lawlor DA, Catov JM. Pregnancy characteristics and women’s future cardiovascular health: An underused opportunity to improve women’s health? Epidemiol Rev. 2014;36(1):57–​70. https://doi.org/​10.1093/​epirev/​ mxt006 70. Lane-​Cordova AD, Khan SS, Grobman WA, Greenland P, Shah SJ. Long-​term cardiovascular risks associated with adverse pregnancy outcomes. J Am Coll Cardiol. 2019;73(16):2106–​2116. https://doi.org/​10.1016/​j.jacc.2018.12.092 71. Skjaerven R, Wilcox AJ, Klungsøyr K, et al. Cardiovascular mortality after pre-​ eclampsia in one child mothers: Prospective, population based cohort study. BMJ. 2012;345:e7677. https://​doi.org/​10.1136/​bmj.e7677 72. Reddy S, Jim B. Hypertension and pregnancy: Management and future risks. Adv Chronic Kidney Dis. 2019;26(2):137–​145. https://doi.org/​10.1053/​j.ackd.2019.03.017 73. Benschop L, Duvekot JJ, Roeters Van Lennep JE. Future risk of cardiovascular disease risk factors and events in women after a hypertensive disorder of pregnancy. Heart. 2019. https://​doi.org/​10.1136/​heartjnl-​2018-​313453 74. Wagner S, Craici I. Hypertensive pregnancy disorders and future renal disease. Curr Hypertens Rep. 2014;16(10):484–​489. https://doi.org/​10.1007/​s11906-​014-​0484-​2 75. Bohrer J, Ehrenthal DB. Other adverse pregnancy outcomes and future chronic disease. Semin Perinatol. 2015;39(4):259–​263. https://doi.org/​10.1053/​j.semperi.2015.05.003 76. Lykke JA, Langhoff-​Roos J, Lockwood CJ, Triche EW, Paidas MJ. Mortality of mothers from cardiovascular and non-​ cardiovascular causes following pregnancy complications in first delivery. Paediatr Perinat Epidemiol. 2010; 24:323–​330. https://​ doi.org/​10.1111/​j.1365-​3016.2010.01120.x 77. Haas DM, Parker CB, Marsh DJ, et al. Association of adverse pregnancy outcomes with hypertension 2 to 7 years postpartum. J Am Heart Assoc. 2019;8. https://​doi.org/​ 10.1161/​JAHA.119.013092 78. Grandi SM, Filion KB, Yoon S, et al. Cardiovascular disease-​related morbidity and mortality in women with a history of pregnancy complications: Systematic review and meta-​analysis. Circulation. 2019;139(8):1069–​1079. https://​doi.org/​10.1161/​ CIRCULATIONAHA.118.036748 79. Lane-​Cordova AD, Carnethon MR, Catov JM, et al. Cardiorespiratory fitness, exercise haemodynamics and birth outcomes: The coronary artery risk development

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Kristi R. VanWinden and Elizabeth Collins in young adults study. BJOG. 2018;125(9):1127–​1134. https://doi.org/​10.1111/​ 1471-​0528.15146 Retnakaran R, Austin PC, Shah BR. Effect of subsequent pregnancies on the risk of developing diabetes following a first pregnancy complicated by gestational diabetes: A population-​based study. Diabet Med. 2011;28(3):287–​292. https://​doi.org/​10.1111/​ j.1464-​5491.2010.03179.x Retnakaran R, Shah BR. Role of type 2 diabetes in determining retinal, renal, and cardiovascular outcomes in women with previous gestational diabetes mellitus. Diabetes Care. 2017;40(1):101–​108. https://​doi.org/​10.2337/​dc16-​1400 Agarwal P, Morriseau TS, Kereliuk SM, Doucette CA, Wicklow BA, Dolinsky VW. Maternal obesity, diabetes during pregnancy and epigenetic mechanisms that influence the developmental origins of cardiometabolic disease in the offspring. Crit Rev Clin Lab Sci. 2018;55(2):71–​101. https://doi.org/​10.1080/​10408363.2017.1422109 Knowler WC, Barrett-​Connor E, Fowler SE, et al. Reduction in the incidence of Type 2 Diabetes with lifestyle intervention or metformin. N Engl J Med. 2002;346(6):393–​ 403. https://​doi.org/​10.1056/​NEJMoa012512 Brown J, Alwan NA, West J, et al. Lifestyle interventions for the treatment of women with gestational diabetes. Cochrane Database Syst Rev. 2017;2017(5). https://​doi.org/​ 10.1002/​14651858.CD011970.pub2 LeFevre ML. Low-​dose aspirin use for the prevention of morbidity and mortality from preeclampsia: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2014;161(11):819. https://doi.org/​10.7326/​M14-​1884 Committee on Obstetric Practice. ACOG Committee Opinion Number 743: Low-​dose aspirin use during pregnancy. Obstet Gynecol. 2018;132(1): e44–​e52. https://​doi.org/​ 10.1097/​AOG.0000000000002708 Koletzko B, Godfrey KM, Poston L, et al. Nutrition during pregnancy, lactation and early childhood and its implications for maternal and long-​term child health: The Early Nutrition project recommendations. Ann Nutr Metab. 2019;74(2):93–​106. https://​ doi.org/​10.1159/​000496471

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A Lifestyle Medicine Approach to Breast Cancer Amber Orman, MD, DipABLM, Radiation Oncologist*

Advent Health Cancer Institute, Kissimmee, FL, USA

Dianne L. Johnson, MD, DipABLM, Diagnostic Breast Radiologist MBB Radiology, Jacksonville, FL, USA

Amy Comander, MD, Hematologist-​Oncologist Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA, USA

Nigel Brockton, PhD, Vice President

Research, American Institute for Cancer Research, Arlington, VA, USA

Meghana Reddy, BS Biomedical Sciences

USF Morsani College of Medicine, Tampa, FL, USA

Gautam Krishna Koipallil, BS Biomedical Sciences USF Morsani College of Medicine, Tampa, FL, USA 20.1 20.2

Introduction..................................................................................................366 Nutrition and Primary Breast Cancer Prevention........................................366 20.2.1 Fiber...............................................................................................367 20.2.2 Carotenoids....................................................................................368 20.2.3 Soy.................................................................................................368 20.2.4 Dairy..............................................................................................369 20.2.5 Osteoporosis..................................................................................369

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Physical Activity and Primary Breast Cancer Prevention............................370 Obesity and Primary Breast Cancer Prevention...........................................370 Sleep and Primary Breast Cancer Prevention..............................................371 Psychological Stress and Primary Breast Cancer Prevention......................372 Tertiary Breast Cancer Prevention...............................................................373 Nutrition and Tertiary Breast Cancer Prevention.........................................373 20.8.1 Soy.................................................................................................375 Physical Activity and Tertiary Breast Cancer Prevention............................375 Obesity and Tertiary Breast Cancer Prevention...........................................376 Sleep and Tertiary Breast Cancer Prevention...............................................376 Psychological Stress and Tertiary Breast Cancer Prevention......................376 Loneliness and Tertiary Breast Cancer Prevention......................................377 Conclusion...................................................................................................377

KEY POINTS • Plant-​predominant nutrition is recommended for both primary and tertiary breast cancer prevention. • Soy intake is recommended for all breast cancer patients/​survivors. • Physical activity is recommended for all breast cancer patients/​ survivors, consisting of cardiovascular as well as muscle training and flexibility exercises. • Maintenance of a healthy body weight is recommended for both primary and tertiary breast cancer prevention. • Emotional support, stress reduction, sleep quality, and healthy relationships are important aspects of breast cancer care.

20.1  INTRODUCTION Breast cancer is the most common female cancer in the United States (aside from skin cancer), with over 275,000 cases estimated in 2020.1 Improvements in early detection and advances in treatment have resulted in 5-​year survival rates reaching approximately 90%. However, breast cancer remains the second leading cause of female cancer death in America, with over 42,000 deaths per year.1 Fortunately, a substantial body of research indicates that several modifiable lifestyle factors can significantly reduce the risk of breast cancer3 and adherence to lifestyle recommendations after a diagnosis can improve cancer-​related health outcomes.4 This chapter will review our current understanding of the role of lifestyle in both primary and tertiary breast cancer prevention as well as breast cancer treatment.

20.2  NUTRITION AND PRIMARY BREAST CANCER PREVENTION Approximately 40% of all cancers could be prevented by following recommendations for modifiable lifestyle factors such as maintaining a healthy body weight, minimizing alcohol intake, being physically active, consuming a healthy diet, avoiding excessive sun exposure, avoiding tobacco use, getting appropriate vaccinations and following

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recommended screening schedules.5–​8 In 2018, the World Cancer Research Fund/​ American Institute for Cancer Research (WCRF/​AICR) published Diet, Nutrition, Physical Activity and Cancer: A Global Perspective, the Third Expert Report, which includes Ten Cancer Prevention Recommendations that are aligned with the six pillars of Lifestyle Medicine.2 These recommendations provide evidence-​based advice to reduce cancer risk, including breast cancer. The recommendations focus on an overall package of habits rather than on individual behaviors. The impact of adherence to the 2007 recommendations3 has been clearly demonstrated, with each one point increment increase in the adherence score resulting in a 10% (odds ratio [OR] 0.90; 95% confidence interval [CI]: 0.87–​0.93] lower risk of breast cancer4, in a linear dose–​response meta-​analysis of 11 prospective cohort studies. Adherence to the 2007 WCRF/​AICR adherence score is associated with similar magnitudes of effect on survival outcomes in both cancer survivors and the general population.4 The Vitamins and Lifestyle (VITAL) prospective cohort study of over 30,000 postmenopausal women with a median follow-​up of 7 years found a 60% reduction in breast cancer incidence in women meeting five or more versus none of the WCRF/​ AICR recommendations.9 The Swedish Mammography cohort prospective study of over 31,000 postmenopausal women with a median follow-​up of 15 years found a 51% reduction in breast cancer incidence in women meeting six or more versus two or fewer of the WCRF/​AICR recommendations.10 Five of the ten WCRF/​AICR Cancer Prevention Recommendations involve plant-​ predominant nutrition2; however, 60–​87% of adults worldwide report consuming fewer than the recommended five servings daily of fruits and vegetables.1 Although there is mixed data regarding the relationship between specific components of a whole-​food, plant-​based (WFPB) diet and breast cancer incidence, a reduced incidence of breast cancer is associated with an overall healthy lifestyle, which includes a high-​quality diet incorporating fruits, vegetable, whole grains, and legumes.13,14 The exact mechanism(s) through which plant-​based nutrition decreases both cancer incidence and all-​cause mortality are not clearly defined, but maintenance of a normal body mass index (BMI), optimized phytonutrient and antioxidant intake, and adequate fiber intake are likely involved.15 The WCRF/​AICR Third Expert Report concluded that the evidence is limited but suggestive that consuming non-​starchy vegetables, foods high in carotenoids, and diets high in calcium may decrease the risk of breast cancer.16

20.2.1 Fiber A recent meta-​analysis of 17 prospective studies demonstrated that overall reduced breast cancer incidence was significantly associated with a high intake of total and soluble fiber. There was an 8% relative risk reduction in the highest fiber intake group compared with the lowest one (relative risk [RR] 0.92; 95% CI: 0.88–​0.95), with a benefit observed in both pre-​and postmenopausal breast cancer. Since dietary fiber is only found in plant foods, it is not surprising that this study also observed that increased fiber intake was associated with higher overall dietary quality and intake of vitamins, minerals, and phytoestrogens.17

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The mechanism by which fiber may reduce breast cancer risk is not completely understood, but fiber may help normalize blood glucose and insulin levels, beneficially affect the gut microbiome, and reduce circulating estrogen.18,19 In addition, as overweight or obesity is associated with an increased risk of breast cancer, postmenopausal women with these conditions have a 20–​40% increased risk of developing hormone receptor-​positive breast cancer when compared to women with a normal BMI.20,21 Due to their relatively low-​calorie density, fiber-​rich foods may help patients achieve a healthy BMI.22,23 Fiber-​ rich plant foods are also a rich source of phytochemicals and micronutrients, which exhibit anti-​inflammatory and anti-​oxidant activities.24,25 Phytochemicals may play a role in cell growth and proliferation, programmed cell death, repairing damaged deoxyribonucleic acid (DNA), eliminating carcinogens or carcinogenic effects, epigenetic modulation, activation or inactivation of oncogenes and tumor-​suppressor genes, angiogenesis, and reducing the damage of oxidative stress.26,27

20.2.2 Carotenoids Carotenoids are phytochemicals which provide yellow/​ orange/​ red pigments in vegetables and fruits and are known for their antioxidant activity. A 2015 prospective case control study with over 20 years of follow-​up observed an 18–​28% lower risk of breast cancer in the quartile with the highest serum carotenoid concentrations versus those with the lowest serum carotenoid concentrations (RR: 0.72; 95% CI: 0.59, 0.88; p < 0.001). There was also a strong inverse relationship between plasma carotenoid concentration and breast cancer recurrence and breast cancer specific mortality (RR: 0.32; 95% CI: 0.21, 0.51; p < 0.001).28 Carotenoids should be obtained by food consumption in food consumption doses, as carotenoid supplements are potentially harmful.29

20.2.3 Soy In 2002, the combined estrogen/​progesterone hormone replacement therapy (HRT) arm of the Women’s Health Initiative trial was closed early due to observed harms, including increased risk of breast cancer, increased risk of coronary artery disease, and overall harm.30 This increased concern about estrogen led to fear that consumption of soy –​a phytoestrogen with a similar molecular structure –​might have the same deleterious effects. Dietary intake of soy foods is associated with as much as a 30% decrease in breast cancer incidence in numerous studies involving thousands of women worldwide.32–​34 A study involving more than 20,000 Japanese women found that those with the highest soy food intake had approximately half the risk of breast cancer when compared to those with the lowest intake.35 Women with breast cancer (BRCA) gene mutations and gene polymorphisms predisposing to breast cancer may especially benefit from dietary soy intake.36 In addition, soy intake in childhood and adolescence may be the most protective.37

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There are likely multiple mechanisms contributing to the protective effects of phytoestrogens. Phytoestrogens may inhibit angiogenesis, affect enzyme activity, and contribute to DNA repair.38 Phytoestrogens have been associated with antioxidative effects, anti-​inflammatory properties, and immune modulating effects.39 Variation in estrogen receptor distribution, binding, and function may also play a role in the differing effects of phytoestrogens versus endogenous/​exogenous estrogen. At food consumption doses, phytoestrogens bind primarily to estrogen receptor (ER)-​beta, producing an antiproliferative, antiestrogen effect. Phytoestrogens may also compete with endogenous estrogen for ER binding.40,41 A more recent epidemiological study of over 52,000 women reported no association between soy and breast cancer risk, but observed a significant reduction in breast cancer risk when substituting soy milk with an equivalent quantity of dairy milk (hazard ratio (HR) = 0.68; 95% CI: 0.54–​0.87, p = 0.002).42 It may turn out that the benefits of soy are related, at least in part, to a decrease in dairy intake.

20.2.4 Dairy Data regarding dairy intake and cancer prevention has been mixed. The WCRF/​ AICR reports “limited evidence” that dairy intake is associated with a lower risk of premenopausal breast cancer,2 and therefore does not make specific recommendations regarding dairy intake relating to cancer risk. When examining potential risks associated with dairy intake, it is important to evaluate the data in the context of recommended intake. The current U.S. Dietary Guidelines recommend three cups of dairy milk per day.43 A recent epidemiological study reported a 50% increase in the risk of breast cancer in the women with the highest 10% of dairy milk intake (consuming approximately one cup per day) compared to those with the bottom 10% of intake (HR = 1.50; 95% CI: 1.22–​1.86; p < 0.001). The risk increased linearly with increased daily dairy milk intake, with no significant difference between full fat and reduced fat milk.42 A deleterious effect of dairy would be consistent with the recent AHS-​2 report suggesting a reduced incidence of breast cancer in vegans compared with nonvegetarians, and no difference in incidence between lacto-​ovo-​vegetarians and nonvegetarians.44

20.2.5 Osteoporosis Inevitably a discussion of limiting dairy intake leads to concerns about calcium intake and osteoporosis. Most breast cancer appears in postmenopausal women who are already at risk of osteopenia/​porosis, most postmenopausal breast cancer is hormone sensitive, and any surgery or treatment that decreases estrogen may contribute to osteoporosis. Aromatase inhibitors target the estrogen biosynthetic pathway and deprive tumor cells of the growth-​promoting effects of estrogen, resulting in prolonged disease-​free survival, as well as a ≥15% increase in fracture risk.45,46 We can leverage Lifestyle Medicine to mitigate this risk by emphasizing a WFPB diet with appropriate calcium balance and vitamin D intake, as well as weight bearing exercise. For more information on lifestyle and osteoporosis, see Chapter 16.

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20.3  PHYSICAL ACTIVITY AND PRIMARY BREAST CANCER PREVENTION Physical activity is associated with many health benefits; however, a recent study of over 300,000 Americans revealed that less than 25% of participants met published exercise recommendations.58 In terms of breast cancer, multiple studies over the last 20 years have demonstrated a 30–​40% decrease in breast cancer incidence in physically active women when compared to sedentary women.59,60 An expert panel at the International Agency for Research on Cancer (IARC) estimated up to a 40% decrease in breast cancer incidence among the most physically active women, regardless of menopausal status or type or intensity of activity.61 The mechanisms by which physical activity impacts breast cancer risk is likely multifactorial, with possible etiologies including a decrease in body fatness, metabolic and hormonal effects, association with other health-​promoting lifestyle habits (e.g., alcohol, smoking. and diet), improved immune system function, and anti-​inflammatory effects.62,63 For cancer prevention, the WCRF/​AICR and the American Cancer Society (ACS) recommend getting at least 150 minutes of moderate, or 75 minutes of vigorous (if possible) physical activity per week supplemented with muscle training and flexibility exercises. The ACS adds that any activity over and above usual activities of daily living is beneficial, and therefore any increase in physical activity should be encouraged. It is especially important to avoid long periods of sitting.64 Patients should be counseled about the importance of physical activity. When appropriate, exercise prescriptions and referrals to physical therapy or medically supervised exercise programs can help patients reach fitness and activity goals.

20.4  OBESITY AND PRIMARY BREAST CANCER PREVENTION According to the WCRF/​AICR, there is strong evidence that overweight or obesity throughout adulthood increases the likelihood of at least 12 different types of cancer, including postmenopausal breast cancer.2 Several of the WCRF/​AICR Cancer Prevention Recommendations address body fatness either directly or indirectly.2 Paradoxically, higher BMI in young adulthood (18–​30 years of age) is associated with a lower risk of both pre-​and postmenopausal breast cancer; however, maintaining a healthy BMI throughout the life-​course is recommended due to the increased risk of many chronic diseases, including post-​menopausal breast cancer, associated with higher BMI. The principle of caloric density can be helpful in addressing overweight and obesity. Whole plant foods and intact or minimally processed whole grains tend to be low in calorie density (calories per weight of food).65 Intake of whole plant foods without added sugars or fat usually results in an average calorie density that allows for intake of a large volume of food and the resulting satiety, without a calorie excess. The WCRF/​AICR recommends a diet with an average calorie density of 567 kcal per pound of food.2 For reference some examples of approximate calorie densities of food items are presented here (calories/​pound): • Tomato = 82 • Kale = 227

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Blueberries = 261 Sweet Potato = 389 Black Beans = 600 Chicken Breast = 748 Walnuts = 2965 Olive Oil = 3998

20.5  SLEEP AND PRIMARY BREAST CANCER PREVENTION Sleep is essential for overall physical and mental well-​being, and many chronic diseases are associated with insufficient quality of sleep.66 Trends toward nontraditional work schedules, increased screen time, and artificial light exposure at night make studying the association of sleep with breast cancer risk very pertinent. The recent explosion of technological devices and their nighttime use contribute to industrialized populations having regular nighttime light exposure, regardless of shift-​ work status.67,68 Analyzing this association can be particularly difficult, as “sleep” is a multifaceted entity, encompassing sleep duration, sleep quality, light at night and many other dimensions. However, because sleep is a modifiable health behavior, understanding whether a genuine risk exists is valuable to oncology practitioners. The most studied associations currently focus on the association of breast cancer risk with light exposure at night and sleep duration. There is evidence that supports light at night as a malignancy risk in humans.70-​72 There are several theories as to how this effect may work. Melatonin level decreases secondary to artificial light at night may lead to increased circulating estrogen levels; additionally, melatonin may have tumor-​suppressing actions, meaning that lower melatonin may increase the risk of malignancy.73–​76 A case-​control study of 410 women found a significantly increased risk of breast cancer with high nighttime light exposure, late sleep timing, night-​shift work, and increased nighttime awakenings. However, the increased risk with light exposure was not clinically significant.77 A more extensive prospective study of females followed for an average of 6 years (n=105,866, with 1,775 breast cancer cases) demonstrated no association between light at night and either overall or breast cancer risk, as well as no association with aggressive phenotypes.78 A systematic review of 12 case-​control and cohort studies also found that high levels of light at night may increase breast cancer risk (RR=1.17), while this risk was not present with ambient light at night exposure.76 These studies support that there seems to be a trend between light at night exposure and increased breast cancer risk, but further study will be necessary to establish a clinically relevant association, and possibly a dose-​dependent risk. There is inconclusive evidence to support any relationship between sleep duration and breast cancer risk. Prospective studies, systematic reviews, and meta-​analyses tend to point toward no conclusive increase in risk. A large early prospective cohort study (n=12,222, with 242 incident breast cancer cases from 1976 to 1996) demonstrated a nonsignificant trend of lower breast cancer risk with extended periods of sleep; this is theorized to be due to greater overall melatonin production during long sleep.80 Many large subsequent prospective cohort studies demonstrated no strong evidence for an association of sleep duration with breast cancer risk.73,81-​83

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Conceivably, although there is some evidence suggesting a link, there is no conclusive consensus of risk. There is a need to continue prospective studies and long-​ term randomized control trials (RCTs) to better classify the association of sleep with primary breast cancer risk. There has even been evidence suggesting that both longer and shorter sleep times (>9 hours and