Live Young, Think Young, Be Young : . . . At Any Age 9781936693245, 9781933503974

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Live Young, Think Young, Be Young, . . . at Any Age Donald Vickery, MD Larry Matson, EdD Carol Vickery, RN, MSN

Bull Publishing Boulder, Colorado

Copyright © 2012 by Bull Publishing Company All rights reserved. No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the publisher, except in the case of brief quotations embodied in critical reviews and certain other noncommercial uses permitted by copyright law.

Published by Bull Publishing Company P.O. Box 1377

Boulder, CO, USA  80306 www.bullpub.com

Library of Congress Cataloging-in-Publication Data

Vickery, Donald M. Live young, think young, be young : --at any age / Donald M. Vickery, Larry Matson, Carol Vickery. -- 1st ed. p. cm. Summary: While there are plenty of books offering advice about how to age, none takes the crucial step back to challenge how people think about aging until now. The Aging Syndrome, the core idea in this book, explains the aging process by using three pillars: intrinsic aging, the aging process that no one understands; disuse, both physical and mental; and chronic disease processes, which begin in childhood or sometimes in the womb. Using practical steps and plain language, this volume is the only guide needed for developing a plan for growing older. By presenting a better way to think about aging, it reveals what everyone can do to live a longer life. Includes bibliographical references and index. ISBN 978-1-933503-97-4 (pbk.) 1. Aging--Physiological aspects. 2. Aging--Psychological aspects. 3. Nutrition. 4. Self-care, Health. I. Matson, Larry. II. Vickery, Carol. III. Title. QP86.V52 2012 612.6’7--dc23 2012024132 Printed in U.S.A. First Edition

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Interior design and project management: Dovetail Publishing Services Cover design and production: Shannon Bodie, Lightbourne, Inc.

To Don

CONTENTS

FOREWORD: VISION—For a New Way of Thinking about Aging

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PART I: WISDOM—To Know the Difference between Aging and the Aging Syndrome

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Chapter 1  Speaking of Aging, Don’t   5 Chapter 2 Real Aging  21 Chapter 3  Lifespan and Life Expectancy   27 Chapter 4  Aging and Death   35 Chapter 5  Aging and Disease   45 Chapter 6  Aging and Evolution   53 Chapter 7  Adaptation to Disuse   61 Chapter 8 Calorie Restriction  79 PART II: KNOWLEDGE—To Understand the Disease Processes That Make Us Old   Chapter 9 Critical Concepts  93 Chapter 10  The Beginning of Disease Processes   105 Chapter 11  Acceleration of Disease Processes   113 Chapter 12 Constricted Circulation  121 Chapter 13 Metabolic Madness  143 Chapter 14 Insidious Inflammation  161 Chapter 15  The Root Causes   177 iv

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Contents 

PART III: COURAGE—The Personal Plan to Change What Can Be Changed

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Chapter 16  Courage to Change   221 Chapter 17  Building Your Personal Plan   233 Chapter 18  The Foolproof Plan for Self-Managing    243 Chapter 19  Take Your Body for a Spin   257 Chapter 20 Use Your Head  285 Chapter 21  Eat (and Drink) Like You Know What You’re Doing   309 Chapter 22  Give Yourself a Break    343 Chapter 23  Cop an Attitude . . . a Positive Attitude   363 Chapter 24 Know Your Environment . . . and What’s Getting into Your Body   391 Chapter 25  Pills and Potions   423 Chapter 26  Connecting the Dots   455 PART IV: RESILIENCE—To Accept What Can’t Be Changed

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Chapter 27  From Acceptance to Resilience   481 AFTERWORD: SERENITY—Leaving This World a Little Better Index  503

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FOREWORD

VISION For a New Way of Thinking about Aging

How many 35-year-olds would take out a full-page ad in a major newspaper like The Washington Post? That’s exactly what Don Vickery did in 1979. Yes, in 1979 at age 35. The purpose: to admonish all of us for not taking greater responsibility for our own health. Don was a self-care visionary even at this early stage of his career. He knew that the best health care is what we do for ourselves—living a healthy lifestyle, taking care of acute problems, managing chronic disease, and being fully involved in our treatment decisions. Don’s journey into self-care began between 1971 and 1973, when he developed an algorithm-based triage system for the U.S. Army. By 1976, at age 32, he had coauthored his first book, Take Care of Yourself, which quickly became the standard self-care manual and is currently in its ninth printing. That book was followed by a guide for parents, Take Care of Your Child, and a lifestyle manual, Lifeplan, as well as numerous articles in medical journals. Don’s research showed that when individuals have good information, they make better decisions, are more satisfied with their care, and have better outcomes at lower costs. He has rightly been called the “father of the self-care movement.” In 1992, Don fulfilled a long-time dream of starting a company, called Health Decisions, with the goal of reducing the demand for medical care by using nurses to counsel people in self-care—from acute problems to major medical decisions, from lifestyle changes to managing chronic disease. Don believed in the power of “watchful waiting”—the “do nothing” approach in which you observe the course vii

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of the condition and seek treatment if it doesn’t improve. He knew that most minor illnesses, and even many more serious conditions, follow a natural course in which our body heals itself. But, in our impatience, we want to be treated now, even if it means enduring some risks and side effects. Health Decisions was ahead of its time. Nurses helped people understand their conditions and provided both estimates of outcomes if the person did nothing or used self-care as well as the benefits and risks of other treatment options. When people were provided with this information and were encouraged to discuss their values and preferences, they often chose less invasive treatment options, perhaps watchful waiting. This led to fewer adverse effects, was less costly, and in the long run, often led to a better quality of life. What a novel approach—better health and lower costs at the same time. Most major health insurers now provide some type of telephone nurse support based on this model. Unfortunately, after a decade of helping people take charge of their health, economic realities forced the closing of Health Decisions in 2001. Don returned to writing—in this case, a self-care book for boomers and seniors. He was working on a chapter on aging, obviously an important topic for anyone over age 50, but as he reviewed the science of

aging, there was little that made sense and little consensus even among the experts. The field was burdened by conflict, controversy, and confusion, all perpetuated by a burgeoning anti-aging industry. Don realized that the real problem is not aging, but why we get old prematurely and what we can do about it. We confuse aging and old. We assume that old is the result of aging, but for the most part it’s not. A new way of thinking about aging was clearly needed. Our current thinking was contributing to an almost universally negative view of aging along with a host of mistaken assumptions and beliefs about it. Misinformation was fostering a sense of helplessness, pessimism, and low expectations for the future. This was all contrary to Don’s core belief that if we take control of our health we can have a better quality of life at any age. A healthier, more positive vision of growing older was needed, one that involved doing more for ourselves and being less dependent on the medical system to take care of us. The self-care book was shelved and this one began. Don had always been fascinated with the idea of heuristics. Heuristics is probably a new term for most—it refers to a simpler way, a shortcut, in thinking about and solving a complex problem. The algorithms for Take Care of Yourself and Take Care of Your Child are examples of heuristics for understanding and managing symptoms. But no

FOREWORD: Vision 

issue Don had tackled was quite as complex as aging. He searched for a simpler way to understand what makes us old and how we can stay young. In the end, the brilliance of this book is the combination of two heuristic tools— a new one that he called the “Aging Syndrome” to explain why we get old, and an old one, the “Serenity Prayer,” to explain what we can do about it. They fit together perfectly.

» First, develop wisdom to know the

difference between what we can and can’t change about getting old. We can change the Aging Syndrome; we can’t change aging.

» Second, use courage to change what

we can change (the root causes of the Aging Syndrome) with a strategy to accomplish the change (selfmanaging).

» Third, accept what we cannot change (aging and other stuff that happens in life for no apparent reason). This results in a new mindset about growing older and a plan to control how fast it happens.

Don lived what he taught—he had an active, informed, and involved lifestyle, despite being diagnosed with rheumatoid arthritis in his early 40s and living on and off with crippling pain for nearly a quarter

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of a century. The disease influenced how he experienced life every day, and it gave him a unique view of aging. He would say, “I’ve been young and old, young and old, young and old, again and again” as the disease waxed and waned. He also said, “I will not claim that mine is a unique experience, or that it has provided me with some secret approach to staying young. I will say, however, that it has provided insights into the difficulty of taking advantage of what science has to offer. And, more than anything else, it has burned the essential rules of dealing with getting old into my mind.” This story should have a happy ending. After all, it is a more optimistic view of growing older. It shows us that we have a lot of control over how we age and the quality of life we live. It begins with a new mindset about aging and growing older, and then provides a new way of thinking about the factors that contribute to growing old. Don’s story is a story of life, and we never know how life is going to unfold. We can do the best we can, but things still happen that we don’t anticipate and have no control over. Life can change instantly, as in serious accidents that we hear about almost daily. Acceptance of these events is part of the process of building resilience. For Don, life changed rather abruptly in the spring of 2008. It wasn’t an accident, but a disease—an aggressive form of lung cancer that began to spread

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rapidly. Because Don had never smoked, there was no explanation for the cancer. Don passed away on November 22, 2008, at the young age of 64. He left behind a large legacy and this book is a big part of it. The Afterword at the end of the book continues Don’s story and includes some lessons

that we learned from him during his last six months—on accepting our own mortality and preparing for the end. No one knows how his or her life will end, but we know how we can make the most of our lives for as long as we do live. Live Young, Think Young, Be Young, . . . at Any Age shows us the path.

PA R T

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WISDOM To Know the Difference between Aging and the Aging Syndrome What we don’t understand is largely the result of the vocabulary we use and the assumptions that we make.

—Albert Einstein

Wisdom—the ability to make sound decisions and judgments based on knowledge, experience, common sense, and insight accumulated over a lifetime. It seems logical that wisdom should increase with age. We do become “older and wiser,” don’t we? In some ways yes, in other ways no. The wisdom we have is based on the life we have lived—the unique knowledge and experience that each of us has accumulated. We’re all wise in some aspects of life, ignorant in others. But wisdom becomes increasingly challenging as the pace of life accelerates and becomes more distracting, and as we become increasingly specialized in our careers. The result is that wisdom is often lacking in many areas. One of these areas is our ability to take care of ourselves, to self-manage the changes that occur in our bodies and minds as we get older. 1

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We all become more experienced with aging as the years go by, but experience alone doesn’t foster any greater insights into the aging process or the wisdom to grow old with strength, vitality, and grace. Our culture is enthralled with youth and winning, which makes aging the adversary and getting older seem like losing. The result is the booming anti-aging industry built on the promise of youth. Henry David Thoreau once said, “It is a characteristic of wisdom not to do desperate things.” The growing use of unproven anti-aging pills and potions is a sure sign of desperation—and a lack of wisdom. Why is wisdom in such short supply when it comes to growing older? Many factors contribute, but a poor understanding of aging tops the list. Most of us are convinced that aging is responsible for most of the problems that become more common as we get older. We know that everything ages, so it’s easy to assume that aging is the cause, at least after age 50. Unfortunately, the belief that aging is our greatest adversary is wrong for one simple but powerful reason: We don’t know what aging is. Even the true experts, the research gerontologists, tell us that it remains a mystery. Science is usually the bastion of truth, but the research on aging struggles to make sense of a quagmire of competing theories and complex biochemical mechanisms, with little consensus or clarity. The research is fascinating

but, quite frankly, not very helpful. With each breakthrough, scientists tell us that they’re getting closer to finding the holy grail of aging and that a true anti-aging drug is on the horizon, but it will take time and money. They’re still working on fruit flies, yeast, and worms—a far cry from humans. Yet, we continue to ascribe our declining abilities and health problems to aging because it’s the easiest explanation and it excuses any personal responsibility. Our beliefs are reinforced by doctors who tell us that our new diagnosis is a disease of aging or that our symptoms are just part of aging. And, of course, most of the information we hear about aging comes from a range of anti-aging “experts” whose businesses depend on aging being the problem and their product the answer. The result of all of this is a distorted mindset about aging that makes us believe we are helpless to do much about it. We expect to go downhill as we get older—to lose abilities, to get stiff and fat and weak, to take more pills to control diseases, to have a poorer quality of life, and so on. Part I of this book examines the roots of this mindset—our mistaken assumptions and beliefs about how and why we grow old. The title is Wisdom because it is about building the wisdom to know what is real about aging and what is not. The first chapter introduces the Aging Syndrome, a new way of thinking about how and why we grow old

Part I: Wisdom 

the way we do. The Aging Syndrome is a combination of factors that we control and that have been proven to cause the problems that we associate with getting old. It removes the notion of inevitability and the feeling of helplessness. Later chapters on real aging (the mysterious process), lifespan and life expectancy, death, disease, evolution, adaptation to disuse, and the practice of caloric restriction (the only proven anti-aging approach) address the fallacies of our current mindset and the clarity that results when we think in terms of the Aging Syndrome. The bottom line: If we want to change how we age, we have to change how we think about aging. We’re in no way denying aging or saying that you won’t get old. What we are saying is that the mysterious

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aging process is a relatively minor factor until the ninth or tenth decade. The Aging Syndrome explains why we get old in our 50s, 60s, and 70s. We can stay as young as possible for as long as possible if we selfmanage the factors that contribute to the Aging Syndrome. This will compress the impact of real aging into the last decade of life. Think of older folks you’ve met who are vibrant, active, and energetic. They show us what is possible. Wisdom is the foundation. It begins with letting go of our current mindset about aging, then letting go of our low expectations for the future. Part I will open your mind to a new way of thinking about growing older and the possibilities that go with it. We ask you to proceed with high expectations.

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Speaking of Aging—Don’t A New Way to Think about What Really Makes Us Old How old would you be if you didn’t know how old you are? —Satchel Paige

Do you think about how you are aging? Are you concerned about getting old? What is your vision of “old”? Is it like that of most people—frail, shrunken, slow, unstable, declining vision and hearing, loss of abilities, and so on? More important, what is your vision of you “getting old”? Is it what you are experiencing right now— weight gain, lack of energy, loss of strength, stiffness, aches and pains, high blood pressure, medications, inability to do activities you used to enjoy? Why does all of this happen? Most of us say “aging” without giving it a second thought. What do you believe about aging? Which of the following statements do you believe?

» » » »

Aging is our greatest adversary as we grow older. Aging determines how long we live.

Aging steals our youth; it makes us old and feeble.

Aging causes chronic diseases, like heart disease, high blood pressure, and diabetes. 5

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» Aging is largely a matter of genes and luck.

» How we age is largely out of our control.

» Science will determine the cause

of aging, and this will lead to the discovery of drugs that will keep us young.

How many of these statements do you think are true? Most of us believe they are all true, at least to some degree. Unfortunately, none of them is true for one simple reason: We honestly do not know what aging really is. Oh, we can define it, such as “everything that happens with the passage of time,” but what is it really? Scientists have been studying aging for decades. They’ve come up with many theories, but there is no consensus and none of the theories can account for the changes that occur in our body and mind as we get older. And, with all of this research, we still have no way to measure the aging process. We don’t know what to measure. Why do we have so many distorted beliefs about aging? That part is simple: It’s because we hear so much about aging and we see the ravages of old age all around us. You will probably hear more about aging than any other topic over your lifetime, and we’re not in the habit of critically evaluating any of this information. We just assume it’s true. “Aging” is

such an easy explanation for problems we develop as we get older. When the doctor tells us that our high blood pressure or type 2 diabetes is due to aging, we accept it and start taking our pills. We have such undying faith in science and medicine. When we hear that scientists have made another discovery about aging, we believe that they really are closing in on a pill to keep us young. When we hear doctors tell us that hormone therapy is the answer or when “entrepreneurs” tell us that a new supplement is an anti-aging miracle, we want to try the treatments because they just may work. As we experience stiffness, aches and pains, or trouble sleeping, the drug industry tells us that it’s all due to aging and that medication is the answer. We believe aging is the cause, so we buy over-the-counter drugs or ask the doctor for prescriptions to help us feel better, sleep better, perform better, and so on. All of this reinforces our mistaken assumptions about the mysterious process of aging that is going on in all of us. How could anyone develop a healthy mindset about aging amid such a sea of confusion and competing interests? This mindset affects our attitude about aging and our expectations for the future. It shapes how we interpret events in our life and the information we read or hear about aging. When we have trouble doing something or when we get fat, feel weak, notice stiffness, or have aches and pains, we

Chapter 1: Speaking of Aging, Don’t 

think we’re getting old. We expect to slow down, get weaker, do less for ourselves, take more medications, and so on. We accept it and go on hoping for the best. At this point you’re probably thinking to yourself, “OK, I get the point about aging and anti-aging, but you’re not trying to say that aging is not real, are you?” Of course not. We all know that aging happens. No one questions that there is an unchangeable, mysterious process going on in every living organism that ultimately limits its lifespan. We know aging exists, but that’s about all we can count on. The fact that it is real, however, provides the thread of legitimacy that makes us buy into all of these unfounded assumptions. But—it’s only a thread. KEY INSIGHT

The key issue about aging is not whether it exists or not, but what we attribute to it. In this chapter, we present a new way of understanding how and why our body and mind get old. It’s called the Aging Syndrome. Our current concept of aging as an unchangeable, negative march toward feebleness is part of it, but actually a surprisingly small part. There are many other factors that contribute, and when we evaluate their impact, we see that agingactually plays a very minor role in how our bodies and minds change over time. We call these other factors “root causes.”

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Our current mindset places the focus almost entirely on aging and distracts us from these root causes. Most important, these root causes are things we can control—as opposed to aging, which we cannot control. When we begin to think in terms of the Aging Syndrome, our focus changes to what we can control. This nurtures a new wisdom about aging that allows us to separate truth from fiction so that we know how to stay in the game right up to the end.

Even Science Confuses Beliefs and Knowledge The term real or biological aging is used to distinguish the unchangeable process from other factors, such as disease and environmental, that can also weaken our body and make us old. But, what is real aging beyond an unchangeable, mysterious process? We turn to science for answers to such questions. Unfortunately, with aging, we’re met with disappointment: a lot of theory but few answers—in other words, a lot of beliefs but little true knowledge. There is an enormous gap between what science believes about real aging and what has been proven about real aging. There’s a big difference between beliefs and knowledge. Beliefs are powerful whether they are true or not. They are true to the believer, and they lead to assumptions that become accepted as knowledge. With time, they become ingrained

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What science believes about real aging is clear.

What science knows about real aging is anything but clear.

There is a real aging process going on in all of us at the cellular level.

There are a half-dozen reasonable theories but no consensus about any cellular mechanisms.

The aging process causes us to grow old and die.

None of the proposed theories has been proven to make us old or cause our death.

Real aging is a major risk factor for the diseases we develop as we age.

None of the proposed cellular mechanisms has been proven to cause disease.

Real aging limits our lifespan to a maximum of 120 years.

There is no convincing evidence that the human lifespan is limited to 120 years.

Caloric restriction can enable us to live longer because it slows, stops, and even reverses real aging.*

Caloric restriction slows, stops, and even reverses disease processes, but its effect on real aging is unknown.*

*Calorie restriction is the regimen (usually a 30%–40% lifelong restriction in calories) that has been shown in animal studies to increase the lifespan. This is the topic of Chapter 8.

in our subconsciousness. A big part of this book is about questioning our longheld assumptions and beliefs about aging. These assumptions prevent us from taking a more active role in self-managing the process of growing older. Those in the anti-aging industry depend on false assumptions to sell their anti-aging products. When we think about aging, it is usually in terms of the changes that occur—gray hair, thin skin, age spots, wrinkles, frailty, loss of height, slowing down, vision and hearing difficulties, urinary problems, and so on. We don’t think

about why these changes occur because we assume aging is the cause. We take aging for granted. We don’t think about the process, just the results. That’s why it’s so important to understand the difference between what science merely believes and what it knows about aging. We can accept aging, but at the same time acknowledge that we know very little about it, especially the role it plays in the changes that we associate with getting old. Therefore, the first step in changing our mindset about growing old is letting go of aging as a cause of anything.

Chapter 1: Speaking of Aging, Don’t 

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Don’t Confuse Real or Biological Age With Real or Biological Aging The two are very different, just like age and aging. Real age is a fun way to estimate the impact of our lifestyle, environment, and other risk factors on our longevity. For example, research suggests that someone who has smoked his entire adult life will die an average of 8 years earlier than someone who has never smoked. Hence, a lifelong smoker’s real age is 8 years older than his actual age. This is an inexact science, but it can show us the effect of our behaviors and exposures in a way that we can all understand. We value life more than anything, so when we see that our excess weight, lack of physical activity, and uncontrolled high blood pressure are making us 10 years older than we really are, it can be a powerful message . . . but it says nothing about aging.

It’s Not about Aging— It’s about Old Of the many definitions of aging, the simplest and most useful is: the process of growing old or maturing. This definition is useful because it gives us a new perspective. We see that understanding “old or maturing” is far more important than understanding any theory of aging. KEY INSIGHT

Understanding how we get old is the key to leaving the confusion of aging behind and getting on with discovering what we can do to stay young. The words old and maturing have very different connotations. Old is mostly negative—slow, weak, frail, wrinkles, and so on. It makes you think that nothing good happens with old age—a bad assumption.

There are actually a number of positive things that happen with older age, including the benefits of more experience, better problem-solving skills, a greater sense of optimism, being less judgmental and less emotionally involved in things. Older folks often have a better understanding of the world around them and are not as bothered by little things. And, we hope, they have earned at least a little wisdom. Maturing, on the other hand, is generally seen in a positive light, mainly in relation to growth and development. But, maturation doesn’t stop when we reach adulthood. We mature throughout life as we grow in wisdom, experience, and serenity. We’ll use maturing for the positive effects of increasing age and growing old for the negative aspects. Our goal thus becomes pretty simple—slow down, stop,

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or even reverse the “growing old” parts, while embracing the “maturing” parts.

The Great Mistake— Confusing Age for Aging Because we use the number of years we have lived as the measure of how old we are, it’s easy to let our subconscious substitute aging for age. This leads to another damaging assumption—that weakness and feebleness, or aging, progress in a straight line in concert with age. Unfortunately, the number of years we have lived is a poor indicator of how we feel and function—in other words, how “old” we are in terms of health and biology. Think of your last high school class reunion, especially if you’ve had at least a 30th reunion. With each reunion, you see more variation in how old classmates appear. By the 30th it becomes a challenge to recognize some folks, while others seem to have hardly changed. It’s clear that people vary greatly in the rate at which they get old. Is this due to variations in the immutable aging process? Hardly. Remember that none of these changes has been conclusively linked to any particular theory of aging. We call this the “missing link” in aging research. Besides, it would be impossible to tell anyway because we have no way to measure aging. One thing we do know, however, is that the number of years we have lived, our numeric age, is not very useful as a measure of aging or biological age.

Another area of confusion between age and aging concerns the risk of chronic disease. Aging is consistently mentioned as a risk factor for most chronic diseases simply because they become more common with increasing age. It makes sense that older age is associated with a greater chance of developing a disease simply because there is more time for the disease to develop no matter what the cause. Age is a measure of time and is, in fact, a perfect risk factor (see box)—straightforward, easily measured, and on a continuum from low to high, or lower probability to higher probability. Aging, on the other hand, cannot be a risk factor because it has none of these characteristics. We’ll come back to this in Part II when we talk about chronic disease, but for now the key point is that risk factors tell us nothing about why things happen. They only predict the likelihood that they will occur. Do you ever think of age as a cause of anything? It’s easy to assume that age and aging go hand in hand. But, when we exchange aging for age in our minds, it changes our thinking. We begin to believe that aging is a real cause of disease. This change has a dramatic effect on our mindset about getting older because we identify so strongly with our age. When we hear that most people are overweight at 40, have a chronic disease by 50, and take multiple prescriptions by 60, and then when we see it in real life, our mindset is confirmed—we’re get-

Chapter 1: Speaking of Aging, Don’t 

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Risk Factors Risk factors are conditions or characteristics that help us predict events, such as a diagnosis or a heart attack. They tell us nothing about what caused the event to occur. We all know that high blood pressure and high cholesterol levels are risk factors for heart disease. This means only that people with these conditions are more likely to be diagnosed with heart disease. It does not mean that high blood pressure or high cholesterol levels cause heart disease. Consider another risk factor for heart disease— family history. If your father had a heart attack at age 47, your risk for having a heart attack is increased, but this says nothing about what would actually cause the heart attack. It could be a defective gene you inherited, a diet you learned from your father, a psychological trait, or any number of other factors that you and your father have in common.

ting old. When we see people who seem older than they really are at our reunions, we attribute it to variation in the aging process—yet another flawed assumption. KEY INSIGHT

Believing that the evidence that supports age as a risk factor also supports aging as a cause is one of the biggest mistakes in our thinking about aging. We’re going to change your thinking about what makes other people seem older than they really are, and what makes you older than you want to be. Satchel Paige pitched in the big leagues into his 50s. Most baseball players are “old” at 40. What was different about Paige? His mindset about aging, which led him to ask “How old would you be if you didn’t know how old you are?” It’s a good question. He re-

ally believed that he was younger than he was—and he performed that way too.

Old Is Not a Function of Age The idea that our body and brain can be old at 40 or young at 70 reflects the central theme of this book—that each of us has a lot to say about how and when we get old. There is a long list of changes that occur in every structure and function of our body as we age (see Tables 2.1 and 2.2 in next chapter). These changes are so common that age is often used to predict them. They’re accepted as “normal” aging. At middle age, the list includes overweight, stiffness, poor stamina, low back pain, high blood pressure, and high cholesterol. At older ages, the list includes frailty, debilitation, dependency, and advanced disease. However, age alone does not dictate any of these changes.

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Lab results and physical findings typical of older people can be seen in young folks, and vice versa—findings associated with a younger age can be observed at older ages. Some change is inevitable, but the time frame is far from inevitable. Age-related changes vary tremendously from person to person. Genes play a role, but so do many environmental and lifestyle factors (i.e., root causes). As we’ll see in the coming chapters, there is a lot more to growing old than aging, or age. The key question shifts from What is aging? to What makes us old? This change in thinking takes us from debating a mysterious concept with no real application to addressing our universal challenge—slowing down the process of getting old. KEY INSIGHT

We do not have to settle for a future predicted by our numeric age. Did your vision of “old” or “getting old” at the beginning of the chapter fit the usual picture? We can change this mindset if we begin to think differently about why we get this way. Think about people you know who are exceptions—vibrant, active, and energetic at older ages. They need to be our models for getting older. Most of these folks are unique in two ways: (1) how they view growing older, and (2) how they manage their lives. Most importantly,

they show us what is possible. The rest, who are the norm, show us what is inevitable if we don’t change our thinking and our expectations, and if we don’t manage our behaviors and exposures in our everyday lives. KEY INSIGHT

Our real age can be much younger than our numeric age. We control our own unique probability of getting old by managing the factors that make us old.

The Aging Syndrome Is What Makes Us Old The most common changes that occur with increasing age involve shrinking, weakening, and stiffening. These problems often result from diminishing stimulation. When not used, the body begins to decay, to weaken, and to break down. The core concept of “old” is weakness, not only of the body but of the mind as well. The most important goal for anyone who wants to stay young is to be strong, physically and mentally. So, what causes us to become mentally and physically weak? Not aging, at least not in the way we usually think of it. If only it was that simple. We’d like to believe the anti-aging folks—just take a collection of anti-aging supplements. Unfortunately, getting old—that is, mentally and physically weak—is a more complex process.

Chapter 1: Speaking of Aging, Don’t 

The truth is that a lot of little things interact to cause our body to weaken and begin breaking down and to allow chronic disease to develop and progress. That’s why we call this process the Aging Syndrome. KEY INSIGHT

A syndrome is a collection of signs and symptoms of disordered function that occur together and form a logical picture of an abnormal condition. In the Aging Syndrome, the abnormal condition is the acceleration of growing old.

What Is the Aging Syndrome? The Aging Syndrome can be defined as the signs and symptoms of being old, categorized by the processes that produced them. These processes are the result of ten primary underlying factors, the ones we call root causes. When you read about their individual effects in Part II, you will see that they cause most of the changes we commonly attribute to aging. Together their effects cause us to age faster than we should. There are several advantages to thinking in terms of the Aging Syndrome. First, it explains the “missing link”—the gap that exists between the theories of aging and the changes that we define as “old.” We may want to believe that observations in worms and yeast also apply to humans, but that’s really quite a stretch. The Aging Syndrome shows us how ten

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key behaviors and exposures do result in the changes we associate with getting old. Second, it takes the mystery out of “aging” and makes it less of a distraction. It provides the wisdom we need to interpret the latest discoveries about aging and to see through the most recent fountain-ofyouth product being hyped on the radio or the Internet. Finally, the Aging Syndrome shows us that growing old has many causes, both known and unknown, and it helps us realize that we have lots of control over some and little or no control over others. It emphasizes the importance of knowing the difference between the two. And, it gives us a plan for focusing our efforts on what we have the most control over and what has the greatest impact. That plan is the focus of Part III.

Description of the Aging Syndrome Figure 1.1 shows the components of the Aging Syndrome. There are three pillars of the syndrome—the three major factors that cause us to grow old: 1. Disuse—When we don’t use our body and brain enough, they get weak— that is, old. It’s the “use it or lose it” law of the biology of adaptation. We can use our body and brain to our advantage to reverse our weaknesses. 2. Chronic disease—Disease processes begin long before there is a diagnosis,

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ROOT CAUSES “A WAY OF LIFE” Physical Disuse

Mental Disuse

Eating Habits

Smoking Exposure

Alcohol Use

Stress Response

Environmental Exposures

Attitude & Emotions

Medications Herbs

Interact with genes leading to

MEGACAUSES Metabolic Madness

Constricted Circulation

Insidious Inflammation

(Fat accumulation, Metabolic Syndrome)

(Atherosclerosis, Increasing blood pressure)

(Chronic inflammation, Immune suppression)

Accelerate disease processes leading to

DISUSE DISABILITY (Loss of function from lack of use)

DISEASE DAMAGE

REAL AGING

(Cumulative effects of chronic disease)

(Mysterious process that limits life)

THE AGING SYNDROME STUFF HAPPENS (Accidents, Injuries, Acute Illnesses)

Figure 1.1  The Aging Syndrome: Interacting root causes lead to megacause conditions that accelerate disease processes leading to disease damage. This combines with disability from disuse, real aging, and things we have no control over to cause the Aging Syndrome.

Chapter 1: Speaking of Aging, Don’t 

but our doctors and health care system pay little attention until the diagnosis is made, at which time considerable “aging” has already taken place.

3. Real Aging—This is the mysterious unchangeable process that we don’t know much about, except that it is minor compared to the other two. The Aging Syndrome teaches us to accept aging and then move on to more important challenges—reversing disuse and slowing chronic disease.

The big issue with these three pillars of growing old is the time and energy we devote to them. How much attention do you pay to each of them? Most of us think more about aging than the other two, which is why we call it the “great distraction.” In the Aging Syndrome mindset, we divert our attention away from aging and focus on disuse and disease. Disuse is the most powerful category for most of us because it not only causes problems on its own but also contributes to nearly every chronic disease process. Still, we ignore disuse even though we know we should not. We underestimate its power, and we associate it with exercise and all the bad things that go with it—discomfort, injuries, bad experiences, looking foolish, and so forth. Muscle and brain cells must be used or they wither away. They are not regularly replaced like most other cell types. Dis-

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use of these cells leads to physical and mental weakness and accounts for a large part of getting “old.” Chronic disease is the most misunderstood part of the Aging Syndrome. We ignore it as well, but at least for good reason: We don’t know why we should pay more attention to it. However, this is changing as more factors (root causes) are associated with various diseases at earlier and earlier stages. The question of cause has created chaos in the understanding of chronic disease. It was much easier to rely on aging as the cause. But, when you see high blood pressure and diabetes occurring at younger and younger ages, even in adolescents, can we really believe that these conditions are caused by aging? An expanding body of research demonstrates a multitude of relationships among causes and diseases (Figures 1.2 and 1.3). In the Aging Syndrome, we simplify disease processes by focusing our attention on the three “megacause” conditions that are the links between root causes and chronic diseases. Real aging will probably turn out to be a combination of many processes that are indistinguishable from what we call disease processes. But, at this stage, we just don’t know. What we do know is that we pay too much attention to aging. Why worry about something we can’t do anything about? In the coming chapters we’ll give you more reasons to ignore aging and to change your focus to the megacause conditions.

Live Young, Think Young., Be Young, . . . at Any Age

“Causes”

somehow lead to

Aging Obesity Diet Lack of exercise Smoking Genetics Environment

“Chronic diseases” Heart disease Stroke Cancer Diabetes Chronic lung disease Arthritis Osteoporosis

Graphic by Stephen P. Wells

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Figure 1.2  Chronic disease as presented in the media—too general to be of any use.

The Three Megacauses Megacauses are the major pathological (disease-producing) processes that result from root cause behaviors and exposures. They show us how diseases develop over the years, eventually reaching the diag-

lead to these

“Chronic diseases” Heart disease

Aging Obesity

Stroke

Diet

Cancer Diabetes

Lack of exercise Smoking

Chronic lung diease

Genetics

Arthritis Osteoporosis

Environment The worst part—boomers you are here

Figure 1.3  C  hronic disease in the media, the next step—specific relationships and interactions result in chaos.

Graphic by Stephen P. Wells

“Causes”

nostic threshold when they are finally recognized by the medical system. The period leading up to the diagnosis is vital because this is when significant damage is being done below the radar, and it is the time when we have the most control over the process (Figure 1.4).

Chapter 1: Speaking of Aging, Don’t 

Graphic by Stephen P. Wells

Several root causes Physical disuse Mental disuse Diet Tobacco Alcohol Stress Environment Medications Attitude Genes Process begins with adaptations to root causes

A few megacauses

lead to

which results in

Metabolic Madness Insidious Inflamation

Accelerates as megacauses advance

Symptoms develop as threshold is reached

Diagnoses made as symptoms are evaluated

Many diagnoses Heart disease Hypertension Lung disease Stroke Cancers Arthritis Diabetes Kidney disease Liver disease Depression

Constricted Circulation

Progresses as reserve capacity diminishes

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Medications prescribed to treat symptoms

Disability/Death as capacity is depleted

Figure 1.4  C  hronic Disease and the Aging Syndrome: root causes lead to a few megacauses, which lead to many diagnoses.

The three megacause conditions— constricted circulation, metabolic madness, and insidious inflammation—play a role in the majority of health and medical issues we will face in our lifetimes. Constricted circulation is easiest to recognize. It has to do with the health of our blood vessels—the buildup of plaque (atherosclerosis) and the stiffening of vessel walls (hypertension). Our circulatory system becomes increasingly constricted and unable to deliver an optimal supply of blood to our cells. Constricted circulation is directly responsible for most heart disease, strokes, and peripheral vascular disease, but it also contributes to every other disease process through its impact on blood flow.

Metabolic madness relates to the changes that occur in our metabolism as a result of overeating, fat accumulation, and inactivity. It begins with muscle cells shrinking and becoming resistant to insulin as a result of disuse. This causes our body to release more insulin, pushing our excess calories into fat cells for storage. Expanding fat cells, especially in the upper body, begin to secrete numerous substances that play havoc with our metabolism and appetite. Obesity, the metabolic syndrome, and type 2 diabetes are the hallmarks of metabolic madness. The third megacause, insidious inflammation, is the rising star of the megacause world. We’re all familiar with the signs

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of normal inflammation—redness, heat, swelling, and pain. It’s our immune system coming to our defense, initiating a healing response. What we’re less familiar with is the chronic, low-grade, silent inflammation that takes place in tissues all over our body in response to abnormal substances or conditions. Many doctors and scientists now believe that virtually every known illness is associated with persistent inflammation. The three megacauses interact with one another, compounding their impact and further accelerating disease processes.

Table 1.1  T he Ten Key Root Causes of the Aging Syndrome 1. Physical disuse 2. Mental disuse 3. Poor diet and nutrition (eating habits) 4. Tobacco exposure (secondhand smoke) 5. Excessive alcohol 6. Stress 7. Environmental exposures 8. Negative attitude and emotions 9. Overuse of medications and herbs 10. Genes

The Ten Root Causes Few abnormal conditions ever have a single cause, and that is never truer than with the three megacause conditions. Multiple factors contribute to plaque buildup, stiffening blood vessels, fat accumulation, insulin resistance, and chronic inflammation. We use the term root causes because they are the source of not only most chronic diseases but also accelerated aging. The ten root causes are listed in Table 1.1. These factors play varying roles in each of our lives. Some have a greater impact than others, but all are important because they interact in subtle but powerful ways. Physical and mental disuse are universally important. Sufficient use is absolutely vital for maintaining physical and mental functioning. When muscle and brain cells are not stimulated regularly, they begin to shut down. Adaptation to disuse is relent-

less in its impact on vitality and disease. In contrast, if you don’t smoke and never associate with smokers, then tobacco isn’t a factor. Similarly, if you don’t drink alcohol or if you use it only moderately, alcohol isn’t much of an issue. The food and drinks we consume, the stress we’re confronted with, the environmental factors we’re exposed to, the medications and herbal supplements we take, our attitude about life and aging, and the emotions we feel all play varying roles in the developing megacauses. Together, they can make us grow old slowly or quickly. In discussing the ten root causes, we will focus on changing what can be changed to reverse the megacauses in order to shift the odds of a long, healthy life in our favor. However, we will all experience injuries and illnesses and losses along the way that can have lasting effects. We

Chapter 1: Speaking of Aging, Don’t 

have to learn to accept what we have no control over and make the best of any situation. That’s where acceptance and resilience come in. If we are not able to accept such situations, the resulting emotions will make us age faster than we would like. Genes are unique in that some aspects of them are changeable, while others are not. Our understanding of genes is changing, but we know that they are not static. They can be turned on and off with various stimuli, including the other root causes. This can work for us or against us. We all have a unique set of genes, or genotype, that increases the likelihood of some problems and reduces the chances of others. Sometimes, no matter what we do, our genetic makeup can set us up for a medical problem. Thus, our genes challenge both our courage to change and our ability to accept what can’t be changed.

Staying Young by SelfManaging the Process of Growing Old Our new way of thinking about aging involves self-managing the process of growing old—that is, the root causes of the Aging Syndrome. Reversing physical and mental disuse is the primary focus, but attention to all of the root causes is important in developing an Aging Syndrome–resistant lifestyle. The Personal Plan (see Part III) is a self-management guide that targets our

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thinking and beliefs about each root cause and then provides the structure for developing a plan of action. In each case, mistaken assumptions are dealt with first, then a new way of thinking about each root cause, followed by rules, strategies, and self-managing. It takes courage to change old habits, but anyone can do it by using a plan of proven self-managing strategies and tactics. KEY INSIGHT

Our lifestyle behaviors and exposures in our adult years provide the best estimate of the rate at which we will get old. Positive root cause behaviors and exposures can prevent a good deal of the weakness and frailty, disease-related disability, cognitive impairment, and depression that often accompany the later years. The earlier we adopt these positive lifestyle behaviors, the better, but positive adaptations can occur at any age. It’s not about aging, genes, or the luck of the draw. It is about the positive habits you develop today. That’s how you take care of your future.

Ten Simple Rules for the Road Ahead These ten rules form the core of the Aging Syndrome mindset. Keep them in mind as you go forward (this won’t be the last time you hear them).

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1. Don’t confuse age (the number of years you have lived) with aging (the mysterious process). 2. Don’t think of aging as a cause of anything, especially how you look and feel. 3. Stop thinking of aging in terms of growing old. 4. Emphasize reversing disuse, both physical and mental, as the key to staying young. 5. Learn about disease processes—the major cause of disability and death. 6. Accept that you have the three megacause conditions going on right now. 7. Understand that the megacause conditions will accelerate if you ignore your root causes.

  8. Pay attention to all of the root causes; their effects interact with each other.   9. Don’t wait for a disease to be diagnosed to take action.

10. Use self-management strategies to improve all of your root causes. So, what will it be? Grow old slowly or quickly? Lose abilities or maintain abilities? More diagnoses or fewer diagnoses? Stay in the game or go to the sidelines? You control the answers. It’s not about aging, and it’s not about luck. Just remember—the default is getting old faster if you don’t begin to think and act differently. Next, we’ll continue building the wisdom to know the difference between what we can and cannot control about growing older by addressing the distraction of the mysterious process of real aging.

Our new mindset We have to change how we think about aging if we want to change how fast we grow old. It’s not aging that makes us old. It’s the Aging Syndrome. More specifically, the root causes and megacauses that make up the Aging Syndrome. There is no magic to staying young and active. The answer is simply not accepting aging as a cause of our problems doing our best to self-manage our root cause behaviors and exposures every day, and accepting what we have no control over When we begin to think differently, our old assumptions crumble and new beliefs are formed; then behaviors follow.

CHAPTER

2

Real Aging The Real Thing or the Great Distraction? Science is the father of knowledge, but opinion breeds ignorance. —Hippocrates

The headline reads “Gene That Controls Aging Found.” It’s intoxicating. Could it really be that easy? The headline draws us in. We might even buy the newspaper or magazine. Unfortunately, the mechanism that controls the mysterious, inevitable process of aging remains a mystery. The research may be fascinating, but we have to take it with a grain of salt. Nevertheless, our mindset that aging is responsible for most of our maladies as we get older keeps drawing us in to the latest “breakthrough” in the search for a way to stay young. There are good reasons to be skeptical about research findings, however. Would you be a little less excited if the headline read “Gene That Controls Aging in Yeast Found”? First things first—three key points about aging that we introduced in Chapter 1: 1. We know aging happens, but we don’t know what it is or how it contributes to making us old.

2. We have no way to measure aging, which limits any conclusions we can make about it. 3. We have no idea what, if anything, we can do about aging. 21

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The downside of aging is that it really is a distraction. It’s natural for us to assume that aging accounts for the universal experience of growing old and dying. We see it in every person we know. But, how much of aging is really due to the number of years lived? We can’t know, but the assumptions we make become our expectations about growing old. In the end, believing that aging causes our challenges as we get older distracts us from the real causes of these problems and blinds us to solutions that are available to all of us. Here are four unproven assumptions about real aging: 1. 2. 3. 4.

It makes us old. It makes us weak and feeble. It causes diseases to develop. It kills us.

These assumptions make us believe that we have little control over how long we live or how we grow old. As a result, we miss the opportunity to change our life course by doing something about disuse and disease processes. On the other hand, if we believe that the answer lies in any of the various anti-aging products, we not only will be distracted from doing things that can make a difference but also we’ll be wasting our time and money. We continue to make these assumptions because aging is the easiest explanation for what we are experiencing and what

we see around us. And, the assumptions are continuously reinforced—when we hear that aging is a risk factor for disease, when our doctor tells us that our disease is due to aging, when we feel sore and stiff after some activity, and when we read the seemingly endless supply of misinformation about aging and anti-aging remedies.

A Brief History of the Science of Aging The work of science is to make sense of observations. Scientists make hypotheses, design experiments, carry them out, analyze the results, and confirm or refute their hypotheses. By the middle of the 20th century, scientists had made some intriguing observations about aging: 1. The pattern of aging seemed to be similar in all mammals—changes in hair color, loss of immune function, decline in cardiovascular capacity, alterations in collagen, changes in proteins, and so on.

2. The lifespan varies markedly among mammals, from three to four years in rats and mice to 120 years in humans. This led to the conclusion that a genetic mechanism must control the lifespan of each species. 3. Extreme calorie restriction clearly increases longevity in mammals. Laboratory mice, for example, live

Chapter 2: Real Aging 

about 40% longer when their caloric intake is reduced by 40%. A separate theory could have been proposed for each of these observations, of course. But scientists have long relied upon the rule of logic known as Occam’s razor, which says that the best explanation is usually the one with the fewest assumptions. In other words, look for a single cause before considering multiple causes. The single-cause hypothesis for aging is called the “master clock” theory. It says that every species has a distinct biological clock ticking away inside that causes it to grow old and die. This idea made sense, except that no one could say what the master clock was. Hundreds of

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theories have been proposed. Most were quickly dismissed, but a few are still being investigated:

» Error catastrophe—There are inevita-

ble accidents in the extremely complex process of DNA transcription and RNA translation (by which genes are passed on). The accidents damage the genetic code, resulting in malfunctioning cells that cause deterioration and eventually death.

» Rate of living—Metabolic rate is

inversely proportional to lifespan. A higher metabolic rate leads to earlier burnout and death, like running a race—the faster you run, the shorter the distance you can go.

Weep Not for the Master Clock Is the idea of the master clock dead? Absolutely not. Consider Werner’s syndrome, a type of early aging or progeria that usually appears in early adulthood. This condition is of great interest to “aging” researchers because it appears to be accelerated “aging.” People with the disease look about 30 years older than they are. They show signs of being old—premature balding or graying of hair, loss of teeth and hearing, wrinkles, cataracts, and the so-called “diseases of aging”: heart disease, diabetes, cancer, osteoporosis, and osteoarthritis. People who have Werner’s syndrome usually die in their 30s or 40s. The cause is a single mutation in a gene that produces an enzyme important to the function of all DNA. This mutation seems to throw a wrench into each cell’s basic functioning. The effects closely resemble old age. So, while the current thought is that intrinsic aging involves many genes, it is possible to imagine that a single gene could alter the basic machinery of virtually every cell in “normal” people. Possible to imagine, difficult to prove.

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» Stress—Chronic stress overstimulates the stress response, leading to chronically elevated levels of stress hormones, especially cortisol, that interfere with many body functions, notably immune function, metabolism, and tissue repair, leading to deterioration and death.

These theories all have one simple but devastating problem—a lack of evidence that they can cause the changes attributed to aging. It’s not because researchers haven’t tried. The connections are just not there. Stress comes closest, at least in terms of its observable effects. But most stress is manageable; it’s a lifestyle issue. Stress is a powerful root cause rather than an immutable process that controls some biological clock.

Cellular or System Aging in Humans With the passage of time, a number of changes do occur in our cells and body systems (Tables 2.1 and 2.2). These changes are referred to as cellular and system aging. It certainly seems possible that these changes could be unalterable and cause us to get old, but no one can demonstrate this. Again, it’s the vital missing link in “aging” research: There is plenty of information about potential mechanisms but no valid experimental model and no true markers of

aging to use as outcomes. And, that’s not the only challenge. In order to prove a mechanism, researchers must be able to isolate it from other factors that could influence the changes. This is virtually impossible, especially in an organism as complex as humans. So, where do we currently stand in our understanding of the science of aging? The notion of a single cause—that is, a master clock—has largely been dismissed as too simple. Current theories are considerably more complicated:

» Multiple mechanisms—increasingly complex, no single mechanism

» Stochastic process—a series of random events

» Evolution—built-in degeneration and demise

» Disease instigator—accumulation of the effects of disease

These theories come no closer to proving that aging exists or even explaining what it is. Scientists must show that the effects are universal and irreversible, that the mechanism is the primary cause of growing old and dying, and that the mechanism ultimately imposes a limit on the lifespan of every species. The bottom line is that there is no scientific basis for distinguishing between the effects of aging and the effects of disease. And, there is little evidence that evolution

Chapter 2: Real Aging 

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Table 2.1  Cellular Aging: Stuff That Happens As Cells Get Older

 Mutations in genes accumulate.  Telomeres (ends of DNA) shorten, leading to the deterioration of chromosomes.  Free radicals accumulate, damaging DNA, proteins, and membranes.  Proteins break down and don’t function opyimally.  Repair of cellular damage becomes less efficient.  Synthesis of new proteins slows. Table 2.2  System Aging: Stuff That Happens As Systems Get Older

 Respiratory 

Decrease in lung capacity and strength of respiratory muscles; reduction in elasticity with cross-linking of elastin and collagen fibers; impairment of exchange of oxygen into blood

 Cardiovascular 

Accumulation of lipofuscin, or “age pigment,” in cardiac muscle; loss of muscle fibers with infiltration of fat and connective tissue; stiffening and thickening of walls of larger blood vessels with increased cross-linking of collagen

 Musculoskeletal 

Loss of calcium from bones; reduction in muscle mass, fibers, capillaries, mitochondria, and enzymes; shift from anabolic (building) to catabolic (breaking down)

 Nervous 

Loss of neurons and neurotransmitters in brain; reduction in blood supply to the brain; slowing of processing speed and reaction time

 Kidneys 

Loss of nephrons; reduced activity of enzymes; reduction in blood flow; more water required to produce the same amount of urine

 Endocrine 

Reduced ability to adjust to stress and control blood sugar; changes in hormone levels, notably a decline in sex hormones

imposes a fixed lifespan on every species. This uncertainty feeds the mystery and leads to a number of important questions:

» What determines longevity and lifespan?

» What causes death, if not accidents or disease?

» What causes disease? » Why do some people “age” faster than others?

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» What roles do evolution and natural selection play?

» Does disuse cause “aging”? » How does caloric restriction extend

The rest of Part I will address these questions. In Chapter 3, we’ll look at the fascinating issues that surround lifespan and life expectancy.

life?

Our new mindset No theory or mechanism of aging yet discovered has been linked conclusively to the characteristics of being “old.” For now, we can ignore the idea of “aging” but not the questions that it raises. By exploring these questions we can begin building the wisdom we need to change how we think about both growing older and staying younger.

CHAPTER

3

Lifespan and Life Expectancy How Long Will I Live? I intend to live forever, or die trying. —Groucho Marx

How long will I live? It’s a question we’ve all pondered from time to time, especially when a loved one passes away or when a friend, colleague, or someone notable who is about our age dies. Two other questions, however, are actually more relevant: 1. What is the limit to the length of human life? 2. How much longer can I expect to live?

These questions correspond to the three terms longevity, lifespan, and life expectancy. As you might expect, these terms contribute to our confusion about aging. They are used interchangeably, and their meanings are obscured by the claims attached to them. However, the definitions are actually refreshingly simple and straightforward. Longevity means simply length of life. Greater longevity means a longer life. Life expectancy is a bit more complex, but straightforward once you understand the basics. It is how long you can expect to live at a particular age. Thus, your life expectancy decreases a little with each year older you get. The key point about life expectancy is that it can vary a lot among individuals who are the same age 27

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Table 3.1  Lifespans of Various Species Species Lifespan Species Fruit flies

Several weeks

Lifespan

Horses   62 years

Common mice   4 years

Elephants   86 years

Dogs

29 years

Humans

122 years

Cats

36 years

Galapagos tortoises

190 years

Polar bears

42 years

Greenland sharks

About 200 years

Goldfish

49 years

Bowhead whales

About 200 years

Chimpanzees

59 years

because of disease, lifestyle, and other factors. Lifespan is synonymous with maximum longevity—the oldest age obtainable for a particular species. As Table 3.1 shows, lifespan varies greatly among species. Lifespan is sometimes used to mean a fixed length of life beyond which no person can go simply because of aging. It is sometimes called the “maximum attainable lifespan.” This concept is built into the definition of aging; that is, aging limits the ultimate length of life, a limit that is unchangeable and not linked to any external factors. Most aging experts believe that the limit to the human lifespan is about 120 years. Some contend that it is actually much longer and that research will eventually unlock the key to aging that will allow us all to extend our lifespan beyond 120 years. The simplest definition of lifespan is the oldest age attained by an individual of the species. For humans, that individual is the French woman Jeanne Calment,

who died in 1997 at the age of 122 years, 164 days. There are unverified stories of greater longevity in the so-called “blue zones” of the world—the Japanese island of Okinawa, the Hunza Valley in Pakistan, the Vilcabamba Valley in Ecuador, the Abkhasia people of southern Russia, and others. Longevity tends to be revered in these cultures, but birth records are often incomplete, which has resulted in accounts of extreme longevity, even up to 160 years. No such accounts have been validated, however. A common practice seems to be the adoption of an older relative’s birthdate, which obviously would be a great advantage in a longevity race. We can say with confidence that 122.5 years is the current maximum attainable lifespan, but it may not be the ultimate attainable lifespan. After all, Madame Calment smoked, albeit fairly lightly, for 96 years, not quitting until she was 117. But, she was also still riding a bike at 100.

Chapter 3: Lifespan and Life Expectancy 

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The Boom in Centenarians More and more people are exceeding their life expectancy. This is a dramatic change from the turn of the 20th century, when families were losing a quarter of their children to infectious diseases and the average life expectancy was 47 years. Centenarians are now the fastest growing segment of our population (by percentage). The second fastest is the age group 1001. Currently, there are about 80,000 centenarians in the United States, or a little more than 1 centenarian per 4000 in the population. More than 85% of them are women.

An organization called the Gerontology Research Group (www.grg.org) documents supercentenarians (people who have passed their 110th birthday). The group maintains a current list of the oldest people. Twenty years ago, the longevity record was just under 115 years, so the lifespan, based on maximum longevity, has increased. However, there is currently no one over 115, so 122 years remains the best estimate of the human lifespan for the foreseeable future. Although the number of supercentenarians does not seem to be increasing much, there is a population boom in centenarians (1001 years). In 1950, there were only a few thousand centenarians in the United States. By 2000, the number had increased to 50,454 (a 35% increase from the 1990 census), and the number is expected to exceed 800,000 by 2050 as the baby boomer generation joins the club (Figure 3.1). Worldwide, the current number of centenarians is estimated to be about

a half a million. The trend is clear: More people are approaching the lifespan of our species. Many “aging” researchers believe that science will gradually identify more and more “aging” mechanisms that can be corrected, and this will allow the true limit of the lifespan to be realized with even greater regularity. If this happened, the survival curve would look more like the one on the far right of Figure 3.2. Would this survival curve be proof of a real aging mechanism? As you might guess, the answer is no. The same effect is observed when multiple causes of death interact. The result is an exponential rise in the mortality rate. This is what happens with chronic disease—multiple disease processes are developing at the same time and interacting with one another. This flattens the survival curve so it looks like the one on the left. When we reach our 70s, most of us are experiencing the acceleration of multiple disease processes. At the same

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1.1 million

Black and other White

580,605 324,000 214,000

131,000 50,454 2000

2010

2020

2030

2040

2050

Figure 3.1  Number of Projected Centenarians by Race, 2000 to 2050. Source: U.S. Bureau of the Census

time, the reserve capacity of our body systems (discussed in Chapter 4) is declining to dangerously low levels and the mortality rate increases. On the other hand, controlling disease processes and maintaining reserve capacities enable the survival curve to approach the one on the right. These two factors—reserve capacity and disease processes—are largely responsible for determining life expectancy at any age. Good management of the root causes of the Aging Syndrome leads to a squaring out of the survival curve, as shown in Figure 3.2. The period of dependence and degeneration is shortened. A better quality of life is maintained longer. It’s basically the same curve that we would see if a true fountain of youth

were discovered or if the cause of aging really was discovered and eliminated by some miracle drug. The difference is that managing root causes is real; it’s about possibilities right now—not some panacea in a distant future. The goal of an active high quality of life for as long as possible can be achieved right now by taking control of these root cause behaviors and exposures. That’s exactly what the Personal Plan presented in Part III will help you do. KEY INSIGHT

The biggest factor affecting our personal longevity is the interaction of advancing chronic disease processes.

Chapter 3: Lifespan and Life Expectancy 

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100 If Aging Syndrome is managed well

Percent Suriving

80

60 2003 1980

40

1950 1900

20

0

0

10

20

30

40

50 Age

60

70

80

90

100

Figure 3.2  Survival Curves of an Aging Population­—U.S. Males and Females. Source: CDC, National Center for Health Statistics

Relationships among Lifespan, Longevity, and Life Expectancy Life expectancy, the expected years remaining, makes no assumptions about cause of death. The health and life insurance industries use statistical methods called actuarial science to assess the probabilities of death and disability. They can predict with surprising accuracy the average life expectancy at any age. This is good because it provides us with a standard way to understand life expectancy. The tricky part of life expectancy is the starting point.

Most statistics involve life expectancy from birth. When we hear that the United States ranks 23rd in the world for life expectancy, it means life expectancy from birth. In 1900 the average life expectancy from birth was just over 47 years. Now it’s pushing 80. The increase has been almost linear since the mid-1800s—about two years every decade. If this trend continued, the average life expectancy from birth in 2150 would equal our current lifespan, 122.5 years. The number of centenarians is doubling every decade. Can the trend in longevity possibly continue?

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Table 3.2  Longevity Changes since 1900 (total years of life)

1900 1950 1980 2003

At birth 47.3 68.2 73.7 77.5 At age 65

61.2

78.9

81.4

83.4

At age 75

NA

NA

85.4

86.8

Source: CDC, Health, United States, 2009

We may not have reached the limits of life expectancy, but it is highly unlikely that the trend can continue. Gains in life expectancy from birth in the first half of the 20th century were largely due to improvements in public health and a reduction in deaths from infectious and parasitic diseases, especially in infants and children. In the second half of the 20th century, improvements

in medical interventions, especially in the treatment of heart disease, have enabled people with advanced disease to survive longer. There is nothing on the horizon that has the potential to match these gains. And, with the epidemic increases in childhood obesity and diabetes, some experts predict that the average life expectancy of our youngest generations may actually begin

Survival Curves A survival curve shows how many people are surviving at a given age. If 1% of the population died every year, the curve would be a straight line to zero surviving after 100 years. In fact, we have relatively few deaths in the first half of life, so the survival curve doesn’t drop much in the first 50 years. It stays pretty “flat.” The slope of the curve increases gradually after age 50 as people begin to die from things like heart attacks and cancer, and then it begins to drop rather precipitously after age 70. More people are living with chronic conditions at advanced stages and surviving longer with these diseases due to advances in medical therapy. However, disease processes continue to advance and interact with one another, gradually eroding what is left of reserve capacity (see Chapter 4) and making control more difficult. This results in an exponential increase in deaths. This is how age works as a risk factor: a measure of the time over which disease processes develop and interact. When we self-manage the Aging Syndrome, we increase our life expectancy at any age and the result is a squaring out of the curve as seen in Figure 3.2.

Chapter 3: Lifespan and Life Expectancy 

Table 3.3  Comparison of Life Expectancy at Birth and Age 50 Men Women At birth

75.1

80.2

Age 50

78.8

82.2

Source: CDC, National Center for Health Statistics

to decline. In terms of managing how we grow older, we are more interested in life expectancy starting at middle age. The second half of life is when disuse and disease processes begin to take their toll. This is when taking control of our lifestyle has its greatest impact.

Life Expectancy Increases with Age We tend to underestimate our life expectancy because we don’t realize that it

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increases with age. Life expectancy from birth means the average age of death for the entire population—75 for men and 80 for women. However, with each passing year, our life expectancy increases slightly because we have escaped a few causes of death. For example, people at age 50 have escaped the accidents and genetic diseases that claim the lives of younger people. A 50-year-old U.S. man can now expect to live to nearly 79, while a 50-year old woman can expect to live past 82 (Table 3.3). If a man makes it to age 65, his average life expectancy is another 17 years, or to age 82. He has gained three years of life since his 50th birthday. For a woman at age 65, life expectancy is another 20 years, or age 85. She has also added three years. The good news is that with each birthday, the expected age of dying moves

Why Does the United States Rank So Low in Life Expectancy? The reason has a lot to do with geographic variability. The United States has more than 3000 counties, and life expectancy varies by as much as 11 years for men and 9 years for women among them. Since the 1980s, some counties have actually seen a decline in life expectancy—shocking for a country that spends, by far, the most money on health care. Appalachia, the Southeast, Texas, and areas along the Mississippi River have the lowest life expectancy. The counties with the greatest declines are those with high proportions of African Americans. This is largely due to higher infant mortality rates and a higher prevalence of chronic diseases, especially obesity and diabetes. To improve the U.S. ranking, we need to improve accessibility to preventive care in these parts of the country, especially in the African American population.

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Table 3.4  Expected Age at Death

Birth

Age 20

Age 40

Age 60

Age 80

White female 80.6 81.3 81.9 83.8 89.3 Black female 76.5 77.8 78.9 82.2 89.3 White male 75.7 76.6 77.9 80.9 87.8 Black male 69.7 71.3 73.5 78.2 87.7 Source: CDC, National Center for Health Statistics

farther out (Table 3.4). At age 80, a man can expect another eight years, a woman nearly ten years. What determines our personal longevity? What will be the cause of our

death? How often do we die from old age? The answers may surprise you. That’s where we’re headed next. These are important questions because they tell us a lot about the course of the Aging Syndrome.

Our new mindset Average life expectancy tells us nothing about possibilities. It can, however, set our expectations much lower than what is possible. If we manage our root cause behaviors and exposures well, we can expect to beat the average. If we ignore these root causes, we will probably not reach the expected average.

CHAPTER

4

Aging and Death As Far As We Know, Aging Never Killed Anyone Death is caused by swallowing small amounts of saliva over a long period of time. —George Carlin

One thing we all have in common is that we will eventually die. Barring an accident or illness, don’t we die of old age? Isn’t that really dying of aging? You may have guessed the answer. As far as anyone knows, aging never killed anyone. This is not a bias against aging. It’s just that the relationship between aging and death is unproven. How could it be proven when we don’t even know what aging is and we have no way to measure it? Let’s begin with a reality check: No death certificate lists “aging” as a cause of death. The International Classification of Diseases, the coding system used to classify diseases and other health problems, includes more than 12,000 diagnoses, but not “aging.” “Aging” was removed from the list of acceptable causes of death in 1951, much to the chagrin of the believers in aging. The reasoning was straightforward: There was no definition or criteria for death due to “aging.” What does it look like? What are the symptoms? How do you verify it in an autopsy? If we were going to allow undefined terms to serve as a cause of death, how about one from a 1922 death certificate, which read simply “All wore out.” Or, another from that 35

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era—”Went to bed feeling fine, woke up dead.” A recent favorite, from 2008, was “failure to thrive.” Is it any surprise that a quarter of us don’t believe the cause of death written on the death certificate of someone we knew? How many people actually look at the death certificate when an elderly loved one dies? Does anybody really care about the cause of death unless it was something mysterious? In fact, we pay little attention to the details of death certificates. If there was no obvious disease, like cancer, we may

assume that the person died of old age. This is another false assumption that has become a core belief: that aging is a real cause of death—in fact, the default cause of death—if nothing else can be identified. We’re back to a familiar dilemma. If we’re not sure what aging is, or how it works, or how to measure it, how could we possibly identify it as the cause of death on a death certificate? Unfortunately, there is a lot of faith in the notion of “aging,” and this faith is strong enough that many still insist that aging is the main cause of death.

Aging Conspiracy Theory Leonard Hayflick, Ph.D., a Nobel Prize–winning aging researcher, had this to say about the cause of death on a death certificate: What is legally written on the death certificates of old people is simply an irrelevant detail. The biological evidence that the direct cause of all deaths in old age is the aging process is incontrovertible, but the statisticians seem to be unaware of this. The statisticians are not alone in their misunderstanding. They have been joined by most of the biomedical community, who are dedicated to the proposition that the study of the leading risk factor for death—the aging process—is unimportant. The irony is that despite the belief of most biomedical professionals that the greatest risk factor for the leading causes of death is the aging process, the resources that they have decided to devote to understanding the aging process are microscopic compared to the resources made available for the study of age associated diseases. This discrepancy in funding is indefensible because the unifying concept that underlies the etiology of all the leading causes of death is the fact that old cells are more vulnerable to pathology than young cells.

It looks like the statisticians and the biomedical community are out to get the “real aging” proponents and deny them the funding that clearly should be theirs. Personally, we are willing to forgo a judgment that there is no such thing as aging, but we are pretty sure that the causes of death on death certificates are not “irrelevant.”

Chapter 4: Aging and Death 

In this chapter, we examine what we know about causes of death, especially as they relate to the Aging Syndrome. After all, the Aging Syndrome is what really makes us look and feel old. How does it contribute to death? A hint: It has to do with the effect on chronic disease processes.

Does Anybody Know Why We Die? Not with any precision. Let’s start with a true story. A 52-year-old man is found dead in his apartment. His family says he had no health problems, although he did smoke. The coroner determines that a heart attack is the cause of death. But, because the death was unexpected and unattended, an autopsy is required. The autopsy reveals a totally unexpected cause of death—meningococcal meningitis, an infection that is both deadly and very contagious. Family members and other contacts are given antibiotics to prevent them from falling victim to the disease. This is a dramatic, but not unusual, illustration of the value of autopsies. A missed diagnosis is not a rare event. Study after study reveals common findings:

» At least one in three death certificates is incorrect.

» Even at major hospitals, such as

Johns Hopkins, one in four autopsies reveals a major disease that was unknown in life.

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» Nearly every autopsy uncovers

something that was not suspected in life.

» In about half of autopsied cases,

awareness of an unsuspected condition would have changed how the patient was treated in life.

» In one in five cases, treatment of the unsuspected condition might even have saved the person’s life.

We really don’t know the true cause of death without an autopsy. But, autopsies have become rare events. In the 1940s, about half of all deaths were investigated with an autopsy. In 1984, the rate was down to about 13%. By 1994, it had fallen to 9%. The National Center for Health Statistics gave up collecting autopsy statistics altogether in 1995. Current estimates suggest that the rate is less then 5%. This is a shame, especially considering what autopsies reveal. An autopsy almost always finds something interesting that was not known during life. Doctors cannot possibly know every detail of each patient’s unique biochemistry and mix of health conditions. Time and resource constraints force doctors to focus on the issue at hand. It may seem incomprehensible that anything could be overlooked with the battery of technology and tests at their disposal. But, evidence suggests that the error rate of diagnoses may actually be going up because

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Why Have Autopsies Become Rare Events? Hospitals used to be required to perform autopsies on a certain percentage of deaths at their institution as a quality control measure. However, that requirement was dropped years ago. Some new hospitals do not even have autopsy facilities. Today, autopsies are usually performed only in crimes or unusual deaths. Autopsies are rare with “natural” deaths. There are also several disincentives to performing this type of autopsy. One is cost—about $2000 to $3000 per autopsy. Insurance usually will not cover the procedure, but Medicare will. Doctors also are not likely to encourage an autopsy because it might turn up something they missed in life, and families often see autopsies as disrespectful of their loved one. The biggest disincentive to autopsies, however, is our unending faith in medical technology. Why do an autopsy if tests have already confirmed the cause of death? There is little thought that anything else could have been involved.

of overrating medical technology. Autopsies are the essential “feedback loop” that enables doctors to improve their understanding of disease processes and to sharpen their diagnostic skills. Autopsies are an essential aspect of quality control in medicine. Figure 4.1 shows the leading causes of death according to the National Center for Health Statistics. “Cause of death” rankings do play a major role in funding decisions for medical research and policies. But, if cause of death is wrong 20% of the time, then the rankings for cause of death could be wrong as well. What if cancer was the leading cause of death in all age groups, instead of trailing behind cardiovascular disease? How often is cardiovascular disease listed as the cause of death when nothing else is apparent?

How often is a heart attack secondary to another disease process? No one knows. Without autopsies from a representative sample of all deaths, we know a lot less about why people die than you may think. The result is that we are more likely to believe that an old person simply died of “old age” or, in other words, aging.

The Argument for Aging As a Direct Cause of Death While proponents of aging admit that there are no autopsy criteria for death due to “aging,” they remain undeterred in their conviction that aging is a common cause of death. There are three arguments for this belief: 1. If an autopsy does not find a cause of death, the cause must be aging.

Chapter 4: Aging and Death 

Heart disease

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28.5

Cancer

22.8

Stroke

6.7

Chronic lower respiratory disease

5.1

Unintentional injuries

4.4 3

Diabetes

2.7

Influenza and pneumonia

2.4

Alzheimer’s disease

1.7

Kidney disease

1.4

Blood infection

21.4

All others

0

5

Causes of Death

10

15

20

25

30

35

Percent of All Deaths

Figure 4.1  Official Leading Causes of Death in the United States, 2001. Source: National Center for Health Statistics

2. Cellular or system aging will kill us unless something else kills us first.

3. Apoptosis, or “cellular suicide,” is aging at the cellular level and is the ultimate cause of death due to aging. Argument One: No other cause is found.

The first argument is usually traced back to a 1982 study by R. R. Kohn that involved 200 autopsies in people over 85. Kohn asserted that “no acceptable cause of death” could be found in a third of the

cases. He proclaimed that these cases represented the proportion of deaths caused by aging or, as he called it, senescence. He even went so far as to propose that senescence be viewed as a disease and be accepted as a cause of death. This study raises two important questions: 1. How accurately do autopsies detect the cause of death? 2. Does the failure to find a cause of death justify the assumption that the death was due to aging?

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The answer to the first question is that autopsies may not be perfect but they are the best way we have of identifying the true cause of death. The real issue is the discrepancy between a clinician’s assessment of cause of death without an autopsy and what is found when an autopsy is performed. As mentioned, at least a third of autopsies result in a completely different cause of death. Even when clinicians are “fairly certain” about the cause, they were wrong in about one in four cases. About half of autopsies produce new findings, and half of these may be clinically significant. Older age does make autopsies more challenging due to more advanced disease processes and more interacting conditions. How often does an autopsy fail to find a cause of death? Kohn’s contention that any unresolved death in an old person must be due to aging fueled another flawed assumption that we have come to accept: Very old people die of “old age” if they escape disease. However, the limited number of autopsies performed on people who died in their 90s or later show that diseases were virtually always found and judged to be the cause of death. These “successful agers” did not escape disease, but disease seemed to progress more slowly. If aging really was a common cause of death in old folks, then the rate of “no cause” findings should be consistently higher in older people than in younger. Unfortunately, only a couple of autopsy

studies have targeted the elderly, so we can’t be sure. One study found no cases of “unknown cause” and the other found only 5% unexplained. Vascular and respiratory disease accounted for more than eight out of ten deaths in these two studies. When all available autopsy studies are analyzed, there seems to be little doubt that the “no cause of death” rate is at least as high in the young as in the old. A 5% “no cause” rate seems to be the general rule. Argument Two: It must have been cellular or system aging.

No one argues that cells and body systems inevitably change for the worse with the passage of time. But much of this has nothing to do with aging. It has more to do with the Aging Syndrome. The changes associated with aging are not at all clear, and they cannot be separated from disease processes, as we’ll see in Chapter 5. Argument Three: Your cells will die if all else fails.

This process of cell death is called apoptosis. It makes for an intriguing argument, but it really is just another assumption about aging. Cells do seem to have mechanisms that trigger them to commit suicide in certain situations. This was once thought to be a mechanism of aging, but our understanding of apoptosis has changed. It is now generally regarded to be a normal mechanism for eliminating damaged or

Chapter 4: Aging and Death 

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Apoptosis About 20 years ago, considerable excitement surrounded apoptosis. It seemed to be a perfect candidate for the “magic clock”—cells committing suicide. The process is rapid and fatal and appears to be entirely orchestrated from within the cell. It doesn’t appear to be associated with any disease or body malfunction. For believers in real aging, it seemed to be a godsend—finally a mechanism for causing cell death that could not be confused with disease. Upon further study, however, the picture changed. Apoptosis is relatively rare, so it was hard to imagine how the death of some cells could translate into the death of the entire organism. It seemed to occur mainly in areas where cell turnover is rapid, such as the lining of the gut, and seemed to be a way of getting rid of cells that are no longer useful. It also occurs more frequently in damaged or aberrant cells such as cancer cells. The more that was learned about apoptosis, the more it seemed to be a specialized mechanism for maintaining healthy functioning in certain organs—another “magic clock” that failed to keep time.

abnormal cells, including cancer cells. It actually seems to be more a process for preserving life than causing death. In summary, there is no persuasive evidence that aging is a direct cause of death. You might think that this would cause the believers in real aging to back away from the assertion that aging is responsible for most, if not all, deaths in the aged. Actually, most are willing to concede that the evidence for aging as a direct cause of death may not be convincing, but only because they have a much better answer for how aging is responsible for most deaths—as the indirect cause.

The Indirect Cause The argument for the indirect cause of death also comes in three versions:

1. Aging weakens the body and reduces reserve capacity so that diseases gradually become more deadly. 2. Aging is the primary cause of all chronic disease.

3. Aging is the major risk factor for all chronic disease. We disposed of the third argument in Chapter 1. Recall that a risk factor says nothing about causation, only association. Numeric age, not aging, is the risk factor for chronic disease. Substituting aging for numeric age is akin to a magic trick. Aging, no matter what you may think it means, has no unit of measure and simply cannot be a risk factor. We’re repeating this again only because it is such an important distinction.

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Reduction in Reserve Capacity All organs and body systems have greater capacity than is required for daily functioning. This provides a safety margin for times when greater demands are placed on the body. The excess capacity is called reserve capacity. The reserve capacity of the heart, cardiac reserve, is most studied but is a bit tricky. The kidneys offer the simplest example. Kidney transplants have become almost routine in modern medicine. The loss of one kidney has little, if any, effect on the donor’s health or kidney function. We can do just fine with only one kidney, which means that the body has at least a 50% reserve capacity for kidney function in young, healthy people. Every major organ has a similar reserve, although it may not be as great or as easily demonstrated as in the kidneys. Problems begin with the gradual decline in organ capacity that accompanies advancing age. The capacity required for daily life remains about the same, so the reserve capacity gets smaller. The big question is why organ capacity declines with age. You can probably guess the bad assumption—that all or most of the decline is due to aging. The “reduction in reserve capacity” concept fits perfectly with definitions of aging and assumptions about how aging causes death. Unfortunately, there is no way to demonstrate how much of the decline in organ capacity is due to aging. Experts estimate that it is probably about 0.5% per year, and no more than 1% per year. On the other hand, there are many ways to show how disuse and disease processes affect capacity to a greater degree. And, there is plenty of evidence showing that the decline in reserve capacity can be slowed by reversing these processes.

The first two arguments fail because of the same fundamental problem—the distinction between real aging and disease. We know that disease processes ultimately cause most deaths. So, if someone really wants to convince us that aging kills, then the claim must be made that aging is an important cause of the reduction in reserve capacity and the diseases that kill. Unfortunately for the folks who make this case, there is nothing that distinguishes aging from disease. This is largely due to the uncertainties surrounding aging.

Without a clear distinction, we cannot say that aging, rather than disease, causes the reduction in reserve capacity (see box). Similarly, if you can’t tell the difference between aging and disease, then it makes no sense to claim that aging causes disease and is not part of the disease itself. In the end, the issue of aging as a cause of death comes down to the oldest continuously running debate in “aging” theory: Is aging a disease? That question is the topic of the next chapter.

Chapter 4: Aging and Death 

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Our new mindset Growing old is associated with a gradual reduction in reserve capacity. Some of this decline is the inevitable result of aging. It’s why we can’t do some things at 80 that we did at 40. But, the average person’s reserves are depleted much faster and to a greater degree by disuse and disease processes than by aging. The reduction in reserve capacity increases our vulnerability and risk for disease, disability, and death. We can handle the decline due to aging if we minimize the decline due to the Aging Syndrome. Self-managing our root cause behaviors and exposures preserves our margin of safety. The Aging Syndrome is the real indirect cause of death.

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CHAPTER

5

Aging and Disease Or, Far More Important, the Aging of Disease It’s far more important to know what sort of person has the disease than what sort of disease the person has. —Hippocrates

Is “aging” a disease? This may be the longest-running debate in the history of medicine, going back at least to the days of the Greek and Roman Empires. Aristotle thought aging was not a disease, describing death in old age as painless, without affliction, whereas Cicero described old age as an incurable disease. There was never a great deal of anxiety about the answer because there was no correct answer. Then along came the 1980s, and the debate intensified as research into the mechanisms of aging took off along with the anti-aging industry. Recall that, in 1982, Kohn proposed that “aging” be declared a disease, since it was responsible for a third of all deaths. At the time, it was firmly believed that the mysteries of aging would soon be explained, and that the aging versus disease debate would finally be put to rest. We’re still waiting. When does aging stop and disease begin? This is an important question because aging must be distinguished from disease. If the two cannot be distinguished, then any claims for aging as a cause of anything fade away. Curiously, the other side of the argument is not that “aging is a disease.” Rather, it is that there is simply no way of distinguishing between aging and disease. As health economist Robert 45

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Evans puts it:

“. . . to draw a distinction between disease and normal aging is to attempt to separate the undefined from the indefinable.”

Currently most aging experts believe that aging is a unique and universal process that is distinct from disease and whose mysteries will eventually be unlocked by research. These researchers have strong opinions on the controversy:

» Thomas Kirkwood: “Is aging a disease? Surely not; it is a normal part of the life cycle.”

» Leonard Hayflick: “Aging is not a

disease and the distinction is central to an understanding of why the resolution of the leading causes of death in old age—cardiovascular disease, stroke and cancer—would tell us little about the fundamental biology of age changes. The resolution of all three conditions would result only in an increase of about 15 years in human life expectancy in the developed world, after which aging will be revealed as the leading cause of death.”

» Nathan Shock: “Aging and disease

are not synonymous. There are processes of aging and etiologies of disease. The relationship between the two is important, but not inevitable.”

» S. Jay Olshansky: “Aging makes us ever more susceptible to such ills as heart

disease, Alzheimer’s disease, stroke and cancer but these age-related conditions are superimposed on aging, not equivalent to it.” For aging to be the main indirect cause of death and disability requires an independent but adversarial relationship between aging and disease. Aging would have to be proven to make us increasingly vulnerable to disease. On the other hand, if no distinction between aging and disease can be established, then the “indirect cause” argument falls apart along with the claims for the existence, uniqueness, and importance of aging. This could be a serious threat to the funding of aging research. To be frank, we believe that Evans’s assessment—that it makes little sense to try to separate the effects of aging from those of chronic disease—is likely to be the correct one.

Is It Just a Matter of Semantics? There may seem little value in the aging versus disease debate, but one positive outcome is that it increases our understanding of chronic disease. First, it helps us realize that there is little to be accomplished by the distinction, so we can ignore it along with every other argument about aging. Second, it helps us focus on chronic disease. Remember that chronic disease is a key part of the Aging Syndrome, so if we can learn more about it, that’s a good thing. Finally, the

Chapter 5: Aging and Disease 

debate introduces us to a vital concept of the syndrome—the aging of disease. This is the key to reducing the threat of chronic disease and slowing the process of growing old. Before we get into the aging of disease, let’s look at a few definitions of disease:

» Any deviation from, or interruption

of, the normal structure or function of a part, organ, or system of the body as manifested by characteristic symptoms and signs; the etiology, pathology, and prognosis may be known or unknown.

» A disorder with recognizable signs and often having a known cause.

» Impairment of the normal state or

functioning of the body as a whole or of any of its parts.

» A disordered or incorrectly

functioning organ, part, structure, or system of the body resulting from the effect of genetic or developmental errors, infection, poisons, nutritional deficiency or imbalance, toxicity, or unfavorable environmental factors.

There are some useful consistencies— for instance, a commendable lack of specificity: “the etiology, pathology, and prognosis may be known or unknown.” In other words, we don’t always know what caused the disease, what it looks like under the microscope, how it does its mischief, or what course it will take. Also, the changes

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are for the worse—that is, away from optimal functioning, as in disorder, impairment, and incorrect functioning. There are also some notable misleading aspects, such as the inclusion of “symptoms.” Nothing is more common than asymptomatic disease. Many diseases show no signs or symptoms, even when quite advanced. If we simply break the word down, dis- means “to separate from,” so disease literally means “to separate from ease.” Ease has several connotations, but one that is appropriate for lack of disease is “optimal function.” Therefore, a simple definition of disease becomes: “anything that separates the body from its optimal functioning.” Note that we say “optimal,” not “normal.” The word normal rivals aging as a source of confusion. Even aging experts use normal inconsistently. Sometimes it is used to mean “expected,” other times “average,” and still other times “optimal.” We briefly discussed this source of confusion in Chapter 1. We’ll stick with the word optimal to reduce confusion.

Age-Related Changes and Disease Time is clearly the key factor in the commonly observed changes that occur with increasing age. Time seems to be the important distinction between age-related changes and changes due to disease. Does

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Normally, “Normal” isn’t Normal We think of the word normal in many different ways—usual, expected, average, mean, common, regular, optimal. Operating normally usually means “without problem.” The trouble starts when we associate “normal” with common or expected, as in the case of age-related changes. Many of the negative changes associated with increasing age, for example, are considered “normal” because they are so common. The same is true for chronic disease at older ages. Most elderly people have multiple diagnoses and are on several prescriptions. This is often seen as normal simply because it is so common. Doctors often perpetuate the misconception by explaining diagnoses as: “It’s just part of aging, the price we pay for living so long.” We expect older folks to have these diseases. However, by definition, disease is not normal in the sense that it represents a disconnect from “proper” functioning. Normal may actually be worse than aging in how it is used.

time play a key role in the development of disease? Do diseases occur spontaneously or within some abbreviated time frame? We’re not talking about acute infections and other short-term conditions here, but rather chronic diseases, which make up the vast majority of disease. In fact, chronic diseases begin long before we realize, they develop slowly, and they last a long time. Like the effects of aging, their effects become more obvious with increasing age. That’s why age is such a strong risk factor for most chronic diseases. Thus, it becomes increasingly difficult to differentiate the effects of aging from the effects of chronic disease with the passage of time. Time is just as important a factor in chronic disease as it is in aging, although many other factors

play key roles in disease too, as we’ll see in Part II. So, it turns out that the difference between chronic disease and aging is not as great as you might think. Those who feel strongly that there must be a difference between aging and chronic disease offer two ideas: 1. Things that go wrong with the body with the passage of time are aging, except for those that are due to disease. 2. Things that go wrong with the body with the passage of time are due to disease, except for those that are due to aging. This is called circular reasoning. It has a certain seductive symmetry, but it’s meaningless. Is there anything more frus-

Chapter 5: Aging and Disease 

trating or less enlightening than circular definitions you see in the dictionary? “old: adj. See senescence.”

“senescent: adj. See old.” The one thing circular reasoning has going for it is that it is logical. A leads to B, B leads to C, C leads to A, and around and around we go. There are no contradictions as long as you limit yourself to the specific concepts and how they relate to each other. However, circular reasoning falls apart when we try to make sense of it in the real world.

Real Aging and Disease Some will contend that the lack of a distinction between disease and aging is simply due to the generality of the terms, and that when “real aging”—the unchangeable, mysterious process—is considered, the differences become apparent. After all, real aging requires that the process be innate and universal and limit the lifespan. Can any disease meet these criteria? Our earlier discussion of real aging left a great deal of doubt as to whether anything can meet these criteria. Remember the “missing link” we introduced in Chapter 1—the gap between the changes with time and a mechanism that limits the lifespan. The connection has never been made. Most of the changes ascribed to aging are the same cellular or system changes that

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occur with disease and disuse. So, any attempt to differentiate real aging from disease is on shaky ground to begin with. Consider again the three criteria for real aging—innate, universal, limits the lifespan. The limit on lifespan is easy. In Chapter 4 we saw that what appears to be a mysterious limit to the lifespan may be nothing more than multiple disease processes interacting with one another and resulting in an exponential increase in mortality rates, exactly the situation that most of us will face in old age. The innate requirement (meaning genes, not environment) is also quite easily resolved. Chronic diseases all have genetic components. This is apparent in the varying predispositions and occurrences of disease. Every chronic disease has multiple root causes that interact with one another, and the response to each of these root causes is affected by a variety of genes. There is no way to distinguish the varying disease processes from any real aging effect. The question of whether any diseases are universally present in humans is more formidable. First, we don’t know for sure, but some disease processes may well be universally present in the elderly. Perhaps the most fascinating is amyloidosis (the accumulation of an abnormal protein in certain organs) because (1) it is mysterious, (2) it is associated with changes usually included in cellular aging, and (3) it may be linked to other diseases, notably

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Table 5.1  Percent of the Population with Chronic Conditions Age (years)

0–19

20–44

45–64

651

Percent with at least one condition

27%

40%

68%

91%

Percent with two or more conditions

7%

17%

43%

73%

Source: Medical Expenditures Panel Survey (MEPS), 2006.

Alzheimer’s. Hypertension and atherosclerosis are also extremely common in the elderly, but we can’t say that they are universal. Some cellular and tissue level changes that are part of disease processes also appear to be extremely common, if not universally present, in the elderly. The best example is deterioration of the elastic membranes in arteries and arterioles. This is almost always cited as one of the first events in the development of atherosclerosis, but it is also often cited as a universal marker of real aging. This example reveals another problem of semantics, or the same phenomenon given different labels by different people—atherosclerosis by the medical people, aging by the aging people. Most important, there is as much mystery about the beginning of chronic disease as there is about the beginning of real aging. Evidence shows that several chronic diseases are developing at younger and younger ages. The unavoidable conclusion is that chronic diseases begin much earlier than generally thought— certainly in childhood and perhaps even at conception. In the end, there is no clear,

fundamental difference between the fuzzy concepts of disease and real aging. Evans was right. It’s like trying to separate the undefined from the indefinable.

The Aging of Disease How many times have you heard a chronic disease, such as heart disease, diabetes, osteoarthritis, or osteoporosis, referred to as an “age-related disease” or a “disease of aging”? How often do doctors tell older patients that their disease is just part of aging? It’s because chronic diseases become more common with increasing age (Table 5.1). By the time we reach our late 60s, a quarter of us will have at least three diagnosed conditions (Table 5.2). This notion, “diseases of aging,” is another grand concept that we’ve got to let go of. It reinforces one of our most damaging assumptions—that chronic diseases become more common with increasing age simply because of aging. We’re not saying that chronic disease is not important to every one of us. In fact, just the opposite: We have three

Chapter 5: Aging and Disease 

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Table 5.2  Percent of the Population with at Least Three Chronic Conditions Age (years) 45–54 55–64 65–74 751 Percent

7% 18% 28% 37%

Source: CDC, National Health Interview Survey; Health, United States, 2007.

very good reasons to be concerned with chronic disease: 1. We have disease processes going on right now. 2. Nearly all of us will suffer disability from one or more of these diseases. 3. Most of us will die from complications of one of these diseases. Actually, an obsession with chronic disease is long overdue. These “diseases of aging” do not suddenly and magically appear at age 50 or 60. They have been percolating inside our bodies for a long time. But, don’t despair. We have an opportunity to embrace a concept that even physicians regularly overlook. KEY INSIGHT

It’s not the diseases of aging that get you; it’s the aging of disease processes.

The Aging of Disease Processes Chronic diseases have a life course of their own. They begin inconspicuously and usually go unrecognized for many years until

there is enough damage to cause signs or symptoms. At that point, we go to the doctor and get a diagnosis. The increasing incidence (i.e., diagnosis) rate with older age does not mean that the disease was not present long before the diagnosis. Nor does it mean that chronic diseases do little harm before they are diagnosed. The reality is that multiple disease processes occurring simultaneously over many years take a toll on our body and make us old. This is what we mean by the aging of disease. Two issues underlie our misunderstanding of chronic disease. First is how and when these conditions begin, and second is how they affect our body over many years. Those who contend that aging is the cause of disease, disability, and death (aging researchers and anti-aging entrepreneurs) insist that problems that develop with increasing age are due to aging even though they have no evidence that this is the case. The more you learn about the beginning and natural course of chronic disease, the more you realize that this is what is causing most of the age-related changes we saw in Table 2.2. The bottom line: Forget about aging and focus on chronic disease.

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KEY INSIGHT

The role of chronic disease in making us old is routinely overlooked. The causes of disease, the aging of disease, and the role of disease in the Aging Syndrome are important concepts: Part II

is devoted to them. Next, we need to address another vexing issue that confuses the understanding of aging—the realities of evolution and natural selection. No matter what you believe about the theory of evolution, the processes involved have set some hard and fast rules that play a major role in the course of the Aging Syndrome.

Our new mindset Chronic disease processes are going on during our entire lifetime, but we ignore them until they cause problems, or at least until they are diagnosed by our doctor. Then, we think we’re getting old. We are getting old, but it is because of disease processes, not aging. A big part of self-managing the process of growing old is managing the root causes of these disease processes before they become evident.

CHAPTER

6

Aging and Evolution At Last, Something You Can Blame Everything On If evolution really works, how come mothers only have two hands? —Milton Berle

Are you tired of hearing that you’re not eating right and not exercising enough, and that it’s all your fault? Take heart, we’ve got some great news: You can blame it on evolution. That’s right. Evolution has failed to give us a body that can handle the “good life”—fast food, cars, couches, cubicles, computers, cable TV, and so on. It’s no one’s fault. Evolution and natural selection have simply been going in the wrong direction for several hundred thousand years. It may seem that unloading our guilt may be all that evolution is good for, but, in reality, there are some new ideas about evolution and it’s worth considering them. We do not have to be concerned with any debate over the origins of man. After all, about 40% of Americans believe that God created man in the recent past (i.e., 10,000 years). Another 10% believe we are the product of evolution alone. The rest feel that we are the result of an evolutionary process that occurred over a much longer time frame directed, or at least initiated, by God. We can actually gain some valuable insights from all of these perspectives. Besides, the current understanding of evolution is wrapped in genetics and is the province of highly advanced mathematics. 53

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Three Key Ideas about Evolution and the Aging Syndrome 1. Until a few years ago, the conventional wisdom was that evolution programmed us to get old and probably created a genetic basis for aging as a way to limit the lifespan. It appears now that not only is that unlikely, but evolution may actually be working to extend our lifespan. 2. Evolution, or more correctly, natural selection, explains a lot about how the Aging Syndrome makes us old by connecting disuse and disease, not by causing aging. 3. Evolution shows us how to counter the Aging Syndrome as individuals and as a tribe.

Darwin’s Legacy—Natural Selection, Not Evolution We usually associate evolution with Charles Darwin and his seminal work, On the Origin of Species. But, Darwin’s real legacy is natural selection, the process by which species adapt over time to increase their likelihood of survival. He didn’t even like the word evolution—mentioned only once in On the Origin of Species. Darwin’s theory of natural selection grew out of his observations of slight differences in the shapes of the beaks of the different species of finch that inhabited the Galapagos Islands. He found that each beak had adapted over thousands of years to a specific food source, and this gave each species an advantage with that particular food source. Over thousands of years, the beaks of each species gradually changed to become increasingly efficient at obtaining their preferred food. Natural selection has

stood the test of time. There is no doubt that species adapt over time and that adaptations that increase survival become part of DNA so they can be passed on.

“Survival of the Fittest” or “Elimination of the Weakest” We can observe natural selection in nature when males challenge each other for breeding rights. The strongest prevail to pass on their genes. We see it in a herd of gazelles being chased by a lion. The weakest is usually caught. The fittest and fastest escape to pass on their genes. In the wild, it’s all about success in reproduction. The fittest reproduce more and have more offspring. But, after the peak reproductive years, there is no survival advantage. There’s always a younger, stronger challenger to fight off or chase down the older individual. Our species has adapted differently. Our survival does not depend on strength

Chapter 6: Aging and Evolution 

or speed, or how many offspring are produced, or who produces them. In a stable society, the impact of natural selection extends far beyond the reproductive years. This is a relatively new finding that disputes one of the common misconceptions about evolution—that it favors the death of older individuals through some aging effect.

There’s More to Reproductive Success than Sex In 2004, a major modification of the core of evolution—“reproductive success”—was presented by University of California demographer Ronald Lee. His contention was that success in reproduction in humans requires a lot more than the birth of a healthy baby. The baby obviously requires help from parents, but also from grandparents and other adults in society, before it can reproduce successfully (at least in the most responsible manner). Thus that baby’s reproductive success depends on what Lee called “generational transfer”—that is, assistance from older generations. Generational transfer is also called the “grandmother effect” because older generations play an important role in the success of the family or tribe. This involvement extends beyond caring for the young to passing on wisdom, history, skills, and knowledge—the positive attributes of older age. The tribe was vital in prehistoric times; the cooperation of members gave the tribe a

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survival advantage. The tribe remains vital today, but it is more a case of extended families and communities. Natural selection actually seems to favor longevity to assure that there are enough elders in the tribe. Mathematicians have also recently challenged the hypothesis that evolution dictates aging. Their highly complex analyses conclude that evolutionary processes are not a major driver of aging.

Natural Selection and the Aging Syndrome Natural selection has shaped our body’s structure and function just as it shaped the beaks of the Galapagos finches. According to evolutionary theory, our most distant ancestor, Homo erectus, evolved in Africa approximately 2 million years ago. However, it was not until about 200,000 years ago that modern man, Homo sapiens, appeared. All of our ancestors lived a physically demanding hunter-gatherer lifestyle at least until the Agricultural Revolution, only 10,000 years ago. This marked the transition from a nomadic hunter-gatherer way of life to farming and more permanent settlements. The Industrial Revolution, just 200 years ago, provided another transition—the move to larger cities and even further from nature. Then, only about 50 years ago, our most recent transition began. This was the Technology Revolution, associated

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The Beginnings of Man—Current Evolutionary Thought Most of human evolution occurred in Africa. Fossils of early humans who lived 2 million to 6 million years ago come entirely from Africa. It is thought that the early humans probably began standing upright and walking on two legs about 3.75 million years ago. A large brain and the use of tools and language developed more recently. Migration into Asia is estimated to have occurred about 2 million years ago, and into Europe between 1 million and 1.5 million years ago. Species of modern humans moved into much of the rest of the world much later—Australia probably within the past 50,000 years and the Americas within the past 30,000 years or so. The beginnings of agriculture and the rise of the first civilizations occurred about 10,000 years ago. This marked a dramatic change in the way humans lived—the transition from an active hunter-gatherer lifestyle to staying put and growing food.

with an increasingly automated lifestyle, jobs increasingly dependent on computers, and yet another step removed from an active lifestyle in tune with nature. If we use a one-year timeline to represent this evolutionary period, the transition from hunter-gatherer to agriculture would have occurred on December 13, the Industrial Revolution on the morning of the last day of the year, and the Technology Revolution only two hours before the end of the year (Figure 6.1). Is it any wonder that our genes have yet to adapt? For at least 10,000 generations, perhaps 100,000 or more, survival depended on physical stamina and strength, including a unique ability to run long distances, which gave humans an advantage in hunting. Survival also required the ability to withstand periods of time with little food. The human body became very effi-

cient at using energy for physical activity as well as storing energy as fat. A preference for fatty foods developed because they are the richest source of calories. A preference for sweets also developed because sugar provides immediate energy, especially for the brain, and it replenishes energy stores in muscle. And, a preference for rest developed to conserve valuable energy. This served man well as a huntergatherer and did not conflict too much with early agricultural lifestyles because the work involved a great deal of physical effort and the food supply was high in lean protein and fiber and relatively low in fat and sugar. But, with the Industrial Revolution, just 200 years ago, machines began to do the work. And, in the last 50 years, the demand for physical activity has declined even further as labor-intensive factories have moved out of the United

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Day 1 (January 1) Homo sapiens appear (look like modern man) January

February

March

April

May

June

July

August

September

October Day 310 (November 6) Humans spread to Americas November

December

Day 347 (December 13) Age of Agriculture begins; hunter/gatherer lifestyle ends Day 357 (December 23) Pyramids built in Egypt Day 364 (December 30) The Renaissance; rise of Western European civilization begins Day 365 (December 31, 9 A.M.) Industrial Revolution begins Day 365 (December 31, 10 P.M.) Computer Age begins

Figure 6.1  A  One-Year Timeline of Human Transitions for Homo Sapiens (200,000 years ago to present).

Graphic by Stephen P. Wells

Day 273 (October 1) Humans spread to Australia

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States, machines have become increasingly automated, and jobs are more dependent on computers. At the same time, the food supply has become increasingly mass-produced to meet the demands of a growing population. Packaged, processed, prepared, and fast foods that are high in sugar and fat make up a bigger and bigger portion of the diet. Caloric intake increased at the same time that caloric expenditure was decreasing in the typical lifestyle. These changes are in direct conflict with the survival advantages that natural selection bestowed upon us over hundreds of thousands of years.

It’s Not Nice to Fool Mother Nature More correctly, you cannot fool Mother Nature. Our efficiency at storing fat, our high-sugar diet, and our reduced demand for physical activity have resulted in a current epidemic of overweight and obesity. Two out of three Americans are now overweight, half (one in three overall) to the point of facing serious health risks. Genes that were fine-tuned by natural selection are now working against us. You might be thinking, “Why aren’t we all fat then? Why aren’t we all affected by the Aging Syndrome?” We all are affected by the Aging Syndrome, just at various stages of development. We all have the same genome, but we are all unique. The transcription and translation of DNA are so com-

plex that there are always some variations in our genes. Some have no effect, while others can cause disease to develop. We also live in different environments and have different lifestyles, attitudes, beliefs, motivations, behaviors, and exposures. Ultimately, all of these factors (i.e., root causes of the Aging Syndrome) influence how our genes are expressed, or activated, as well as how fat we get. You will read more about this in Chapter 10. Natural selection has also led to the development of our remarkable reserve capacities. These reserves allowed our prehistoric ancestors to survive emergencies and hardships, and they allow us to feel fine even as chronic disease is developing. However, these disease processes, combined with disuse, will eventually deplete our reserves so that we have little margin of safety for emergencies or unusual activities. Overweight, high blood pressure, high blood sugar, and elevated cholesterol levels are all indicators of disease processes—the higher the numbers, the more advanced the disease. No two people are exactly the same. That’s why one person can eat a high-fat diet and not have a cholesterol problem while another can eat healthy and still have a cholesterol problem. We cannot assume anything based on a single lab test result. You might have a healthy level of cholesterol but poor insulin sensitivity. Also, remember that half of heart attacks occur in people who do

Chapter 6: Aging and Evolution 

not have a cholesterol problem. Some of us are more susceptible to the harmful effects of a fast-food diet, a sedentary lifestyle, stress, or environmental toxins. Native Americans are a good example. Many are only a few hundred years away from a hunter-gatherer lifestyle, so they tend to be very sensitive to the modern lifestyle, as observed in their epidemics of obesity, the metabolic syndrome, and type 2 diabetes. Self-managing the root causes of the Aging Syndrome is important because it addresses all disease processes at the same time, rather than taking a separate medication for each diagnosed condition. It’s about being aware of, and living more in tune with, how our body is designed to function. This is not easy in today’s world. It requires a mindset of being conscious of our behaviors and exposures, of compensating for indulgences, and of living as close to nature as possible.

Religion and Natural Selection We said that both sides of the origin of man debate had something to offer in developing wisdom to manage the Aging Syndrome. What role does organized religion play? First, it can help foster spiritual growth in some people. Obviously, we don’t need religion to experience spiritual growth, but for some of us, it helps. Spiritual strength helps us deal with the big

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questions in life—our purpose, what happens to our soul when we die, and so on. And, it can help us accept the events in our lives that we have no control over—the injuries, illnesses, and losses that we all experience. Recall that managing the Aging Syndrome is about the courage to change what can be changed, but also the resilience and serenity to accept what cannot be changed. Spiritual strength can help foster serenity and resilience. It can also make us feel more optimistic about the future, which has a positive effect on the course of the syndrome. Another positive aspect of nearly any form of religion is the fostering of connections with others. The need for interacting socially, belonging to a group, and working together for a common good is a basic human need. It becomes more important with increasing age. Isolation is as strong a risk factor for disease events and death as any other. We are a social species. We need our families, communities, organizations, and tribes. For many people, the church/synagogue/temple/mosque is their tribe. It is a place that everyone, rich and poor, can count on for social support.

Putting Evolution in Its Place In summary, evolution does not limit our lifespan or contribute in any significant way to aging. It only reinforces how the Aging Syndrome causes us to grow old. It

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may even favor longevity when we are part of a tribe. Natural selection also adds nothing to our understanding of aging, but it does add to our understanding of the relationship between disuse and chronic disease in the Aging Syndrome, especially as it relates to metabolic madness.

In the next chapter, we will look at disuse, the source of adaptations that are the primary driving force behind the Aging Syndrome. It’s a picture of our body’s “evolution” in our own lifetime—the adaptation to how our body is used or not used, and the resulting consequences.

Our new mindset Our body has adapted over thousands of generations to help us conserve and store energy. Conserving energy was a survival advantage for hundreds of thousands of years. It explains why it is so easy to gain weight and so hard to lose it, and why the Aging Syndrome develops. And, it shows us why becoming more active, eating less, consuming foods closer to their natural form, and having a tribe to belong to are essential for managing the Aging Syndrome.

CHAPTER

7

Adaptation to Disuse Didn’t Use It, Lost It Life is like riding a bicycle. To keep your balance, you must keep moving. —Albert Einstein

Want to know what old feels like? Go to bed, and stay there for a week or two. When you get up, you’ll be weak, stiff, unstable, a little disoriented. Everything will be an effort. You’ll be old. A great deal of research has gone into the effects of forced inactivity, thanks largely to the space program. The early astronauts experienced a multitude of unfavorable effects after being exposed to weightlessness, a form of accelerated inactivity. Similar effects are seen in people confined to bedrest. In both cases, the effects are the same—the shrinking and weakening of virtually every structure and function of the human body. This is why extended bedrest is seldom prescribed for anything, and following even major surgery, patients are up and walking as soon as possible. As it turns out, most of the short-term effects of disuse (Table 7.1) are identical to the “age-related changes” that accompany growing old—the same changes usually attributed to “aging.” We could call it instant “aging,” but it’s really instant “old.” The cause is simple—disuse of the body and brain. 61

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Table 7.1  Short-Term Effects of Disuse—Weightlessness and Bed Rest Cardiovascular

Heart contractions weaken Volume of blood decreases; fewer red blood cells means less oxygen for cells Resting heart rate increases; capacity to exercise decreases Arteries stiffen and lose their normal elasticity Dizziness upon standing becomes more common (heart cannot compensate) Blood thickens, with increased risk of clots forming

Musculoskeletal

Bones and muscles get smaller and weaker; tendons also weaken Energy production in muscle cells decreases Strength and mobility decrease; stiffness increases Motor coordination deteriorates

Metabolism

Levels of stress hormones increase Muscle cells become resistant to insulin and require less glucose Insulin increases to counteract resistance in muscles Catabolic processes accelerate; tissue building and repair slow down Metabolic rate decreases

Mental

Blood flow to the brain decreases Cognitive functioning slows down

Immune

Immune system is suppressed; immune response weakens Latent viruses may be reactivated

Inflammation

A low-level inflammatory response occurs in most systems

Recall from our previous forays into defining terms that dis- means “separation from,” so disuse means “separation from use.” It fits our other “dis” words: disease, “separation from ease or health,” and disability, “separation from ability” (Figure 7.1).

Disuse is the cornerstone of the Aging Syndrome because it affects both body and brain. The brain responds to use and disuse just like every other part of the body. The term inactivity is sometimes used, but it doesn’t fit mental functions or account for

Chapter 7: Adaptation to Disuse 

Disuse

Dysfunction

Disease

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Disability

Figure 7.1  Talk about Getting “Dissed”

improper use, which is an important part of physical disuse. Activity does have the advantage of relating well to unintentional physical use, which is called non-exercise activity thermogenesis (more commonly known by its acronym, NEAT). NEAT includes the energy expended for everything we do that is not sleeping, eating, or exercising. Thus, it is primarily the activity daily life. You probably haven’t heard of NEAT, but it is extremely important and will play a key role in how we manage the physical disuse component of the Aging Syndrome.

The Wisdom to Know the Difference: Disuse, Aging, and Old Disuse is not a new concept. Hippocrates, the father of modern medicine, recognized its importance 2500 years ago: all parts of the body, if used in moderation and exercised in labors to which each is accustomed, become healthy and well developed, and age slowly; but if left unused and idle they become liable to disease, defective in growth, and age quickly.

Clearly Hippocrates understood the connection between disuse and disease and knew that disuse (a body “unused and idle”) resulted in a loss of health, a loss that might be more accurately described as a loss in function. However, he also alluded to the relationship between disuse and aging: “. . . if left unused . . . age quickly.” We already know that there is very little that we can confidently blame on aging. So, why are the effects of disuse often confused with aging, even by Hippocrates? The answer is simple—because the changes that occur with disuse are identical to the “age-related” changes that become more common with increasing age (Table 7.2). It’s a heck of a lot easier, and more acceptable, to blame them on aging rather than disuse. Remember that for a change to be truly caused by aging, it must meet three criteria: 1. It happens to everyone, not at the same age but it is inevitable. 2. It becomes more common with increasing age.

3. It is not modifiable by changing the environment—in other words, it is independent of outside influences.

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Table 7.2  Comparison of Changes with Age, Disuse, and Increased Physical Use Increasing Age

Disuse

Increased Use

Aerobic capacity (VO2 max)

2

2

1

Heart function

2

2

1

Elasticity of arteries

2

2

1

Blood pressure

1

1

2

Muscle tissue and strength

2

2

1

Flexibility

2

2

1

Bone density

2

2

1

Fat mass

1

1

2

Blood volume/red blood cells

2

2

1

Formation of clots

1

1

2

Triglycerides

1

1

2

Good cholesterol

2

2

1

Bad cholesterol

1

1

2

Glucose tolerance

2

2

1

Insulin sensitivity

2

2

1

Immune function

2

2

1

Sleep patterns

2

2

1

(1) means increase; (2) means decrease

The last criterion differentiates disuse from aging. And, it rules out aging as a cause of every change listed in Tables 7.1 and 7.2. There’s only one requirement for a change to be due to disuse: It can be reversed by increased use—practice, training, or just doing it more. Old is another story. Disuse makes us old because disuse makes us weak. In our

current mindset of aging, when we feel weak, we start thinking we’re old. If we begin to believe that we’re weak because we’re getting old, then we accept it, and we do less about it instead of more. And, the Aging Syndrome accelerates. When was the last time you tried to play a sport that you hadn’t played in years, such as baseball? You might have noticed that it didn’t

Chapter 7: Adaptation to Disuse 

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More Sedentary Than You Think Do you realize how much more you sit than you used to? Most of us become more sedentary as we get older without realizing it. It often begins when we become parents. Life slows down, although joyfully, as we raise a family and activities revolve around the kids. We gradually do fewer and fewer of our own activities. We become more of a spectator than a participant. Then, when the kids move on, we have fewer obligations. We may take the time to read more and watch more movies and more TV, with movies delivered wirelessly or right to our door and TV channels for every possible interest. We tend to do less strenuous work around the house and fewer vigorous recreational activities. We’re drawn to the path of least effort. Every single day our body is adapting—with cross bridges forming in collagen (connective tissue) and adhesions between muscle and fascia making us stiffer, muscle cells shrinking and capillaries drying up because blood flow is not stimulated. We get weaker, muscles do not support joints as well, fluid in joints declines, overuse or unusual use results in microscopic damage to muscles and joints, and aches and pains increase. How we use our body and mind affects not only how we function but also how we feel.

go quite as you expected. Your arm wasn’t as strong as you thought it would be. You couldn’t hit the ball with the power you expected. You didn’t run the bases or field ground balls or run down fly balls in the outfield like you used to. In fact, the experience may have been down-right humiliating. Then you were reminded again the next morning when you tried to get out of bed. Talk about instant old. Did you think, “I’m too old for that”? The difficulties were largely the result of adaptations to disuse. The specific muscles involved in throwing a baseball or swinging a bat had not been used in that activity, so they got weak. The neural pathways in your brain that used to make hit-

ting or catching a fly ball routine had not been used for years. Like an overgrown trail in the woods, they became more difficult to follow. Your performance would improve if you practiced. Your body and brain would adapt to throwing, catching, fielding, and hitting. You’ll never be as good as you once were, but you could certainly be much better than you were on that first day you gave it a try. There are senior leagues all over the country that show that we can still play, if we keep playing.

Use It or Lose It There is great wisdom in these five simple words. You may have thought that the only given in life is death, but you’d be mistaken.

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The Alexander Technique—Exploring the Subtleties of Use and Disuse FM Alexander was an opera singer in the late 19th century who lost his voice unexpectedly and with no explanation. He suspected that he was somehow causing the problem himself, so he commenced an intensive study of his own posture and body use through the use of mirrors. He discovered that the way he was using his body was not as he perceived it. In particular, he discovered that the alignment of his neck on his torso changed slightly when he sang. This was impairing his vocal cords. Simply by becoming aware of how he was holding himself, he regained his voice. His studies led to the Alexander Technique—a method of analyzing the way we use our body in everyday life. There are now teachers of the technique all over the world. The premise is that how we use our body in standing, sitting, breathing, walking, bending, and so forth affects how it functions. Becoming aware of our habitual patterns of improper use and consciously improving them can often reduce pain and slow disease processes.

There is one other—adaptation. Adaptation is as inescapable and inevitable as death itself. All body parts and functions are constantly being remodeled in accordance with the demands placed on them. We become what we do, or don’t do. A lack of use causes a loss of function, whereas increased use makes functioning easier, more efficient, and more enjoyable. Increasing use leads to order, while disuse leads to disorder. Disuse can make us feel old rapidly. There are no age limits. Even college athletes experience signs and symptoms of being old after a week of bedrest. The most vivid example occurs in muscle. We’ve all seen the extremes— the massive muscles of bodybuilders versus the shrunken remnants of muscle after a cast is removed from a broken arm or

in a frail elderly person. Every muscle in our body, just like our heart, brain, lungs, and blood vessels, adapts to the stimulus placed on it. Disuse leads to shrinking, weakening, and diminishing function. KEY INSIGHT

Adaptations to disuse make us old. They are at the heart of the Aging Syndrome and the main reason we often grow old before our time.

The Single Most Important Health Issue in Middle Age Disuse becomes increasingly important as we get older for several reasons: 1. Disuse causes much of the loss of functioning attributed to aging.

Chapter 7: Adaptation to Disuse 

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Table 7.3  Disease Processes Accelerated by Disuse Alzheimer’s

Low back pain

Dyslipidemia

Chronic obstructive pulmonary disease

Anxiety

Metabolic syndrome

Gallbladder disease

Congestive heart failure

Cancer (some types—e.g., breast, colon)

Obesity

Hypertension

Depression

Cardiovascular (atherosclerosis)

Osteoarthritis

Insomnia

Diabetes type 2

Cerebrovascular (stroke)

Osteoporosis

2. It is the strongest risk factor for chronic disease.

3. It is the single most important reason for disability. 4. It is the most important cause of an accelerating Aging Syndrome.

There have been many, many studies on the effects of disuse. The outcomes can be summarized in three simple, but powerful, generalizations. First, disuse degrades every function of our body. Second, no function can be maintained without proper use. Third, disuse accelerates most disease processes (Table 7.3). It is far more accurate to refer to these conditions as diseases of disuse rather than diseases of aging. The conclusion is that use determines function. Optimal use leads to better function and slower disease processes at any age. Obviously not all of the deterioration in function that occurs with increasing age

is due to disuse, but a surprising amount of it is. Aging does take a toll, but it is subtle. Professional athletes provide a good example. As they get older and the end of their career is in sight, these athletes want to stay in the game as long as they can for the spotlight as well as the paycheck. They train harder than ever, but eventually they can’t keep up with the younger athletes who challenge them every year. Some decline in function with increasing age is unavoidable. Maximum heart rate declines by about a beat a year in everyone, from professional athletes to couch potatoes. Most body systems decline by somewhere between 0.5% and 1% per year after about age 30 or 35 due to some aging effect. This happens in even the most highly trained athletes where disuse is not a factor. This decline is insignificant to the average person, but to an athlete at the highest level of competition it’s a huge difference,

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Decreasing Activity

More Time Sitting

Desk Job, Commuting Weight Gain Declining Strength

Give up Strenuous Activities Functional Decline Reserve Capacity Diminishing Increasing Weakness, Stiffness, Loss of Stamina Greater Difficulty w/ Physical Tasks

Diagnosed with Hypertension, High Cholesterol, etc. Medications Disease Process Accelerates

Feel Older Act Older

Believe Old

Slow Down, Do Less Stiffer, Weaker Injuries

Figure 7.2  The Disuse Path to “Old.”

Disabilities

Old

Graphic by Stephen P. Wells

Lower Expectations

Chapter 7: Adaptation to Disuse 

especially in sports that require speed and power (e.g., basketball, football, track). Experience and training can compensate for a while, but eventually the drop-off in speed and power that occurs in the late 30s, along with the inevitable decline in motivation, is too much to overcome.

Disuse on Top of Inevitable Decline For those of us who are not professional athletes, losing 0.5% to 1% of capacity is not a big deal. It is easily offset by our reserve capacity, at least until our eighth or ninth decade. Normal, everyday functioning uses such a small percentage of our capacity that we don’t notice. However, when disuse occurs on top of the aging effect, it can become a big deal. That’s when we notice that we’re getting old. Disuse contributes significantly more to the decline in function and performance than aging. Consider the best measure of fitness—maximal oxygen consumption (VO2 max), or aerobic capacity. Picture yourself jogging along a road that goes up a hill that gradually gets steeper and steeper. As you continue up the incline, you breathe harder and harder as your muscles require more and more oxygen. Your heart rate increases and contracts more forcibly to push more blood out to your working muscles. The blood vessels in those muscles relax to allow more blood to reach the capillaries of each fiber to

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deliver the oxygen and energy needed to keep going. Eventually you’ve got to stop because you’re exhausted. You’ve reached the maximal amount of oxygen that you can breathe into your lungs and exchange with carbon dioxide in your blood, pump out to your muscles, and use in muscle cells to produce the energy needed to keep you moving. This is your aerobic capacity. The intrinsic decline in aerobic capacity is about the same 0.5% to 1% per year in everyone. This is what highly trained athletes experience after their mid-30s even if they continue working out at the same level. On the other hand, a sedentary person may experience a rate of decline up to four times higher as a result of adaptations to disuse on top of the intrinsic decline. A fit younger person will always have a higher capacity than a fit older person at the same level of use or training. But, a fit older person may have a higher capacity than an unfit younger person simply due to the disuse factor. In fact, the difference can be the equivalent of 30 years worth of aging. In other words, a highly fit 65-year-old may be as fit as an inactive 35-year-old (Figure 7.3). Constricted circulation is the major megacause of the Aging Syndrome. A key part of the constriction is due to arteries losing their normal elasticity. The inner lining of arteries, called the endothelium, contains smooth muscle that constricts and relaxes, which causes the

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Regular exercise

Sedentary

60

Fitness VO2

40

(ml/kg/min) 20

35

65

50

Age

Figure 7.3  Effect of Age and Disuse on Decline in Fitness Note: Does not include additional decline in capacity due to chronic disease processes.

artery to either close down or open up. This helps keep our blood pressure from rising or falling abnormally, and it helps move blood around the body to where it is needed more. Exercise keeps arteries elastic as we age because it stimulates the endothelium to dilate. Without the stimulation of exercise, arteries get stiff over time. When young and old sedentary people are compared, the younger have more flexible arteries. The good news is that we can make our arteries more elastic through exercise, and this adaptation occurs at any age. A three-month brisk walking program can restore the elasticity of the arteries of men in their late 50s to that of men in their late 20s.

Preserving Capacity to Prevent Frailty We’ve talked about the importance of preserving reserve capacity as a margin of safety against unforeseen challenges. It’s also vital in protecting against frailty, which occurs when the reserve capacity of the cardiovascular and musculoskeletal systems diminishes. Frailty results from a decline in physical activity due to either disuse or disease. It results in weakness, injuries, disease-related events, and disabilities. Our goal in self-managing the Aging Syndrome is to maximize the distance from frailty. This means maintaining as large a reserve as possible in our

Chapter 7: Adaptation to Disuse 

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60 50

Fitness VO2

Lif elo

ng

Lif elo

ng

ina

40

cti

ve ,u

nfi t

(ml/kg/min)

ac Yo tiv e, fi wi ung th er t tra ini ng

30

O wi lder th tra in

ing

20 Threshold for remaining independent 30

40

50

60

70

80

90

Age

Figure 7.4  Comparison of Aerobic Training on Arteries in Young and Old Note: Does not include additional decline in capacity due to chronic disease processes.

cardiovascular and musculoskeletal systems. This is a sign of strength.

The Good News about Disuse The good news about disuse is that it is reversible. It is the best investment we can make in ourselves. 1. Every body function can be improved with increasing use. 2. Increasing physical use improves both physical and mental function. 3. Increasing mental use improves mental function. And, age doesn’t matter. People in their 90s can build muscle and increase

strength with resistance exercise and improve their heart and lung capacity with aerobic exercise. The percentage improvement in an inactive person is about the same at any age (Figure 7.4). There are countless stories of older people taking up a fitness program and being astonished at what they could do. Mavis Lindgren, a frail northern California woman, began a walking program at age 62 to see if it would help her lung disease. A couple of years later she thought she’d give jogging a try. At age 70 she ran her first marathon—then went on to do 74 more marathons over the next 20 years. At age 80, her VO2 max was tested; she had the heart and lung efficiency of a

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Table 7.4  Age Group World Records Men 50 60 70 80 90

100 m 10.95 11.70 12.76 14.35 17.53

400 m 51.39 53.88 1:00.77 1:12.85 1:38.69

1 mile 4:27.90 4:54.07 5:23.58 7:08.83 13:43.6

Marathon 2:19:29 2:38:15 2:54:48 3:39:18 5:40:01

Long jump (m) 6.84 6.07 5.19 4.19 3.26

Women

100 m

400 m

1 mile

Marathon

Long jump (m)

50 60 70 80 90

12.50 13.89 15.16 18.42 23.18

1: 58.51 1:06.69 1:18.26 1:40.45 3:02.14

5:02.80 5:48.94 7:15.68 9:00.52 NA

2:35:46 3:11:57 3:46:03 4:31:42 8:53:08

5.40 4.75 4.16 2.78

Source: http://www.mastersathletics.net/World-Records-Masters-Athletics-Trac.684.0.html

22-year-old. At last check she was 103 years old and still walking. In the last two decades, the performances of Masters athletes have improved at a faster rate than any other age group (Table 7.4). Part of it is numbers—

an increasing number of older folks are continuing to compete in various athletic endeavors. Another part is simply the realization that our body adapts so favorably to increased use at any age.

Two Cautions to Keep in Mind about Disuse 1. Positive adaptations are short-lived—they are quickly reversed with decreased use. Disuse is the default. You have to take action for positive effects to occur; become less active for any reason and negative adaptations begin almost immediately. 2. Adaptations to increased use are specific to the type of use. If you do only arm curls, they won’t do any good for the muscles of your legs. If you begin a jogging program, adaptations will occur in your heart and lungs, but your upper body will not get stronger. A variety of use is essential, including activities that challenge both your upper and lower body as well as your brain.

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Table 7.5  Effects of Increasing Mental Use on the Brain Age-Related Change

Effect of Increasing Use

Brain weight

Decreases

Increases as blood flow improves

Brain cells

Shrink or die

Get larger, healthier, more dendrites

Neural pathways

Slower, less efficient

Stronger, more efficient

Nerve conduction

Slows

Gets faster

Brain arteries

Stiffen, reducing blood flow

Become more elastic, increasing blood flow

Neurotransmitters

Decrease in number and function

Increase in number and function

Metabolism

Becomes impaired

Improves

Oxidative stress

Increases

Is reduced

Mental functioning

Declines

Improves

Mental Disuse— Under-Recognized, Under-Appreciated We seldom reflect on the different ways we use our brains, and how we do fewer of these activities as the years go by. Combine the trend of declining use with the expectation that we will become forgetful and unable to learn new tricks as we age, and we’ve set the stage for mental disuse to take a toll. The truth is that mental functioning is as good an example of “use it or lose it” as physical functioning. It becomes harder to learn new tricks because we quit trying

to learn new tricks. Every mental function is capable of being improved (Table 7.5). Virtually none of the decline in mental functioning is inevitable or irreversible— that is, due to aging. And, better yet, evolution supports continued mental activity. However, a couple of challenges make mental disuse more formidable than physical disuse. First is the mind-numbing complexity of the brain—100 billion nerve cells (neurons) making 100 trillion connections, each requiring a variety of chemicals (neurotransmitters) to communicate. The second challenge is the variety of ways in which we use our brains. It is

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overwhelming to think of understanding, measuring, and training all of the unique aspects of mental functioning. The good news is that we don’t have to be concerned with the complexity. In fact, we’re better off ignoring it, and simply becoming aware that both physical disuse and mental disuse are key parts of the Aging Syndrome. We’ll get into the specific effects of each when we talk about root causes in Part II and then what we can do about them in Part III.

Expectations with Increasing Age Mental difficulties that become more common with increasing age are usually attributed to aging until they become severe enough to be labeled dementia. These difficulties include:

» Forgetfulness, especially short-term

memory (repeating things, forgetting names)

» Slower processing of information » Difficulty learning new tasks or techniques

» Increasing rigidity in thinking, less able to consider alternatives

» Poorer motor control—problems with balance and coordination

» Poorer concentration

All of these processes are reversible with increasing mental activity. Neurons,

neurotransmitters, and neural networks get stronger and more efficient. The intensity of the connections between neurons is strengthened, making thinking and processing information along these paths easier. There is tremendous variability in mental functioning at older ages. This is further evidence that aging is a minor factor. Much of the decline with increasing age is simply due to lack of use. Much of it can be reversed by training, although not as completely in older folks as in younger. Four key research findings support the view that a decline in mental functioning is not inevitable: 1. The level of mental functioning in older people is directly related to the mentally stimulating activities they do over their lifetimes. More learning and more education build the mental capacity to offset the declines.

2. Neurons respond to use. Areas of the brain that are used frequently show more extensive neuronal networks, new neurons, and less oxidative stress. This can be seen on PET scans. 3. Declining mental function is often related to dementia. It now appears that increasing mental use offers some protection against even Alzheimer’s disease (see box—The Minnesota Nuns Study).

4. Greater physical activity is associated with better mental functioning

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The Minnesota Nuns Study— Mental Disuse and Alzheimer’s Disease The Nuns Study is an ongoing study of aging and Alzheimer’s disease. It is following hundreds of Roman Catholic sisters whose similar lifestyle and environment make them an ideal group to study. They undergo annual functional assessments and comprehensive medical exams, and they have agreed to donate their brains to science upon their death to confirm any diagnoses. One of the most fascinating examples of the interaction between disuse and disease concerns two sisters—call them Sister A and Sister B. Sister A was a schoolteacher until age 93. She died at 96, and her autopsy revealed extensive Alzheimer’s disease that was never suspected in life. The intensive mental activity of teaching seems to have preserved her mental capacity despite her Alzheimer’s. Sister B was much less mentally active and was actually thought to have Alzheimer’s when she died in her late 60s. But her autopsy revealed no signs of Alzheimer’s disease. Her declining mental functioning was attributed largely to a lack of mental stimulation.

because activity helps maintain healthy blood circulation to the brain and every movement stimulates the brain, especially new activities and those that require coordinated movement.

If Disuse Is So Important, Why Is It So Ignored? There are two main reasons that disuse does not get the respect it deserves. First, our culture promotes disuse in many ways, and second, the aging experts and the anti-aging industry ignore disuse. Aging researchers are interested only in finding a magic gene or some error in biochemistry that could lead to a drug to stop aging. Disuse is not as interesting, and it’s not conducive to re-

search with worms and fruit flies. Besides, we want a quick and easy answer. We don’t want to hear that exercise is the answer. The anti-aging folks, on the other hand, believe they already have the answer in their pill or potion. They can’t make a profit on reversing disuse, so they have no interest in it. This promotes a mindset that dismisses the role of disuse. We hope to change that mindset. In the end, there are few remaining questions. The case has been proven. Reversing disuse is the single most important “anti-aging” intervention we will ever have. We know we should be more active. So, why aren’t we? The answer lies in four obstacles that we’ve got to overcome—evolution, employment, environment, and education.

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Evolution

We alluded to this in Chapter 6. Conserving energy (that is, rest) was essential for our hunter-gatherer ancestors because they had no choice but to be on the move. They had to rest at every opportunity. The same is true for wild animals. In anthropology, it’s called the principle of least effort. We naturally choose the path of least resistance or “effort.” It’s part of our makeup. Unfortunately, the preference for rest (as well as eating whenever possible) that was once a survival mechanism is now a lifestyle, and it’s working against us. Employment

During the last 50 years, physical activity has largely been eliminated from most jobs, especially higher paying jobs (except, of course, professional athletes). And, as we become specialized, the work (both physical and mental) tends to be the same day in and day out. We use a fraction of our potential, and disuse affects every capacity, every muscle, and every neural network that is not stimulated. Environment

The principle of least effort became a mantra for America in the last half of the 20th century. A steady stream of labor-saving devices was introduced with the age of automation. It was all intended to reduce the need to use our body and brain—electric appliances, remote controls, calculators,

elevators, escalators, moving walkways, and ultimately the supposed “greatest invention ever,” the human transporter. We don’t realize how little we use our body. The design of newer subdivisions and communities discourages walking, with greater distances to shopping and schools, lack of sidewalks and bike paths, and so on. The suburbs were designed for cars, not people. Fortunately, this attitude is changing, but not fast enough to reverse disuse. Education

The concept of physical education has been denigrated to the point that today it has been banished from the curricula of many schools beyond the elementary level. Even when present, these classes offer little real education. The objective should be an appreciation of the importance of lifelong activity and the cultivation of lifelong recreational interests, but, unfortunately, many of us are left with only a disdainful taste for exercise.

Social Learning Theory Provides Additional Insights Research on how our behaviors are shaped has provided two important findings: 1. We’re influenced by other people’s behaviors—the more we see others doing something, the more likely we are to do it ourselves or at least

Chapter 7: Adaptation to Disuse 

to give it a try. When more people are taking the escalator or using the moving walkway in the airport, we’re more likely to use it too. By the same token, if we see more people out walking, jogging, or riding bikes, we’re more likely to consider these activities as well. Mindsets are changed by the momentum of thought. As more of us view growing old as a syndrome of many factors that we control, we will think differently about aging. And, as we realize the impact of disuse and the importance of reversing it, more of us will become active, doing things that were unheard of at older ages a generation or two ago. 2. We’re more likely to engage in behaviors that we believe we can be successful at. We enjoy what we do well; we avoid what we don’t do well. As we gain weight and lose strength from disuse, we find it more difficult to climb the stairs, so we avoid them. We don’t want others to see us struggling, and we don’t want to feel the discomfort. The cycle of disuse is a vicious cycle—“don’t do it” soon leads to “can’t do it.” The less we actually do for ourselves, the less we can do for ourselves. The less we walk, the harder it is to walk. It’s a simple formula that leads to increasing

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disuse, helplessness, disease, and disability. Combine it with the tendency of our culture to suggest that, after age 40, any difficulties we experience are due to aging, and we have the recipe for the disaster of disuse. On the other hand, like Mavis Lindgren, we can take the first step, and as we begin to walk more, it becomes easier. We enjoy it more, so we do it more. The next thing we know, we’re going farther, then maybe joining a group for a hike, then we’re giving jogging a try. Or, our newfound confidence leads us to try another activity, like tai chi or weight lifting or yoga. The contrast is remarkable—“can’t do it” leads to “give it a try,” which leads to “can do it” and eventually to “can’t live without it.”

Disuse Is the Problem, Use Is the Solution Increasing use is incredibly powerful. If it were a drug, no one would believe the proven claims that could be printed on the label. KEY INSIGHT

It’s not that you don’t do it because you can’t do it; you can’t do it because you stopped doing it. Use it and get it back. Keep using it and don’t lose it.

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We’ll get into more specifics on the effects of disuse in Part II, but first we have one more important topic to cover

in Part I—the wisdom that can be gained from the only proven “anti-aging” strategy, calorie restriction.

Our new mindset Adaptation to disuse, rather than aging, is the real cause of our declining function and abilities as we age. Our body cannot adapt to a 21st-century lifestyle, so our behaviors must adapt to the way our body is designed. Using our body and brain more, and in a greater variety of ways, is a key to slowing or reversing the process of getting old. This requires courage to overcome the barriers and a strategy that assures success. You’ll get both in the Personal Plan presented in Part III.

CHAPTER

8

Calorie Restriction Less May Really Mean More . . . Years of Life Anyway Mankind, since the improvement of cookery, eats about twice as much as nature requires. —Benjamin Franklin

There may really be a life-extending miracle after all, and nothing could be simpler—just cut the calories you consume by about 40%, and do it for the rest of your life. At first glance, this strategy, known simply as caloric restriction, or CR, may seem to be a little out of its league among such heavyweight topics as evolution, death, disease, and disuse. But, it has one unique feature that places it legitimately in this group—it is the only proven method to increase longevity. And, if that’s not enough, consider this:

» CR is the gold standard by which every anti-aging therapy is judged. » Its mechanism is considered to be the Holy Grail of “anti-aging” research— the mysterious cause of real aging.

Don’t confuse this type of calorie cutting with a weight loss diet. CR is a way of life. Weight loss happens with CR, but that’s not the goal. The people who practice CR believe that it really does slow aging and will enable them to live at least 79

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30 years longer. However, these folks have to be very smart about nutrition to make sure that they get all the vitamins, minerals, and other nutrients that their body needs. There’s no room for empty calories. That’s why the plan is called caloric restriction with adequate nutrition. The last part is the challenge, along with overcoming the not so small matter of hunger.

The Research— Cause for Enthusiasm The potential benefits of CR really do sound like a miracle cure:

» » » »

Increased lifespan by 30% to 40% Reduced body fat

Reduced incidence of chronic disease

Improved cholesterol levels and blood pressure

» Reduced glucose and insulin levels, improved insulin sensitivity

» Reduced oxidative stress, fewer free radicals produced

» Reduced inflammation » Strengthened immune system CR has been shown to increase the lifespan of every species tested, which so far includes worms, fruit flies, spiders, insects, and rodents. Studies of monkeys are currently in progress. CR seems to work best when it is started early in life, but it has positive effects even when begun in

adulthood. The general rule, however, is the earlier begun, the greater the impact, at least in terms of longevity. Rat and Mice Studies

The first study of CR to report an increase in longevity involved rats and was published in 1935. Since then, hundreds of studies have confirmed the impact of CR on longevity in a variety of short-lived species. Rat and mice studies provide the bulk of the evidence. Here are some of the significant findings:

» In young rodents, the increase in

lifespan is roughly proportional to the reduction in calories—30% to 60% CR increases lifespan by about 30% to 60%.

» In adult rodents, the effect is less

dramatic—40% CR seems to increase lifespan by only about 10% to 20%.

» There is less chronic disease,

especially diabetes, heart disease, and cancer at any age; chronic disease develops slower and later in life.

» There is less deterioration of nerves and neural networks in the brain. Studies on Monkeys

The first primate studies of CR began in the 1980s, using rhesus monkeys because they develop many of the same chronic diseases as humans at older ages.

Chapter 8: Calorie Restriction 

The monkeys’ average life expectancy at birth is about 27 years and their lifespan is about 40 years. The animals were young adults when they began the study, so the survivors today are elderly. A 2009 report showed that, at late-middle age to early old age (about 20 years), half of the control animals had died compared with only a fifth of the CR animals. The CR monkeys also had only half the cancer and cardiovascular disease and no diabetes. Studies in Humans

Does CR work in humans? That’s the big question. Unfortunately, research in humans is in its infancy, and obviously it will take a long time to determine whether CR has an impact on longevity. We’re very different from short-lived animals like rats and mice. From an evolutionary perspective, when these animals experience food shortages, their metabolic rate and core body temperature drop and reproduction is shut down until the food supply is restored. We don’t have these survival mechanisms. Our primary survival mechanisms are the ability to store large amounts of energy in fat and the ability to cover long distances walking and running to move to where food is more plentiful. We also have other differences in physiology, metabolism, and immune function that may change our long-term response to CR. However, if the trends in the monkey studies continue, then all bets are off.

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They are much more similar to us. What we do know about the human response to CR comes from four sources: 1. The island of Okinawa, Japan, where the oldest generation has lived a calorie-restricted lifestyle most of their lives 2. An unintended “experiment” in the Biosphere-2 project

3. A series of six-month to one-year pilot studies sponsored by the National Institute of Aging, the first randomized controlled trials in humans

4. Observations of people who have chosen CR as a way of life and belong to an organization called the Calorie Restriction Society The Okinawa Experience  Many human populations have been forced to survive famines, but most were malnourished. The exception is the oldest generation of Okinawans. From their early years, prior to World War II, they consumed a low-calorie but nutritionally adequate diet. Even today, they consume 20% to 30% fewer calories than people in the rest of Japan. Their rates of death from cardiovascular disease and cancer are also about 30% lower. And the incidence of diabetes is much lower. Okinawa has the highest density of centenarians in the world. But, none have lived longer than the oldest

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people in other parts of the world who have not experienced consistent CR. This supports CR’s positive impact on disease and the Aging Syndrome, but not on aging itself. Biosphere-2  This was a project in which eight people (four men and four women) chose to live completely independently for two years inside a 3-acre self-contained “ecological mini-world” near Tucson, Arizona. It was the largest closed system ever created, including insects, birds, and even fish in a lagoon. The participants had a garden and raised goats, pigs, and chickens. All food was produced inside the compound. This was a highly motivated group of people who viewed the experience as an adventure, and the media coverage reinforced their motivation. A study of calorie restriction was not part of the plan. However, when food production fell short of expectations, the team leader, a physician named Roy Walford, convinced the crew that a calorie-restricted lifestyle would not only enhance their health but also provide a great research opportunity. For the first year, the people lived on about 1800 calories per day. They reported feeling hungry much of the time. In the second year, food production increased and caloric intake increased to 2200 calories a day. Dr. Walford and an outside medical team monitored everyone’s health. The participants were free to leave at any time

if they felt their health was being compromised. Over the two years, no one left and their health remained excellent. The predicted effects of CR were observed (similar to the monkeys):

» Body weight and body fat decreased substantially.

» Body temperature lowered. » Blood pressure dropped. » Blood glucose and insulin levels dropped.

» Total cholesterol and both LDL

and HDL levels fell, although bad cholesterol fell proportionally much more than good cholesterol.

» Immune system became stronger. » Metabolism became more efficient.

The participants were able to maintain their level of physical activity, which is a concern with CR. Some CR animals become weak and lethargic due to a lack of energy. Despite the positive effects on their health, however, none of the participants continued the regimen after they left Biosphere-2. Their health data gradually returned to pre-Biosphere levels. The CALERIE Studies  The initial CALERIE (Comprehensive Assessment of Long-Term Effects of Reducing Intake of Energy) studies were conducted at three different sites and included healthy, sedentary, overweight, but non-obese,

Chapter 8: Calorie Restriction 

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Table 8.1  The Original CALERIE Study Designs Study Site

Duration

Sample Group

Intervention

Washington University

12 months

50–60 year olds

20% CR diet vs. 20% increase in calories expended in exercise

Pennington

6 months

25–50 year olds

25% CR diet vs. 12.5% CR diet with 12.5% increase in calories expended

Tufts

6 months

24–42 year olds

25% CR diet with high vs. low glycemic load

men and women (Table 8.1). A second phase is currently under way using normal to only slightly overweight men and women, 25 to 45 years old, following a 25% CR regimen for two years. The Washington University study showed that a 20% CR regimen over one year has a similar effect whether it comes from decreased food intake or increased exercise. The exercise group had the added advantage of an increase in fitness (VO2 max), strength, and preservation of bone density. The Pennington study confirmed that a combination of exercise (12.5% increase in expenditure) and CR (12.5% reduction) is just as effective as 25% CR alone, again with the added benefit of increased fitness in the exercise group. You may be wondering how much exercise these folks were doing. On an intake of 2500 calories per day, a 12.5% increase in expenditure is the equivalent of about 300 calories a day. This amounts to about 60

minutes of brisk walking daily. It depends on your weight (more weight, more calories burned) and how fast you walk (faster, more calories burned), but this is about what you would have to do if you walked at a pace of 3 miles per hour. It doesn’t have to be all at once; you could do three 20-minute walks in place of a one hour walk. The third research group, from Tufts, addressed the composition of the diet— specifically the effect of varying the glycemic load (the amount and type of carbohydrates). Their results confirmed previous findings that it is the caloric deficit and not the composition of the diet that is important. There was no difference in outcomes with varying glycemic loads as long as the deficit was the same. The Caloric Restriction Society (CRS) This is a group of people who are committed to a CR lifestyle for the rest of their lives. Most are more than willing

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to be evaluated to confirm that their sacrifice is worth it. Researchers from Washington University are monitoring a group of CRS members. The participants were average for their age on most health variables when they began a CR lifestyle. The results so far suggest the same adaptive responses that have been observed in laboratory animals. Their heart became stronger, blood vessels more elastic, and blood

pressure dropped to that of a child. Lipid levels improved to the top 10% for their age. Insulin sensitivity improved so much that the fasting insulin level dropped to one-fifth of what it was when the regimen began. Chronic inflammation decreased to a similar degree. Together, these results indicate a strong deceleration of the effects of the Aging Syndrome (Table 8.2).

Table 8.2  Comparison of 33 CRS Members to a Matched Normal-Diet Group after Six Years of CR Normal Diet

Calorie Restricted

Age (years)

52.3

51.4

Males:females

29:4

29:4

Body mass index (kg/m2)

24.8

19.6

Body fat (%)

23.1

8.4

Systolic blood pressure (mm Hg)

130

103

Diastolic blood pressure (mm Hg)

81

63

LDL cholesterol (mg/dl)

122

86

HDL cholesterol (mg/dl)

52

64

Total cholesterol:HDL cholesterol ratio

4.2

2.5

Triglycerides (mg/dl)

143

58

Glucose (mg/dl)

95

84

Insulin (µUI/ml)

7.4

1.5

C-reactive protein (mg/L) (inflammation)

1.1

0.2

Source: J. O. Holloszy and L. Fontana, Caloric restriction in humans, Exp. Gerontol. 42, no. 8 (2007): 709–712.

Chapter 8: Calorie Restriction 

The Mystery—How It Works “Aging” scientists are fascinated with the CR research because they believe it is a connection to the secret to aging. Discover the mechanism of CR and you have not only the cause of aging but also the means to develop the biggest blockbuster drug in history. Or so the thinking goes. This mindset reflects, once again, the mistaken belief that there is a single cause of aging. The way the body responds to CR seems to be an evolutionary adaptation, but exactly how it works remains a mystery. Several mechanisms have been proposed but none confirmed. The effects are so widespread that it is futile to try to single out one mechanism as responsible for all of the positive effects. Three mechanisms seem to play key roles: 1. Reduction of oxidative damage as metabolism becomes more efficient

2. Lowered glucose and insulin levels as insulin sensitivity improves 3. Activation of multiple defense mechanisms as “hormetic” effects Oxidative Damage

Oxidation is one of the most damaging processes in the body as well as a dominating theory of aging, so it makes sense that CR would affect it. Oxidation occurs whenever oxygen combines with another substance. We see it when iron rusts, copper gets a patina, or a cut apple turns

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brown. It also occurs with every breath we take. Oxygen enters our bloodstream and is delivered to every cell in our body, where it is used to produce the energy currency of our body, ATP. ATP is produced in mitochondria (the powerhouses of every cell). When we digest food, glucose from carbohydrates and fatty acids from fats enter the mitochondria and move through a chain of reactions with oxygen that results in the formation of ATP (energy). The problem is that during this process a few lone electrons are released, and they are very reactive. They are called free radicals. Most combine with oxygen and then hydrogen to make a harmless byproduct, water. But some do not. These free radicals can react with other molecules and steal electrons from them. This destabilizes that molecule and causes even more free radicals to be generated. It can result in widespread damage—to mitochondria, cell membranes, proteins, lipids, even DNA. The good news is that this is a normal process and our bodies are constantly repairing free-radical damage. We have enzymes that detoxify them and a host of antioxidant molecules that “trap” them to neutralize them. The bad news is that oxidative processes that generate free radicals are accelerated by many factors in our lives, including overeating, stress, smoking, excessive alcohol, overexertion, excessive sun exposure, and environmental toxins (i.e., root causes). The

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result can be a chronic overload of free radicals, which overwhelms our defenses. This condition has been linked to several disease processes, including heart disease, liver disease, and some cancers. CR reduces the production of free radicals. It makes metabolism more efficient—less food consumed, less metabolism occurring, less oxygen required, fewer free radicals generated, and less oxidative damage. CR also activates enzymes that neutralize free radicals. Rodent studies show that normally fed older animals put most of their genetic effort into repairing damage, while CR animals have less repair to do, so energy goes into building new proteins and other cellular components—more like younger animals. Glucose and Insulin Overload

A common finding with increasing age is a rise in the fasting blood glucose level. Muscle cells use less glucose as we become less active. They become resistant to insulin, the hormone that helps glucose get into muscle cells. Insulin becomes less effective at reducing the level of glucose in the blood. Our body responds by releasing more insulin to overcome the resistance, so insulin levels rise too. This is the core of the megacause metabolic madness (Chapter 13). Many problems develop when blood glucose levels remain higher than normal. Glucose attaches to other cells in a process called glycosylation. Glycosylated hemo-

globin (or hemoglobin A1c) is used to measure glucose control over several months because it measures the amount of glucose that has attached to red blood cells, which are replaced every three to four months. Long-term diabetes is often considered to be a form of accelerated “aging” due to the extensive glycosylation that occurs over time. But you don’t have to have diabetes to experience this. It happens long before the diagnosis of diabetes, as muscle cells are becoming resistant to insulin and glucose levels are starting to rise. Eventually, excess glucose reacting with proteins, fats, lipids, and even DNA can form toxic chemicals called advanced glycation end products, or AGEs. This is the same process that turns meat brown. This kind of damage accumulates over a lifetime even in people who do not have diabetes. It contributes to nerve problems, kidney damage, atherosclerosis, loss of vision, cataracts, and impaired immunity. The brains of Alzheimer’s patients contain extensive amounts of AGEs. Caloric restriction has a powerful effect on glucose and insulin levels. It reduces them to the low end of the normal range, increases insulin sensitivity, and ameliorates all of the related pathologies. Hormesis

Hormesis is the biological response to an agent that is harmful at higher doses but helpful at low doses. Vaccines are a classic example. A very small dose causes anti-

Chapter 8: Calorie Restriction 

bodies to develop in our body that protect us from the disease. Alcohol is another example. A little alcohol has some positive effects, but larger amounts become increasingly harmful. Sunshine is another. We need some sunshine to boost vitamin D production, but we all know the damage caused by too much sunlight. The effect of stress on performance is yet another example. A little stress heightens arousal, increases our focus, and gets us ready to perform our best. Too much stress interferes with our ability to perform. CR is a low-intensity stressor. We know this because it causes a mild increase in corticosterone, a hormone linked to stress. As a mild stressor, CR turns on a variety of defense mechanisms. These defense mechanisms help us get through food shortages, but they also protect against oxidative damage, inflammation, and metabolic and immune dysfunction.

With CR, the defense adaptations remain activated and assist in preventing disease and may enhance longevity. However, there is a fine line with CR. If nutritional deficiencies develop, then the stress becomes more intense and damage increases. Likewise, if there is excessive fatigue, then physical exertion is more likely to cause excessive oxidative stress along with inflammation.

Calorie Restriction and Disease Processes You may have noticed that we have often mentioned the effect of CR on chronic disease. That’s because CR has a beneficial effect on virtually every disease process that has been studied, especially heart disease, diabetes, cancer, and rheumatoid arthritis (Table 8.3). This is an impressive list, worthy of blockbuster status if it could be packaged into a pill.

Table 8.3  Diseases That Have Been Shown to Benefit from Calorie Restriction

 Some types of cancer (breast, colon, prostate, lymphoma, and others)

 Alzheimer’s disease  Atherosclerosis  Autoimmune diseases (e.g., lupus,

rheumatoid arthritis, multiple sclerosis)

 Cardiovascular disease  Cataracts  Cerebrovascular disease

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 Cholesterol disorders  Diabetes  Hypertension  Kidney disease  Liver disease  Metabolic syndrome  Osteoarthritis  Parkinson’s disease  Peripheral vascular disease

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Caloric Restriction and Disuse

A Tough Pill to Swallow

Many of the effects of CR are similar to the effects of reversing disuse. Exercise can even substitute for part of the calorie deficit. This is critical because few people can sustain a long-term 25% or 30% reduction in caloric intake. Like CR, physical activity is a mild stressor of many body systems. Mild stress makes us stronger and increases our ability to cope with physical and mental demands. Exercise also has hormetic properties. As the intensity of exercise increases, the positive effects diminish and the damaging effects increase. That’s why keeping exercise to a moderate intensity is best, or at least limiting vigorous intensity to short periods of time. Debating the virtues of CR versus exercise is sort of like debating the importance of fitness versus leanness. Which is more important? In the end, both increasing fatness and decreasing fitness make us old. It’s not one or the other; it’s both. Both increasing fitness and reducing fatness are essential in managing the Aging Syndrome. This is the advantage of combining an increase in activity with a low level of calorie restriction. The clincher is: What is more livable? What makes you feel better? Clearly the answer is the combination. It allows you to eat more, to feel more satisfied and less deprived. And, by including exercise in your lifestyle, you increase your strength and stamina, have healthier bones, and have a greater capacity for life.

CR, even at a modest level, is difficult to maintain. It can be uncomfortable and frustrating, and it forces you to become an amateur nutritionist, or at least to have access to one. Table 8.4 lists some other potential disadvantages as well. Age is also an important consideration. The risks associated with CR increase with age (especially bone health). The adaptations to CR decline somewhat with age, as do the positive effects. So, the balance of benefits and harms gradually shifts toward the harm side with increasing age. Table 8.4  The Downside of Long-Term Calorie Restriction

 Thinner, more gaunt appearance  Weaker and more porous bones as calcium is drawn out

 Greater sensitivity to cold  Less cushioning (sitting) and protection of internal organs (due to fat loss)

 Smaller energy reserves with more

difficulty withstanding food shortage or exhaustive activity

 Decline in strength, stamina, and physical work capacity

 Slower healing and recovery from accidents, surgeries, and injuries

 Menstrual irregularities in premenopausal women

 Decreased testosterone levels in men

Chapter 8: Calorie Restriction 

Caloric Restriction and the Aging Syndrome The important thing about CR is what it tells us about the Aging Syndrome. Most important, it provides a large body of evidence showing the reversibility of most age-related changes. If a condition improves with CR, then it was not caused by aging. This research confirms what we’ve been saying all along: Many, if not most, of the changes that we think of as “aging” are not inevitable and are not caused by the mysterious real aging process. CR also shows us how the parts of the Aging Syndrome are connected. It gives us a great example of how root causes accelerate megacauses, and how they interact to make us old. CR has a powerful positive effect on all three megacauses—constricted circulation, metabolic madness, and insidious inflammation. Adaptations in one system affect adaptations in other systems. CR results in positive changes occurring simultaneously in virtually every body system and disease process.

Putting the Research to Work— Managing the Aging Syndrome The good news is not how CR works but what it shows us is possible. It confirms that we are our own worst enemy when it comes to risk factors, diseases, and growing old. We may never know whether CR can actually increase our lifespan, but we

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do know right now that it will improve our disease processes. And, we know that it will slow the effects of the Aging Syndrome. We also know, however, that very few of us—only one in a thousand by one estimate—can sustain this type of lifestyle. In the end, CR is a great research tool, but not much of a real-life tool. We can still get some of the benefits of CR with little of the pain. Researchers at the University of Florida have shown that an 8% CR combined with a moderate increase in physical activity can extend the lifespan of rats and significantly reduce cell and organ damage. That means only a couple of hundred calories a day, the equivalent of a few different choices or smaller portions. A couple of hundred calories can be burned in a 40-minute walk. That’s sustainable. With the Aging Syndrome, we take it a few steps further with our ten root causes. Small changes are easier to accept and to achieve. Several small changes can replace one big change. Big changes are doomed to failure, as any habitual dieter will tell you. If we could conduct research studies using the entire Personal Plan for self-managing the root causes of the syndrome (see Part III), we think we would find many of the same outcomes. And, it would be much more pleasing to the palate. A final observation about the CR research is the resemblance of the average overweight, under-active American to

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the control rats in the CR studies. These rats ate “ad libitum,” meaning as much as they wanted. Food was plentiful, and their caged environment discouraged physical activity. Does that sound familiar? These studies allow us to glimpse the impact of overeating and under-activity in a very compressed time frame. Control rats gain weight, develop disease, and die prematurely. These animals are “poster rats” for the Aging Syndrome.

They show us what makes us old, while the CR rats show us what is possible. We want to be more like the CR rats and less like the control rats. Next, we’ll get into the nuts and bolts of the Aging Syndrome in Part II. It begins with a better understanding of chronic disease processes and then the root causes and megacauses that affect these processes. This is where possibilities become realities.

Our new mindset The key to the benefits of CR is that it is a way of life. We can still get many of the benefits without the sacrifices—lots of little changes, adjustments in our lifestyle that we can handle. Eventually, we will not be able to live without them. Selfmanaging the Aging Syndrome is a different mindset more than anything—a mindful approach to how we eat, how much we eat, how active we are, how we use our brain, how we respond to stress, how we use alcohol, how we control our environment, how we think about life, how we use medicines and supplements, how aware we are of our inherited risks, and so on. Small changes in each of these root causes will interact and make us stronger.

PA R T

II KNOWLEDGE To Understand the Disease Processes That Make Us Old

In part i we learned that our thinking about “aging” is built on a foundation of flawed assumptions and beliefs. There is no solid foundation to aging. We can’t define it, we can’t describe how it works or what it causes, we can’t differentiate it from disease or disuse, we can’t even be sure that it causes death. In a word, it’s confusing. And confusion opens the door to a deception-filled anti-aging industry that is thriving even in our struggling economy. Do you see how our assumptions and beliefs about “aging” can be a distraction? They make us feel powerless to the changes that happen to us as we get older. And, they keep us from making positive changes that can actually prevent many of these changes. We hope you now have a new perspective on “aging” and a new respect for this thing we call the Aging Syndrome. Part II is devoted to understanding how the Aging Syndrome develops from a set of root causes in our daily lives. This involves the central part of the syndrome— chronic disease processes. It includes disuse because disuse affects virtually every 91

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disease process. This is the part of the syndrome that threatens both our quality and length of life. Advanced chronic disease causes most disabilities and death and is the biggest drain on our health care system, accounting for three of every four dollars spent on health care. It’s all because we ignore the early stages of disease processes. We wait until medical therapy is required, and then we become dependent on increasingly expensive medical therapy as the disease process advances. Self-managing of the Aging Syndrome is largely about slowing the development of chronic disease before it is ever recognized by the health care system. The next seven chapters explore the critical concepts of chronic disease that are overlooked by both the research and medical communities. Chapter 9 presents a new way of thinking about chronic disease—as a lifelong process that we have a great deal of control over. Chapter 10 explores the beginnings of disease processes. Chapter 11 describes the crucial intermediate stage—what we will call the megacause conditions that develop when we ignore our root cause behaviors and expo-

sures. Mega means “very large” or “of great significance or importance.” This stage is the time when disease processes are accelerating toward a diagnosis, but before medical care is authorized. We call it the “black hole” in our thinking about chronic disease because our health care system provides little recognition and support. One of our most harmful assumptions is that chronic disease is not an issue until it is diagnosed. We are still in control of the Aging Syndrome at this stage, but we are approaching a tipping point when disease damage gets more difficult to reverse. Chapters 12, 13, and 14 address the three megacauses—constricted circulation, metabolic madness, and insidious inflammation—and how they make us old. Chapter 15 includes a brief overview of each of the ten root causes. The focus is on the adaptations that result when we ignore them, especially how they contribute to the developing megacause conditions. Chapter 15 sets us up for the presentation of the Personal Plan in Part III because the plan shows us how to think and act differently about each of these behaviors and exposures.

CHAPTER

9

Critical Concepts Stuff You Need to Know about Chronic Disease All diseases run into one. Old age. —Ralph Waldo Emerson

“Why? What caused it?” asks a dismayed patient after feeling blindsided by the diagnosis of a chronic disease. We want to know why it happened now and what caused it—a bad gene, a defective organ, a chemical imbalance, a germ or virus. The doctor’s response is not very satisfying: “It’s just aging. You’ve reached that age when we develop a number of chronic diseases. We call them ‘diseases of aging.’ If we live long enough, we all get them. The good news is that we can control them with medication.” So, why now? Will it get worse? Am I going to be on medication the rest of my life? The diagnosis of a chronic disease often seems like a milestone, a sure sign that we’re getting old and that our life will never quite be the same. In Chapter 5 we introduced the role of chronic disease in the Aging Syndrome. These were the key points:

» The damage caused by chronic disease is often interpreted as “getting old.” » It’s impossible to distinguish the effects of disease from “aging.”

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» Aging does not cause chronic disease to develop.

»  Accepting that chronic disease is an inevitable consequence of “aging” is wrong.

In this chapter, we’ll present a new way of thinking about chronic disease— as a lifelong process that we control rather than a milestone of getting old.

Current View—A Case of Mistaken Assumptions Chronic disease is a bigger deal than we realize (Table 9.1), and not simply because it is the greatest threat to our future quality of life. The big deal is what it is doing to us right now. Two faulty assumptions contribute to our misconceptions about chronic disease. The first is

that we don’t have a chronic disease until it is diagnosed. We call this the “diagnosis delusion”—that the diagnosis occurs soon after the disease began. This delusion is tied to our second bad assumption that we have already alluded to—that the disease was caused mainly by aging. This is the typical explanation for why the diagnosis came out of the blue. We finally reached the age when it becomes a problem. This thinking feeds into our belief that we’re getting old.

The Diagnosis Delusion Our health care system is built on diagnoses—everyone benefits from a system that is based on a point of diagnosis. It makes everyone’s job easier. It’s when the system kicks in, when disease is recognized, med-

Table 9.1  The Impact of Chronic Disease

 Chronic disease is responsible for 75% of total health care spending.  Chronic disease is the leading cause of death and disability, responsible for seven out of ten deaths.

 Heart disease, cancer, and stroke cause more than half of all deaths.  Nearly half of all adults have at least one chronic condition.  Chronic disease becomes more common with older age; by age 65, nine out of ten

people have at least one chronic condition, three out of four have at least two, and one in four have three or more chronic conditions.

 The use of medications for chronic diseases increases with age; by age 65, the average person takes six unique prescription drugs yearly.

Source: CDC, National Center for Health Statistics; MEPS, 2006

Chapter 9: Critical Concepts 

ications indicated, and treatment reimbursed. Unfortunately, this system is not always in our best interests. Why? Mainly because of inconsistency in how and when diagnoses are used. The point at which a diagnosis is made is arbitrary. There are no rules for when a diagnosis should be made. Even when the diagnostic criteria are clear, diagnoses are inconsistent. How close to the beginning of a disease does a diagnosis typically occur? Most of us assume that chronic diseases don’t develop at least until middle age, and usually later. We don’t think about exactly when or how these conditions begin. The simple, but powerful, point is that chronic diseases do not appear overnight. They are processes that occur over a lifetime. The diagnosis may seem like a milestone, but it is really only a marker of the progression of the process. The only consistency in the diagnosis is that it almost always occurs late in the disease process. KEY INSIGHT

Believing that a diagnosis occurs near the beginning of a disease is a mistake. This delusion about when chronic disease begins diverts our attention away from the process. We pay little attention to the beginning, the causes, and the progression of the disease. And, we miss a critical window of opportunity to change the course of the condition. It’s much

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easier to change the course earlier in the process than later. It’s easy to ignore the disease before it is diagnosed because it is not interrupting our life yet. Another part of the diagnosis delusion is “no diagnosis, no harm.” Damage is more obvious after the diagnosis just because the process is “aging.” It’s getting worse. It leads to more symptoms, more related diagnoses, more prescriptions, more tests, and so on. After the diagnosis, disease processes are better understood. Doctors and insurance companies, perhaps even telephone nurse counseling services, follow patients and help them manage their disease. Table 9.2 presents the traditional view of chronic disease management—making regular visits to the doctor, monitoring symptoms and lab results, adjusting prescriptions, changing and adding medications, managing side effects, and so on.

How Many Chronic Diseases Do You Have Right Now? Most of us would say none, unless we’ve already been diagnosed with something. If a doctor has not told you that you have high blood pressure, does that really mean that you do not have it? More important, does it mean that you have normal or optimal blood pressure? National statistics tell us that 32 out of 100 adults have high blood pressure,

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Table 9.2  T he Conventional View of Chronic Disease— Beginning with the Diagnosis 1. Diagnosis prompts a treatment plan; medication is the first step. 2. The disease progress is monitored by periodic lab tests. 3. Medications are adjusted to improve control; others are added as needed. 4. Organ function becomes impaired; new medications are added. 5. Mental and/or physical abilities begin to be affected; they get attributed to aging. 6. Disability develops, activities are limited, and the quality of life declines. 7. The goal is to prevent complications for as long as possible.

which means 140/90 or higher. What does that say about the other 68 out of 100? A person who has a reading of 139/89 or 130/85 is not diagnosed with high blood pressure, but is that blood pressure normal or optimal? Hardly. Studies clearly show that health risks increase at any level above the optimal level, which is about 110/70, even lower than the standard “normal” of 120/80. We tend to assume that if our level is not “high,” then it’s OK—no diagnosis, no prescription, no disease, no worries. We now call readings between 120/80 and 140/90 “pre-hypertension.” The same point can be made about other easily measured risk factors, such as blood sugar and cholesterol levels. The numbers in Table 9.3 are misleading. They do not present the true prevalence of the conditions, but rather only the

diagnosed cases. How many more cases have just not yet been diagnosed or are in the pre-diagnosis stage? We have fewer data, but the CDC tells us that, besides the diagnosed cases:

» Nearly another third of adults have pre-hypertension, and 7% have undiagnosed hypertension.

» More than a third of adults have

pre-diabetes, and more than half of people over age 65.

» Another third of the population is overweight but not yet obese.

The pre-diagnosis stage is evidence of the disease process. Unfortunately, this stage of chronic disease is like the proverbial elephant in the room—the health care system doesn’t recognize it and doesn’t want to deal with it. Treatment is more

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Table 9.3  P  revalence of Disease: Percentage of Adults Aged 20 and Older with the Diagnosis Disease Percentage

Disease Percentage

Obesity

34

Ulcers 9

Hypertension

32

Diabetes

8

Arthritis

23

Cancer

8

High cholesterol

16

Asthma

7

Heart disease

12

Chronic lung disease

6

Source: CDC, National Center for Health Statistics.

difficult because medication is not yet indicated. Lifestyle changes are the best approach, but the system does not recognize this, and doctors lack incentives to address things like exercise, diet, and stress. The same pre-diagnosis stage applies to all disease processes—in our lungs, kidneys, heart, brain, digestive tract, blood vessels, nerves, joints, bones, muscles, and so on. We just don’t have a simple measure like blood pressure to monitor the developing process. The important point is that the process begins long before it reaches the diagnostic threshold of a lab test.

The Fallacy of “Diseases of Aging” Our second bad assumption is that aging is a major cause of the developing disease process. This misconception is understandable because the prevalence of virtually every chronic disease increases across age groups (Table 9.4). But, the reason is not because some mysterious “aging” mechanism kicks in at age 50, 60, or 70. These are diseases of life that are simply diagnosed more frequently as the years go by because the disease process has

Table 9.4  Prevalence of Diagnosed Hypertension with Increasing Age (%)

35–44 years

45–54 years

55–64 years

65–74 years

75+ years

Men 21 36 50 64 65 Women 13 36 54 71 80 Source: National Center for Health Statistics, Health, United States, 2009.

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been ignored. Eventually the diagnostic threshold is reached, and, voilà, a “disease of aging” has appeared. The diagnosis tells us that the process is advancing, but it also confirms our belief that we’re getting old. As conditions like obesity, hypertension, diabetes, high cholesterol, arthritis, and depression become increasingly common, we begin to accept them as part of aging. It’s easy to accept aging as the cause. It’s easy to believe that these conditions are inevitable. It’s easy to accept medications as the answer. These ideas contribute to our laissez faire, defeatist attitude about our ability to exert any control over chronic disease. After all, isn’t it just a matter of time, genes, and luck before we get them? In reality, time, genes, and luck all play minor roles.

A New Way to Think about Chronic Disease The only way to think about the changes that occur as we get older is as a process. When we think of chronic disease as a process, and aging as simply the passage of time, we see that age is only an estimate of how long the disease processes have been going on. This allows us to change our mindset from “diseases of aging” to the “aging” of disease processes. It also removes the notion of inevitability. KEY INSIGHT

It’s not the diseases of “aging” that get you; it’s the “aging” of disease.

With this point of view, we also see the diagnosis for what it really is—just another point along the way. We can then look at the “aging” of disease from two perspectives: before diagnosis and after diagnosis. The medical system focuses on the latter. Self-managing the Aging Syndrome focuses on the former—the “aging” of the disease process before the diagnosis. It is getting harder and harder to ignore this part of the process. Not only do we hear more about the pre-diagnosis stage, but we see disease processes accelerating at younger and younger ages. This is all too obvious in the alarmingly high rates of obesity, diabetes, and hypertension in children and adolescents (Table 9.5). And autopsies of young people show significant atherosclerosis (plaque deposits on the inner walls of arteries) already occurring. KEY INSIGHT

The most important part of chronic disease processes occurs before the primary disease is ever diagnosed. Chronic disease is very different from acute illnesses. Doing nothing is often a reasonable course of action for acute problems. Most are self-limiting; that is, our body tends to heal itself. Chronic diseases are different. They don’t resolve on their own. If we ignore them, they get worse. Our innate healing mechanisms (e.g., im-

Chapter 9: Critical Concepts 

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Table 9.5  Prevalence of Chronic Disease in Children and Adolescents Condition

Age

Prevalence (%)

Obesity

2–19

16

High triglycerides

10–18

14

High cholesterol

10–18

10

Hypertension 8–17

3

Pre-hypertension

8–17

14 (boys) 6 (girls)

Metabolic syndrome*

12–19

10 (overall) 29 (of obese)

*Diagnosis is made by the presence of three of five criteria (elevated blood pressure, large waist circumference, low HDL, high triglycerides, and high blood sugar)—discussed in Chapter 13. Source: CDC, NHANES 1988–1994, 2003–2006.

mune system) are often diminished by the disease process. The effects are subtle and gradual, but they persist and accumulate if the underlying causes are not changed. We don’t notice the effects because our reserve capacities allow us to function quite well. We may move a little slower, think a little slower, and have a little less energy, but we pass it off as aging. What we don’t realize is that our reserves are slowly being depleted, leading to a vicious cycle of declining energy and declining activity that feeds the disease process. Declining activity leads to weight gain and further deconditioning. Physical exertion becomes more difficult, so we stop doing more and more activities. This leads to increasing dependence and a growing sense of helplessness and pessimism. It worsens all three megacauses (circulatory, metabolic, and inflammation

problems) and accelerates all disease processes. Eventually, symptoms appear or we go to the doctor because we just don’t feel well or our lab tests come back positive, and then the disease is diagnosed. KEY INSIGHT

Individual diagnoses cause us to miss the forest for the trees. For every disease process, there may be a series of diagnoses along the way. The most recent diagnosis becomes the point of focus for our health care. If the diagnosis is a high cholesterol level, then that becomes the treatment target, which usually results in one of the 253 million annual prescriptions for cholesterol-lowering drugs, such as Zocor (94 million prescriptions in 2010). Zocor works by inhibiting an enzyme that our body needs to produce cholesterol. The

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drug often lowers cholesterol levels, but is this enzyme really the cause of cholesterol problems for the many millions who take the drug? Is elevated cholesterol the only, or even the most important, issue? Probably not on either count, but don’t stop taking your medication. The real problem is that we’re not dealing with the root causes. High cholesterol may be just the tip of the iceberg. Below the surface are multiple chronic disease processes and the Aging Syndrome, which are greater threats. Isolated diagnoses overshadow the overall process. The medication to lower cholesterol may even have detrimental effects on other aspects of the Aging Syndrome (see Chapter 10). The bottom line: Our narrow obsessions with each diagnosis often cause us to miss the forest for the trees.

If Not “Aging,” What Is the Cause? The question of cause poses a dilemma for both doctors and patients. There is no simple cause, as there often is for acute problems. We don’t just “get” diseases like hypertension, diabetes, heart disease, lung disease, osteoarthritis, and osteoporosis. Both doctors and patients overlook the underlying process because it involves many different factors. Chronic disease processes begin with adaptations to interacting root causes.

These adaptations vary depending on each person’s unique set of behaviors, exposures, and genes. Inevitably they lead to the megacause conditions and then to outright disease and disability. Age plays a relatively minor role, as we know from the evidence of atherosclerosis in most 20-year-olds and the rising incidence of high blood pressure and diabetes in adolescents. KEY INSIGHT

Chronic disease processes have multiple root causes, one of which is always genes. The only rational explanation is that the same disease processes are occurring at younger and younger ages. Adaptations to root causes occur at any age. They are a function of behaviors and exposures (i.e., root causes), not age. It is the behaviors and exposures that are occurring at younger ages. We introduced the ten primary root causes in Chapter 1. Here they are again:

» » » » » » » » » »

Physical disuse Mental disuse Poor diet and nutrition Tobacco (smoking or exposure to secondhand smoke) Excessive alcohol Stress Negative attitude and emotions Environmental exposures Medications and herbs Genes

Chapter 9: Critical Concepts 

There is really nothing new and exciting in this list. That may be frustrating if you were hoping for something shiny and new. That’s why fad diets, exercise gadgets, and new supplements always sell but seldom result in long-term success. They appeal to our desire for a magic potion that will take the work out of staying healthy and fit and give us quick results. Our answer may not be the kind of breakthrough you were looking for, but it is a breakthrough. The breakthrough is a different way of thinking about each of these behaviors and exposures in your life along with an approach to self-managing them that results in a lifestyle that resists growing old. Most important, this approach can guarantee long-term success. KEY INSIGHT

Root cause interactions are not a problem but rather an opportunity to decelerate disease processes. The cause of chronic disease processes is complex because all of the root causes really do contribute, and genes affect the response to each of them. But, there’s no need to despair over the simple realization that there are so many causes. Interactions can work in our favor just as they can work against us. Improving one root cause magnifies the positive effects of others. Positive adaptations reinforce one another. For example, increasing physical activ-

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ity not only improves fitness and strength; it also enhances mental use by improving blood flow to the brain, is one of the best stress management tools around, helps balance hormones that influence attitude and appetite, may allow a reduction in medications, and so on. And, it has a positive effect on all three megacauses as well as many different disease processes. We’ll get into all of these interactions in Chapter 10. The important point for now is that root cause interactions have a powerful influence on chronic disease processes and their combined effect is greater than their individual effects. It works both ways though. Just as combinations of positive root causes are really good for the Aging Syndrome, combinations of negative root causes are really bad for it.

The Process Is Unpredictable Sir William Osler, the “father of modern medicine,” described the unpredictable nature of disease: “Variability is the law of life, and as no two faces are the same, so no two bodies are alike, and no two individuals react alike and behave alike under the abnormal conditions which we know as disease.” Chronic disease processes vary from person to person. When exposed to the flu virus, not everyone gets sick. And, those who do get sick experience different degrees of severity. The variation results from each individual’s general health, genetic makeup, and immune system robustness.

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If there can be such variation in a simple infectious disease, think of the variation that must exist in chronic disease processes. There are many other sources of variation—root causes, lifestyle, medical history, coexisting disease, genes, occupation, living situation, injuries, fitness, reserve capacity, and so on. The variation shows up in the type of diseases developed and in the rate at which they progress. We can’t predict how each disease process is going to affect us. We can get a glimpse from our parents’ experience, but the root causes we face are far different from those our parents experienced. Family history cannot be ignored, but it may not be as important as we think. The bottom line is that we have to assume that the process is happening faster than we think. After all, acceleration is the default if we are mindless about our thoughts, behaviors, and exposures.

The Aging Syndrome View of Prevention The Aging Syndrome concept gives us the tools we need to change how we think about prevention. After all, we can’t prevent a process that is already happening. But, we can change it in three ways—accelerate, decelerate, or reverse. The direction and rate of change can change from day to day. Our body is in a constant state of change. Our root causes change daily and disease processes are constantly

adapting to them, so the process can slow down one week and accelerate the next. The key is the big picture—the trend over months and years. KEY INSIGHT

The Aging Syndrome view of prevention is not about preventing the disease; it’s about slowing the disease process. Acceleration happens when negative root causes continue to interact. This is when age becomes a factor because the longer root causes favor acceleration, the stronger the interactions, the more rapid the depletion of reserve capacity, and the greater the acceleration of disease processes. On the other hand, deceleration can happen with good self-managing. The more root causes we modify in a positive direction, the greater the deceleration. Some effects can even be reversed. People with type 2 diabetes have seen their disease “disappear” after several months of exercise and weight loss. And, there are instances of atherosclerosis regressing following aggressive lifestyle changes. With chronic disease processes, the longer you wait to do something (i.e., wait for a diagnosis), the less control you have. Think of the people you’ve known who didn’t get serious about making any changes until they had a heart attack or suffered complications from diabetes. At that point,

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A New Way of Thinking about Chronic Disease         

Chronic disease is a process rather than an event. The process begins long before a diagnosis is ever made. Disease processes may be labeled with different diagnoses along the way. Chronic diseases have multiple, interacting causes called root causes. Root causes lead to three key abnormal conditions called megacauses. Megacauses accelerate disease processes. We can’t prevent disease, but we can slow down or even reverse disease processes. When root causes are improved, disease processes slow down. Waiting for a diagnosis results in missing the best chance to change the process.

Rules for Our New Way of Thinking about Chronic Disease   1. Think “chronic disease process” instead of “chronic disease.”   2. Think “aging of disease processes” instead of “diseases of aging.”   3. Accept that these processes are going on right now.   4. Keep the focus on the process rather than any diagnosis along the way.   5. Learn about the megacauses—where disease processes accelerate.   6. Don’t wait for a diagnosis—the longer you wait, the less you control behaviors and exposures.   7. Root causes determine the course.   8. Assume the process will accelerate if you ignore the root causes.   9. Disease processes are constantly changing—the trend is the key. 10. Monitor the trend by tracking signs, symptoms, outcomes, and behaviors. 11. Prioritize root causes by their impact and what you can do about them. 12. Develop a plan that includes small changes in every root cause that needs changing. 13. Use the Personal Plan presented in Part III to improve how you think about every root cause in your life.

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disease processes were well advanced and the Aging Syndrome had won. KEY INSIGHT

The earlier you do something about a disease process, the less damage you will suffer later. Thinking of chronic disease as a lifelong process helps us see that it results from the slow but steady accumulation of adaptations to root cause behaviors and exposures. It explains how disease processes begin slowly, lead into megacauses, and then accelerate toward diagnoses. It takes the mystery out of the “Why me, why

now?” question. It reduces the shock of the diagnosis and the stigma that goes with it. It shows us that diagnoses do not have to be life-changing events, but they do have to be lifestyle-changing events. And, most important, this viewpoint gives us a strategy to slow the process and reduce the impact of chronic disease in our life. If everyone—patients, doctors, insurers—accepted the “process,” the diagnosis would not be the defining issue, the explanation would be easier, and the treatment plan would be clearer. More responsibility would be placed on patients earlier in the process, less emphasis on medical care, and health care costs would be reduced. That would be good news for all of us.

Our new mindset The effects of developing chronic disease processes are often confused with “aging.” These processes are the major driver of the Aging Syndrome, but they are under our control. That’s good news because we can slow them down by self-managing our root causes. But we can’t wait for a diagnosis. Harmful root cause behaviors and exposures can cause a lot of damage before we are ever diagnosed with anything.

CHAPTER

10 The Beginning of Disease Processes Root Causes of the Aging Syndrome Every human being is the author of his own health or disease. —Buddha

You should now have a pretty good idea why we need to think in terms of a lifelong process, not only for chronic disease but also for growing old. Our health care system and our current thinking about chronic disease actually hasten the process of growing old by ignoring the period leading up to life-changing diagnoses. We are coaxed into complacency at a time when we should be getting serious about our lifestyle. In Chapter 9, we put the bull’s eye squarely on our root cause behaviors and exposures as our biggest challenge in slowing disease processes and the Aging Syndrome. In this chapter, we’ll describe how adaptations to these factors lead to inevitable declines in function and capacity—in other words, aging. We’re familiar with the ten primary root causes, but we underestimate the effects of most of them and certainly the power of the interactions among them. It is the total picture of these behaviors and exposures that accelerates the pathological processes that we call megacauses. Megacauses are the intermediate phase of most chronic disease processes, the link between root causes and diagnoses. They allow us to judge the rate at which the process is developing. In this chapter, we will look at

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how the process begins with adaptations to our thoughts, actions, and exposures. These effects are vital to understand because they lead to constricted arteries, disrupted metabolism, inflammation, and the erosion of the reserve capacity of every system in our body. At the end of the chapter you should have a much greater appreciation for why changing our root causes is the only way to change how we grow old.

Why Don’t We Pay More Attention to These Root Causes? If these issues really are that important, why don’t doctors discuss them more? Why don’t they push us harder to change? The sad reality is that our doctors’ hands are tied by a health care system that is based on diagnostic codes. Root cause behaviors and exposures are not diagnoses that can be coded, even though they initiate processes that lead to our most serious, and costly, health problems. This is another aspect of the diagnosis delusion—misuse of the power of diagnoses. The treatment of root causes is seldom reimbursed, and then only if associated with a serious diagnosis, such as exercise rehabilitation after a heart attack or weight loss after an obesity-related disease is diagnosed. Smoking cessation is the lone exception, with fairly wide coverage owing to the overwhelming evidence of its cost effectiveness for insurers. The bottom line is that root cause changes remain largely ignored by our health care system as

they push disease processes toward serious diagnoses. Even obesity has only recently been recognized as a diagnosis by insurance companies. However, the root causes that lead to obesity (poor eating habits and inactivity) remain largely ignored by the insurance and pharmaceutical industries—except for an occasional token public service announcement that is more about marketing the company than truly promoting the lifestyle change. Here’s the kicker: If the cause is genetic, it will almost surely have a diagnosis and reimbursable treatment, even if it is a relatively unimportant contributor to the disease process. Such is the case with several genetic cholesterol disorders.

Another Case of Mistaken Assumptions We hear a lot about some root causes, like getting more exercise, eating right, and losing weight. In fact, we probably hear too much. It’s the same as with “aging.” The overwhelming amount of advice and information ends up having the opposite of the intended effect—confusion from mixed messages and cynicism over what really is true. A lot of people are out there trying to make a buck on the promise of change. We don’t know what to believe. Some of it is at best misleading, at worst fraudulent. It all contributes to a state of confusion and a recurring theme—mistaken assump-

Chapter 10: The Beginning of Disease Processes 

Bad assumptions (diet is the answer) Incorrect beliefs (need to find the right diet) Repeated diets fail Discouragement grows Hope and confidence diminish Give up trying Megacauses worsen/ disease processes accelerate Figure 10.1  T he Cycle of Mistaken Assumptions.

tions leading to incorrect beliefs that keep us from making positive changes. The case of weight loss is a great example: Mistaken

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assumptions lead us to believe that diet is the answer, so we try a diet plan that sounds good; it doesn’t work, we try another, and it doesn’t work; we think it’s our fault, and we give up trying to lose weight (Figure 10.1).

A New Way of Thinking about Root Causes Root cause behaviors and exposures are responsible for most of the conditions we attribute to “getting old.” They are an issue long before we realize it because our reserve capacity masks them. Think about the last time you did something really strenuous. Was it more difficult than you anticipated? If so, why do you think it was? It is mostly because of adaptations to disuse that have gradually reduced your capacity so that everything seems a little harder than it used to. Improving root causes is not about living longer; it’s about living better—having

Some Mistaken Assumptions 1. Root causes are not an important issue until I have a problem because of them. 2. Root causes are overrated—exaggerated by people selling programs or products. 3. Changing root cause behaviors is very difficult and takes the fun out of life. 4. I’m already doing enough; these issues are not a problem for me. 5. I’m different, I’m healthy; I don’t have to worry about chronic disease. 6. My parents lived to 80 and didn’t give a hoot about any of this, so why should I? 7. The older I get, the less important it is to change anything. 8. I’ve got plenty of reserve capacity. If I can’t do something, I must be too old to do it anyway.

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the energy and vitality to do more of what we enjoy and to be able to do it longer. Positive root cause behaviors become increasingly important as we get older because of the gradual decline in reserve capacity due to aging. This loss of capacity is inevitable, and it reduces what we have left to compensate for negative adaptations to our daily way of life. Changing negative behaviors and exposures into positive ones preserves our reserves, and strengthens our ability to withstand all kinds of challenges. We cannot ignore any root cause, even though some are more important than others. The power comes from a collective lifestyle, rather than individual factors. KEY INSIGHT

The combination of positive root causes offers the best opportunity to slow disease processes and the Aging Syndrome. Genes may not play as big a role as we think, but they do influence our response to every other root cause as well as every megacause and disease process. Some genes help, some harm. One person can smoke throughout his or her entire life (recall Jeanne Calment, the oldest person on record) and not get lung cancer, while another person can quit smoking early and still develop cancer. Unfortunately, we don’t know which will be the case for us. We cannot make assumptions about the impact of any root cause in our life.

As our life circumstances change, the influence of our root causes may change. Some may become bigger, others less significant. They’re not equal in their impact on our life or our ability to change them. These two factors, impact and ability to change, are the key issues in prioritizing desired changes. Setting priorities doesn’t mean ignoring lower priorities, but rather making simpler changes to address lower priorities. At the core is our mindset about each root cause. If we don’t believe that a particular change is important, then we’re not going to do it. But, if a positive change becomes part of our usual routine—something we do without thinking or planning—then we’ll do it, and keep doing it. KEY INSIGHT

The best way to prevent a chronic disease process from ever reaching a major diagnosis or a serious related event (e.g., heart attack) is to modify every root cause that needs to be modified, and to do it sooner rather than later.

Rating the Root Causes It’s not possible to produce a completely objective and precise rating system for any individual’s root causes. However, by using the two factors we just mentioned— impact and ability to change—we can provide a general rating that can help you assess your own behaviors and exposures.

Chapter 10: The Beginning of Disease Processes 

Table 10.1  Real Causes of Death Cause

Number (%)

Tobacco smoking

467,000 (19.5)

High blood pressure

395,000 (16.5)

Poor diet*

341,000 (14.2)

Overweight and obesity

216,000 (9.0)

Physical inactivity

191,000 (8.0)

High blood glucose

190,000 (7.9)

High LDL cholesterol

113,000 (4.7)

Excessive alcohol consumption

64,000 (2.8)

*Includes diets high in sodium, trans fats, or saturated fats, or diets low in omega-3 fatty acids, fruits and vegetables, or polyunsaturated fatty acids. Source: G. Danzaei et al. “The preventable causes of death in the United States: Comparative risk assessment of dietary, lifestyle and metabolic risk factors.” PLoS Medicine, 2009.

This requires that you honestly and objectively assess each factor in your life. Rating Impact What would be the best measure of the impact of a root cause on the Aging Syndrome? Clearly, a root cause’s contribution to death is one factor. Table 10.1 provides estimates for some root causes. It shows that four root causes—physical inactivity, poor nutrition, tobacco use, and excessive alcohol consumption—are responsible for nearly half of all deaths and, if you include the megacause-related conditions

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(high blood pressure, obesity, high blood sugar, and high cholesterol), the percentage climbs to more than 80%. You can see the challenge in pinpointing the contribution of a specific root cause. All of the root causes contribute to the megacauses, and they interact with one another. Most of us would probably agree that quality of life is at least as important as length of life. The burden of chronic disease lasts a long time and, at advanced stages, can severely impair the enjoyment of life. Most of us will not suffer serious impairments, but many of us will have disease-related problems that undermine our quality of life. Unfortunately, we don’t have a good way to measure this impact. Hospital admissions, hospital days, absenteeism, dollars spent on health care, and self-reported health status have all been used, but all have limitations. There is plenty of research on the relationships between root causes and various health impacts, but it provides only a snapshot through a fairly cloudy lens because root cause behaviors and exposures never exist in isolation. It becomes very difficult to assess specific contributions. And, we don’t have good ways to measure the impact of some root causes, such as mental disuse, stress, negative attitude, environmental exposures, and long-term medication use. In the end, we have used the available evidence to develop an estimate of the relative impact on the Aging Syndrome.

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Rating Ability to Change The second factor in ranking root causes is how easily they can be changed. It doesn’t make much sense to spend a lot of time on things you can’t change. In rating “changeability,” we give the greatest weight to what you can do for yourself and less weight to changes that you have less control over, such as certain environmental exposures. Again, there is no objective measure of changeability. It comes down to each person’s perception of his or her ability to change each root cause. If we feel strongly that the benefits of the change outweigh the difficulties, then we will rate changeability higher. This is the key to success in self-managing—identify-

ing small changes that are important to us and that we are confident we can accomplish. We don’t ignore the benefits of more difficult changes; we just don’t start with them. We build confidence first by focusing on things we know we can do. Using the typical A–F grading system, Table 10.2 has our general rating for the ten primary root causes. The ratings in Table 10.2 can help you assess your own priorities, knowing that your particular ratings may be somewhat different. For example, if you smoke, then quitting is clearly your highest priority. We do not even consider smoking as a root cause because so few health-conscious people continue to smoke. People who still smoke need to put all of their energy into quitting. If

Rules for Root Causes 1. Accept that all of the root causes are important. 2. Evaluate your root causes objectively (we’ll help you in Part III). 3. Prioritize your needs by their impact on your health and your ability to change them. 4. Target initial efforts on changes with the greatest impact that are easiest to change. 5. Attempt smaller, simpler changes for lower-priority needs. 6. Try to do something positive for all root causes to take advantage of the power of interactions. 7. Re-evaluate and re-focus regularly; root causes change (e.g., stress of a job loss or separation) and needs within each root cause change (e.g., more resistance exercise and stretching with increasing age). 8. Prioritize, plan, practice, perform, and persist—use the Personal Plan presented in Part III as your guide.

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Table 10.2  Root Cause Ratings Impact on Syndrome

Changeability

  1.  Physical disuse

A

A

A

Easily number one, determines quality of life

  2.  Mental disuse

B

A

A

A solid second, overlooked by most

  3.  Poor diet

B

B

B

Vital but a source of great confusion

 4. Stress

C

B

B

Affects both biology and behaviors

  5. Negative attitude and emotions

C

B

B

Growing evidence but still underrated

  6. Excessive alcohol

C

A

B

Can help a little but also do great harm

  7. Secondhand smoke

C

B

C

Less common, but underrated when exposed

  8. Environmental exposures

C

C

C

Increasingly important in ways we don’t anticipate

  9. Medications and herbs

C

C

C

Increased use may create unforeseen challenges

10. Genes

D

F

D

Affects everything, but we still don’t know how much

Root Cause

excessive alcohol consumption is a chronic issue, then it probably takes precedence as well. For most of us, however, the ratings will ring pretty true.

Overall Rating

Comment

A high quality of life 10, 20, 30, or 40 years from now won’t just happen. It’s not a matter of luck and genes, as some of us would like to think. It’s the outcome of

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of these root causes. Taking care of them is the best way to manage how you are going to age. In Chapter 11, we’ll begin to examine the megacauses. These are more complex

processes, but we’ll keep the discussion as simple as possible. Having some understanding of these critical processes in your body will make you appreciate the root causes even more.

Our new mindset Root cause behaviors and exposures are our focus. If we ignore them, there will be consequences—worsening megacauses. If we focus on only one or two, we’ll miss out on their collective power. Adaptations become stronger when they are reinforced in different ways. If we can have a positive influence on each root cause, we will be doing the best we can to combat the Aging Syndrome.

CHAPTER

11 Acceleration of Disease Processes Megacauses of the Aging Syndrome If people are constantly falling off a cliff, you could place ambulances under the cliff or build a fence on the top of the cliff. We are placing all too many ambulances under the cliff. —Irish physician Denis Burkitt

Let’s look ahead for a moment to age 70—it will be here sooner than you think. If you are like most, you will have several diagnosed conditions and will be taking at least as many different prescription medicines. And, the doctor could probably rattle off a dozen or so additional diagnoses that are quite possible over the next 10 years. We know that such diagnoses do not serve us well. They occur late in the disease process and foster a continuing dependence on medications and the medical care system. We saw it happen to our parents and grandparents, but we don’t anticipate it happening to us. But it will—unless we become more mindful of the process that leads up to these diagnoses. Welcome to the “black hole” in our traditional thinking about chronic disease—the crucial period between changing root causes and diagnoses. We feel fine, life is busy, and we take our health for granted. However, subtle changes are occurring below the surface as a result of our behaviors and exposures. We’re not aware of them, and our doctors don’t seem to be concerned with them. These changes 113

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are the domain of prevention in our health care system—a low priority for an insurance industry that focuses on short-term risk, controlling payouts to sustain annual profits. The health care system is not overly concerned with distant health problems. The chances are that someone else, probably Medicare, will be paying those bills. The result is a disregard for developing disease prior to the diagnosis and an epidemic of advanced diseases (diagnoses) later in life that gets attributed to aging. The longer we wait, the more expensive these conditions are to manage—more dependence on medical care, more medications, more adverse effects to deal with, more tests, more doctors to see, more doctor visits, and so on. The treatment of chronic disease eats up 75% of our health care costs. It’s no wonder that Medicare is in crisis. If we dealt with disease processes before the diagnosis, we could reduce costs and control the Aging Syndrome at the same time. So, what’s happening during this “black hole” in the process? Subtle adaptations to root causes are converging into three conditions that accelerate disease processes. We call these conditions megacauses because they really are the biggest causes of advanced disease and getting old. These three megacauses are: 1. Constricted circulation Changes in our blood vessels that gradually impede the flow of blood to every

cell in our body; it is mainly due to the buildup of plaque inside arteries (atherosclerosis) and the stiffening of artery walls (increasing blood pressure).

2. Metabolic madness  Problems with how our body converts food into energy; it is mainly due to fat accumulation, especially around the belly, and resistance to insulin in muscle cells that are not used enough.

3. Insidious inflammation  A persistent, low-level inflammatory response that occurs in tissues all over the body; it is our body’s response to any abnormal substance or minor injury—the problem is that it continues as long as the stimulus is present. Constricted circulation is the most important megacause because every cell depends on healthy circulation to receive oxygen and nutrients and to eliminate carbon dioxide and waste products. When blood vessels are constricted, cells cannot function optimally. And, both metabolic madness and inflammation also affect the circulation. Metabolic madness is rapidly becoming a powerful force in the Aging Syndrome as obesity and diabetes become more and more common. Poor control of blood sugar is especially damaging to the smallest blood vessels, the capillaries. Insidious inflammation is the newest megacause, at least in terms of its recogni-

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» Drug therapy is fairly ineffective,

Constricted Circulation

except for isolated parts (e.g., hypertension).

» The risk of disease increases as the megacause progresses.

Insidious Inflammation

Metabolic Madness

Figure 11.1  Megacause Interactions.

» The “safe” lower limit keeps getting

lower the more we learn about them.

» Genes play an important role in how they develop and the diagnoses that result.

» Root causes affect the expression of tion. It plays a key role in the beginning of most disease processes, especially atherosclerosis.

The Making of a Megacause You may be wondering, “What makes a megacause a megacause?” All the megacauses are abnormal conditions that meet four criteria: 1. Are extremely common; affect virtually everyone 2. Affect many disease processes, including nearly every body system 3. Are responsible for substantial disability and death 4. Have a reasonably well-defined process of beginning and progressing The megacauses have a few other important characteristics in common as well:

» They are affected by most root causes.

genes involved in their development.

KEY INSIGHT

Megacauses are remarkably sensitive to root cause changes. Megacause conditions improve as root causes are improved; they get worse when root causes are ignored.

Constricted circulation, metabolic madness, and chronic inflammation are the only conditions that clearly meet all these criteria. Not only do they account for a substantial portion of the disease, disability, and death that we will experience as we get older, but they account for most of it. Why don’t we hear more about them? There are three reasons: 1. Complexity—All three are complicated processes. There is still a lot we don’t understand about each of them.

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New Way of Thinking about the Black Hole of Chronic Disease 1. Thinking in terms of “the diseases of aging” obscures the megacauses. 2. Thinking in terms of “the aging of diseases” places the focus on the megacauses. 3. Megacause conditions are the inevitable result of ignored root causes. 4. Megacause conditions are developing in children because poor root cause behaviors are occurring at young ages. 5. Chronic disease diagnoses confirm that megacauses have been ignored for years. 6. A diagnosis is often the tip of the iceberg. 7. Megacauses affect all disease processes; other diagnoses may be just below the surface.

2. System of medical care—As discussed, our health care system is built on diagnoses and heavily influenced by the insurance and pharmaceutical industries. These industries don’t get involved until a problem is diagnosed. No one is in our doctor’s ear pushing changes in our lifestyle and new ways of thinking before the diagnosis, the way pharmaceutical reps are pushing the latest drugs after the diagnosis. When we go in for a checkup, most doctors will tell us we should try to get more exercise and lose some weight, but that’s about it. They don’t have the time or incentives to explain why or to help us change our habits. And they certainly do not address the full range of healthy habits or how we think about any of them. Most

doctors are pessimistic about people’s ability or desire to change anyway. So, everyone waits for the diagnosis to begin addressing the problem. 3. Thinking and expectations—We have all come to accept minor changes in our body as we get older—the increase in blood pressure, weight gain, weakness, stiffness, lack of energy—as “normal aging.” In reality, they are indications of problems with the megacauses. We can’t see or feel atherosclerosis, stiffening arteries, chronic inflammation, or insulin resistance, so we don’t think of them as contributing to these problems. Megacauses are easily ignored, but ignoring them means missing your best chance to control the Aging Syndrome, to

Chapter 11: Acceleration of Disease Processes 

Health Care System (diagnosis delusion)

Ignore Megacauses Complexity (how and why they develop)

Beliefs and Expectations (part of “aging”)

Figure11.2:  Why We Ignore Megacauses (triangle of complexity, system, expectations).

be as young as you can be, and to prevent chronic disease diagnoses and the stream of prescriptions that follow.

Dealing with Complexity We said that understanding the megacauses will simplify chronic disease for us. How can that be when they are such complex processes themselves? They are complicated when we look at the biochemical processes involved, but we don’t have to be concerned with biochemistry. In fact, we’re better off not being concerned with it. Complexity opens the door to charlatans who use fragments of research to develop theories and propose quick and easy solutions. The more complex, the easier it is to offer a “new” answer. And, the easier it is for us to believe that the answer is real. Consider the variety of diet plans that are presented as breakthroughs for weight loss or cures for a particular chronic disease. Or, con-

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sider the variety of “anti-aging” supplements that “science” has shown can make us younger. There are shreds of truth in all of them, but they are mostly based on extrapolations from research that is far from conclusive—and ultimately they are not that effective. Thinking in terms of the megacauses reduces the clutter of multiple diseases and diagnoses that occur as we age. By focusing on the three megacauses, we can improve most disease processes. All we really need to know about them is how they accelerate disease processes and how they respond to root cause behaviors and exposures. That’s it. These three processes ultimately make us old and diseased. And, they show us why changing our root causes is the only way to slow down “growing old.” KEY INSIGHT

By focusing on the three megacauses, we can improve most disease processes. Focusing on the megacauses is an effective way to think about chronic disease for three reasons: 1. Helps us see chronic disease as a lifelong process

2. Shifts attention away from diagnoses, so we escape the diagnosis delusion 3. Focuses attention on the root causes, the only way to improve the intermediate stage of disease

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Mistaken Assumptions

Facts

Everything about our body gets worse with age because of aging.

Just about everything about our body gets worse when root causes are ignored.

A little rise in blood pressure, cholesterol, or blood sugar or a little weight gain is no big deal.

These changes are a big deal because they indicate an acceleration of the megacauses.

If I’m still within the normal range, I’m fine. After all, my doctor says I don’t need medication yet.

“Normal” is very different from optimal. The optimal levels of blood pressure, blood sugar, and bad cholesterol keep getting lower as research shows that any increase above optimal increases the associated risks. But medication isn’t helpful at this stage of disease; it is for more advanced disease. A prescription means you’ve waited too long.

If I feel fine, the megacauses are not an issue.

Reserve capacity hides the early effects of root causes on megacauses. The “cost” is the erosion of the reserve capacity, which makes us more susceptible to illness, injury, and disease processes. Then we start feeling “not so fine.”

KEY INSIGHT

Take care of the root causes and you take care of the megacauses; take care of the megacauses and you defeat the Aging Syndrome.

From Root Causes to Megacauses Every root cause behavior or exposure exists on a continuum from negative to positive for every one of us. Our set of root causes is the life we have grown into;

it is the life we defend (if people try to tell us we need to change) and the life we adapt to. We control our position on the continuum of negative to positive for every root cause, with the possible exception of genes (although we have more power than we think over how our genes are expressed). The combination of all of our root causes determines the trend of our megacauses. Some behaviors or exposures obviously have a greater impact than others, but they all contribute. What may seem like a minor role for one root cause

Chapter 11: Acceleration of Disease Processes 

can compound the effects of others. The more that root causes go unchecked, the greater their cumulative impact. How do you know when your megacauses are getting worse? The first sign is often a change in body composition—an increase in fat and a decrease in muscle. This aggravates all three conditions and initiates interactions among them. Other subtle signs follow—declining energy, accumulation of fat around the middle, a little more difficulty climbing a few flights of stairs, a little more stiffness, and a slight rise in blood pressure, bad cholesterol, triglycerides, blood sugar, or inflammatory markers; all are essentially negative adaptations to root causes.

The Age Effect The aging of disease processes that occurs with time is largely about the developing megacauses—atherosclerosis (plaque deposits on artery walls) develops, blood pressure increases, inflammation becomes more widespread, the ratio of fat to muscle increases, resistance to insulin builds, and the control of blood sugar deteriorates. We associate all these conditions with age because they get worse with older age, but age is really just the length of time over which the adaptations to negative root causes have occurred. Interactions become more complex as more coexisting disease processes reach advanced stages.

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As we get older we tend to get more set in our thoughts, behaviors and exposures. At the heart of it is the “master” root cause, physical disuse. The decline in strength and energy saps our motivation to manage the other root causes. Old and new injuries become bigger challenges with increasing age. All of the root causes remain important, but the influence of some increases with age. Medications often take on a bigger role because we’re taking more of them. Environmental exposures tend to become more significant because of the accumulating impact of years of exposure. And, we often become more sensitive to toxins, alcohol, medications, and certain foods, and less efficient at detoxifying and digesting.

Bottom Line Megacause conditions are happening inside you right now, whether or not you’ve paid any attention to them, have any diagnoses related to them, or have ever been tested for any of them. They are a “black hole” because we can’t see how they are impairing our organs and body systems, eroding our reserve capacity, and accelerating our chronic disease processes. In the next three chapters we’ll take a closer look at each megacause. Keep the big picture in mind: These are the conditions that lead to disease damage and gradually make us old—the conditions we target when we manage our root causes.

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Our new mindset If we keep in mind how the megacauses develop, we can see how important it is to become vigilant in managing our root causes as we get older. This is how we control all three processes at the same time. The challenge is to take charge before diagnoses are made and prescriptions written, before we get swallowed up by the medical care system and lose control of our health future. This is the time when disease processes are still responsive to simple and safe interventions—the things we can do for ourselves.

CHAPTER

12 Constricted Circulation The Great Accelerator of the Aging Syndrome A man is as old as his arteries. —Thomas Sydenham, English physician (1624–1689)

How old do you think your arteries really are? It’s a legitimate question. Remember when we talked about biological or real age versus chronological age. Biological age actually turns out to be an estimate of the status of the Aging Syndrome, and it applies to our arteries more than anything else. There can be a big difference between your age and the “age” of your arteries. A healthy and fit 70-yearold can have the arteries of a healthy 40-year-old, or an unhealthy 40-year-old can have the arteries of a typical 70-year-old. Constricted circulation is about the “real age” of your arteries. Constricted circulation is the most important megacause because healthy blood circulation is the best defense against every disease process. We all know what happens when blood flow stops—cells die and tissues are damaged. But, we overlook what happens when the flow of blood is merely reduced. Every organ and body system suffers. Individual cells are starved for oxygen and nutrients. They struggle to produce energy. We have less stamina, especially when more effort is needed. Injuries heal more slowly. Two processes form the core of constricted circulation: atherosclerosis, the buildup of plaque, and hypertension, the increase in pressure 121

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inside arteries. The degree of constriction is mostly a function of the extent of these two processes, and our energy level is actually a reasonable indicator of just how constricted our circulation is. KEY INSIGHT

Most chronic diseases that we experience as we grow older involve a problem with constricted circulation.

Structure and Function of Arteries Our first task is to get a better understanding of our circulatory system, particularly the arteries that carry blood from our heart to every cell in our body. Blood is pumped out of the heart through the aorta, our largest artery, which is about the size of your thumb. The aorta divides into a few major branches that successively branch into smaller and smaller vessels that reach every part of the body. This network of arteries eventually reaches the smallest arteries, called arterioles, which feed the capillary beds of every organ and tissue. Capillaries are a single cell thick, or about 1/100 millimeter in diameter. This is where oxygen and carbon dioxide are exchanged, and where nutrients are delivered and wastes removed. Capillaries drain into venules, beginning the network of veins that returns blood to the heart. Our concern in constricted circulation is the arteries and capillaries.

Artery walls have three layers:

» Inner layer—A thin layer of flat cells that is in direct contact with the blood. This layer of cells is called the endothelium, and the cells are called endothelial cells.

» Middle layer—A combination of

muscle and elastic fibers. This layer contracts and relaxes like any muscle. When it contracts, it constricts the artery, reducing blood flow. When it relaxes, the artery expands and blood flow increases.

» Outer layer—Mostly connective

tissue that protects the vessel and anchors it to surrounding tissues.

The larger arteries nearer the heart have a middle layer that is mostly elastic fibers. These arteries stretch with each beat of the heart, then recoil between beats. This process evens out the pressure and keeps blood flowing smoothly. As arteries get farther from the heart, the middle layer gradually becomes more muscular and less elastic. By the time arteries are about the size of your little finger, the middle layer is mostly muscle. This muscular middle layer determines the blood flow and pressure in the artery by how contracted or relaxed it is. This is controlled by the nervous system along with substances in the blood that interact with the endothelial cells that line the artery.

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The Big Job of Circulating Blood The amount of blood in our body depends on our size. A medium-sized man (150 pounds) has 5 to 5.5 quarts of blood, a 200-pound man nearly 7 quarts. On the other hand, a 110-pound woman has only about 3.5 quarts. Blood circulates continuously through 60,000-plus miles of blood vessels, the result of about 100,000 contractions of the heart every day. About two-thirds of our blood is in our veins and venules at rest; they act as a storage reservoir for when more blood is needed. About 10 trillion endothelial cells (enough to cover more than an acre if laid flat) line our blood vessels and control the state of these vessels.

We will soon see that the endothelium is the key to constricted circulation. When arteries reach the size of a pencil lead, they are considered arterioles. They still have three layers, and the middle layer is still mostly muscle. But, as they get closer and closer to their target tissues, they lose the middle and outer layers and become just a layer of endothelial cells with a few muscle fibers. These tiniest arterioles largely determine blood pressure. In relative terms, they have the greatest dilation potential, expanding to three times their usual size when their muscle fibers relax. Dilation dramatically increases blood flow and reduces pressure. Arterioles connect to a microscopic bed of capillaries that infuse tissues and connect to venules, the beginning of the system of veins that carries blood back to the heart. The walls of capillaries contain just a single layer of endothelial cells with a membrane, so substances can pass easily through

them. Most tissues, especially muscle, contain excess capillaries, which allow more blood to be delivered.

An Old Artery Versus a Young Artery In a “young” artery, the inner surface of the endothelium is smooth. Blood moves smoothly through it even as flow increases. The artery dilates as flow increases. The endothelial lining is fragile, however, so it is easily injured. When this happens, an inflammatory response occurs as part of the healing process. Plaque forms over the injury to protect it from further damage. In young arteries, the injury heals, the inflammation stops, and the endothelium returns to normal functioning. The artery retains its ability to dilate when the demand for blood increases. In “old” arteries, the surface of the endothelium is repeatedly injured by high blood pressure and abnormal substances

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in the blood. It remains chronically inflamed and becomes rough and uneven, causing blood to flow more turbulently. Plaque development becomes ongoing. Artery walls get thicker and stiffer, and the opening for blood flow shrinks. Pressure must increase to maintain the flow.

The Key Role of the Endothelium Constricted circulation begins in the endothelium, the thin single-cell lining of all arteries. This layer of cells is like the circuit board of the body. It is constantly “reading” the blood and responding to changes in temperature, pressure, flow, pH, hormones, and a long list of other substances in the blood, both normal and abnormal. The endothelium plays a vital role in maintaining a healthy, functioning artery. One of its most important functions is controlling the tone of the artery wall. The endothelium produces molecules that cause the muscular layer of the vessel wall to either

contract or relax. The usual tone of this layer is slightly contracted to maintain blood pressure because too great a drop in pressure can be life threatening. But if the endothelium is not working properly, the vessel wall will not dilate sufficiently. The result is a gradual stiffening of the vessel—a hallmark of aging. This was once thought to be the result of inevitable structural changes, especially plaque buildup and connective tissue infiltration. But then researchers began to notice that some normal-appearing arteries were also not dilating properly. This led to the observation that constricted arteries had one thing in common: reduced production of a substance called nitric oxide.

Nitric Oxide— The Key to Vessel Health For decades nitric oxide was ignored, thought to be just another ubiquitous byproduct of metabolism—until it was found to play the key role in male sexual performance (erections). The pharmaceu-

Vital Functions of the Endothelium      

Repairing damage to the blood vessel wall Forming and dissolving clots Managing the immune response to pathogens, infections, injuries, and so on Controlling the tone of arteries and arterioles (i.e., constriction or dilation) Controlling the viscosity (thickness) of the blood Maintaining the permeability of the vessel wall to substances in the blood

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tical companies quickly jumped in to use the new findings to develop drugs to treat erectile difficulties. Needless to say, we’re all too familiar with the products of this research. Research has now clearly established the vital role of nitric oxide in maintaining blood vessel health. It is the most important dilator produced by the endothelium and hence the key to maintaining vessel elasticity and keeping blood vessels young. Endothelial cells have receptors that sense the stress of blood flow against the artery wall. When this stress increases, nitric oxide is released and the artery wall relaxes. This allows the flow of blood to increase and the stress against the wall to decrease. This is a vital function of nitric oxide, but nitric oxide does a lot more. It dampens inflammation, inhibits plaque development, and reduces clot formation. And, it helps reduce the abnormal thickening of the vessel wall. We want our blood vessels to be producing an optimal amount of nitric oxide all the time. It’s possible to have too much, but that’s very unusual.

When the Endothelium Is Not Working Properly The endothelium is highly vulnerable to “short-circuiting.” This happens when normal functions, such as inflammation, clot formation, membrane permeability, and the immune response, become chron-

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ically stimulated and don’t turn off. The result is a decline in nitric oxide production. When this happens, vessels stiffen and pressure increases. Reduced levels of nitric oxide  have been associated with a long list of conditions, including atherosclerosis, cholesterol problems, diabetes, hypertension, smoking, oxidative stress, and, of course, “aging.” KEY INSIGHT

Endothelial dysfunction is a hallmark of the Aging Syndrome. Most root causes affect endothelial cell function, especially the production of nitric oxide. So, what causes the endothelium to stop producing nitric oxide? In healthy “young” arteries, when blood flow increases, the pattern of flow remains the same, just faster. The stress against the wall increases directly with the increase in blood flow. This triggers nitric oxide to be produced, and the vessel opens up. On the other hand, in “older” vessel walls that are damaged and scarred by the chronic effects of root causes, inflammation, high blood pressure, and plaque buildup. The surface becomes uneven and irregular, and blood flow becomes more turbulent. When flow increases, the stress against the wall becomes even more abnormal. The result is that the endothelium does not function normally. Less nitric oxide is produced because the vessel wall is not

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stimulated normally. Inflammation persists, clots are more likely to form, and substances that usually pass through the vessel wall cannot get through any more.

Development of Constricted Circulation For large and mid-sized arteries, constricted circulation results mainly from the buildup of plaque and the loss of elastic fibers in the middle layer. For small arteries and arterioles, constricted circulation has more to do with the endothelium, especially a reduction in nitric oxide production. In capillaries (the tiniest, most fragile arteries), the damage is mostly due to high blood pressure and high blood sugar, as seen in the complications of long-term diabetes. The process of damage is different, but the end result is the same—diminished blood flow due to impaired circulation.

The Age Effect We’ve long known that arteries get stiffer with increasing age. The walls gradually accumulate calcium and collagen and lose elastic fibers. The endothelium works less efficiently, and less nitric oxide is produced. Even in healthy men who have no major risk factors, vessel dilation declines by about 0.5% to 1% per year after about age 40 (similar to the decline in reserve capacity). In women, the decline is steeper but begins about a decade later, probably

related to the effects of estrogen. We used to think that arterial stiffness was due to aging. That was the easy answer. We now know that there is an aging effect, but no aging factor has been shown to initiate or accelerate constricted circulation. The “missing link” is still missing. Age-related constriction of arteries is more closely related to the aging of the disease process in blood vessels than to aging itself. The same effects are seen in younger folks who have cardiovascular disease, in direct relation to the extent of the disease. In the end, the age effect is more about longterm effects of root causes on disease processes than anything else. Age, as usual, is mainly an estimate of the duration of the disease process.

Atherosclerosis Atherosclerosis is the progressive accumulation of fatty materials (plaque) in the walls of large and medium-sized arteries. Plaque is mostly cholesterol and lipids but also contains fibrous materials and calcium. It hardens as it ages, which stiffens the vessel wall. Plaque is less important in smaller arteries, where endothelial problems and high blood pressure are bigger issues. It’s hard to overestimate the importance of atherosclerosis. Every mediumsized and large artery can develop it, and every tissue can be damaged or destroyed by it. Atherosclerosis is responsible for nearly

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Changes in Blood Vessels As Constricted Circulation Develops          

The surface of the endothelium gets rougher and more irregular. Blood flow becomes more turbulent. The endothelium becomes increasingly impaired; vessels do not dilate efficiently. Muscle in the middle layer stiffens. Vessel walls become stiffer and thicker. The proportions of calcium and collagen in the walls increase. Elastic fibers decrease, especially in larger arteries. Resistance to blood flow increases. The pressure increases, making the heart work harder. The heart becomes enlarged, requires more blood, and does not relax efficiently between beats.

all heart disease and more than half of all deaths in the United States. If you live long enough, you will develop a problem related to atherosclerosis. Even in those who die of “natural” causes or “old age,” the underlying cause is most likely atherosclerosis. The disease label you end up with simply reflects the signs or symptoms that first appeared (i.e., diagnosis delusion once again). Unfortunately, a common presentation of atherosclerosis-related heart disease is a heart attack—often with no warning at all. KEY INSIGHT

We all have some degree of atherosclerosis. It’s just a question of how much. Autopsies of young people who have died from various causes have shown that

virtually every one had some atherosclerosis. You don’t have to have symptoms and you don’t have to have a test to know that you have atherosclerosis. There is nothing more certain in medicine than the fact that everyone has atherosclerosis, at least by early middle age. Size Matters, Especially in Arteries The size of the opening in an artery is the biggest factor that determines the amount of blood that ultimately reaches the target tissues. It’s simple physics: A small reduction in the size of a cylinder has a dramatic effect on the flow of a liquid through it. In the same way, a small narrowing of an artery has a large effect on blood flow. Imagine drinking a glass of water through a quarter-inch straw.

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Then, switch to an eighth-inch straw and suck in with the same force. How much less water do you think you will get? The answer is about one-sixteenth as much. The rate of flow is proportional to the fourth power of the difference in the radius, as long as pressure and length stay the same. The radius of an eighth-inch straw is half that of a quarter-inch straw, so the flow is only one-sixteenth as much (½  ½  ½  ½). But, the process works both ways—switch from an eighth-inch straw to a quarter-inch straw, and you get 16 times as much. Don’t get hung up on the physics—the point to take away from this is that a small reduction in the opening of a blood vessel has a much greater effect than you would think on the flow of blood through it. KEY INSIGHT

Even a slight narrowing of an artery as a result of atherosclerosis can have a large impact on the flow of blood through that artery. According to physics again, as the opening is reduced, the effect on flow is exaggerated. If an artery is 10% blocked, the blood flow is reduced to two-thirds of normal; if an artery is 25% blocked, flow drops to one-third of normal. And, if the vessel is 50% blocked, the flow is cut to only one-sixteenth of normal. Again, the

good news is that the process works both ways. Atherosclerosis is reversible, so if we reduce the plaque by 10%, we can increase blood flow by one-third. You may be wondering how you could survive with only one-sixteenth of the blood getting through. After all, we hear of people with arteries 90% blocked who didn’t even know it. How can that be? The preceding discussion is based on pure physics where everything is constant (pressure, viscosity of the fluid, length of the tube). Fortunately, our body works quite differently. It is constantly changing—in this case, compensating to maintain blood flow in the presence of narrowed vessels. The primary response is an increase in blood pressure to force more blood through the narrowed vessel. A small increase in pressure can offset a small decrease in the opening. This is one reason high blood pressure is so common. We take blood pressure–lowering drugs to help our body compensate, to make our blood thinner so that it flows easier, or to help our blood vessels relax. It would be far better to reverse the process by changing our root causes. The Traditional View of Atherosclerosis In the old view of the cardiovascular system, the heart is a pump, arteries are simple conduits to deliver blood throughout

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Mistaken Assumptions

Facts

Blood vessels are simply a system of tubes that deliver blood around the body.

Blood vessels are dynamic structures that continuously monitor the blood, producing numerous substances that control its functioning.

Heart disease is mainly about the heart.

Most heart disease is about constricted circulation that makes the heart work harder while reducing its own blood supply at the same time.

Atherosclerosis is caused by too much fat in the blood, especially too much cholesterol.

Most victims of heart attacks actually have “normal” cholesterol levels by current standards..

Atherosclerosis clogs arteries until Most heart attacks and strokes are not caused by a it finally causes a heart attack or gradually developing blockage. They usually occur stroke. when a plaque bursts, and a clot forms that abruptly blocks blood flow. The best treatment is to find the area of the artery that is narrowed, open it up, and put a stent in to keep it open.

Atherosclerosis is a systemic condition. There are probably many areas of the artery that contain plaque. The best treatment, if the condition is not too advanced, is an aggressive lifestyle approach, combined with medication as needed.

Atherosclerosis is like sludge building up in a water pipe. It slowly accumulates and, once in place, is there for good.

Atherosclerosis is an inflammatory condition that impairs the functioning of the vessel wall, but it is more reversible than ever thought.

If test results for cholesterol, blood pressure, and blood glucose do not indicate the need for drugs, then they are no problem.

The optimal levels of these and other risk factors have been steadily going down for 20 years. Problems occur at levels far lower than you might think.

Risk factors can predict heart disease risk quite accurately.

Approximately half of all heart attack victims had no established risk factors other than age and gender.

There is no need to worry about atherosclerosis until it causes symptoms or is diagnosed.

We can’t measure atherosclerosis without a risky and costly procedure, but we can accept that it is going on and focus on slowing or reversing it.

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the body, and capillaries are sites for cellular exchange. Atherosclerosis was thought to develop primarily from too much cholesterol in the blood. Cholesterol thickens the blood and leads to deposits building up on artery walls, sort of like sludge in a pipe. The plaque gradually narrows arteries, hardens, and permanently reduces the blood flow. Eventually, plaque may completely block an artery enough to cause symptoms or, worse, a heart attack or stroke. The extent of the obstruction was the key factor in the old view, and cholesterol was the main culprit. This led to the belief that controlling cholesterol was the most important thing to do to prevent heart attacks. This view made sense until researchers began to notice that about half of all heart attacks were occurring in people who had “normal” cholesterol levels, many without any traditional risk factors other than age and gender. Then it was found that in three out of four cases, the plaque that caused the heart attack was not significantly obstructing flow or causing symptoms. There was obviously much more to heart attacks than cholesterol and plaque development.

New Way of Thinking about Atherosclerosis Over the last decade, the focus has turned to the endothelium, with the realization that blood vessel walls are constantly

changing. They are very biologically active, and the process is all orchestrated by endothelial cells interacting with the blood on one side and the middle layer of the vessel wall on the other. This view of atherosclerosis shines the spotlight, not on cholesterol, but on nitric oxide. KEY INSIGHT

Atherosclerosis begins with damage to the endothelium. As mentioned, the endothelial lining of arteries is easily damaged by a number of mechanisms, including high blood pressure and the effects of most of the root causes. Individual endothelial cells have junctions between them that allow substances, such as cholesterol and glucose, to penetrate the interior of the vessel wall. The higher the level of these substances, the more this happens. Bacteria and viruses can also penetrate, causing infections and an inflammatory response to “attack” the intruder. Endothelial cells release substances that make the vessel wall more permeable to facilitate the immune response. White blood cells are attracted to capture the foreign substances. They penetrate the vessel wall and go after substances like oxidized LDL (bad) cholesterol that has already entered (especially if blood cholesterol levels are high). These white blood cells become known as foam cells as they load up on cholesterol and other fatty substances. They produce fatty

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streaks in the artery wall. They also release substances called cytokines that trigger an ongoing inflammatory response in surrounding tissues. As foam cells grow, some break through the lining of the artery. This initiates a clotting reaction: Platelets in the blood are activated and attach to the area. Smooth muscle cells and other types of white blood cells move in to assist. The smooth muscle cells become foam cells too, consuming oxidized fats. The plaque grows as cell debris, cholesterol, and another immune system product, called tissue factor, accumulate. Eventually, a fibrous cap develops around the plaque and becomes part of the artery wall. KEY INSIGHT

Heart attacks and strokes are less about the obstruction and more about the condition of the plaque. The fibrous cap that encompasses deposits of plaque varies. In some cases, it is quite solid and stable. In other situations, it is not so well developed and hence is thinner and more fragile. This fragile type of plaque is a problem because it is more likely to rupture, which causes a blood clot to form. Such clots may continue to grow or break loose and obstruct blood flow somewhere else. In the heart, a clot can cause a heart attack;

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in the brain, a stroke; in the lungs, a pulmonary embolism. This is why so many heart attacks are unsuspected and unrelated to risk factors. KEY INSIGHT

Symptoms of atherosclerosis occur very late in the disease process. A more solid plaque impairs blood flow gradually, so it allows time for compensating mechanisms to occur. It takes a surprising amount of atherosclerosis to cause symptoms. An artery can be blocked by 50% or more and the tissues supplied not yet show signs of insufficient blood supply. This is the result of the compensating adaptations—increased pressure and collateral circulation where new arteries or arterioles develop to meet the demand for more blood flow; there is also excess capacity for blood supply that enables basic needs to be met even when the flow is significantly compromised. However, an increased demand for blood, as in an emergency effort, may spell trouble. Most middle-aged adults have the compensating adaptations working for them. Their plaque is not life threatening, but it is taking a subtle toll. We think we’re “aging” because we don’t have the energy we used to have, when in fact we are suffering from constricted circulation.

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KEY INSIGHT

Cholesterol is overrated as a cause of atherosclerosis. We sometimes obsess about cholesterol because we hear so much about it. But this has more to do with drug advertising than with the relative impact on atherosclerosis or heart disease. There’s no doubt that lowering our level of bad (LDL) cholesterol and increasing our level of good (HDL) cholesterol are good for us. But this is only one piece of the puzzle. A narrow focus on cholesterol can cause us to neglect other factors that are at least as important. Remember that half of all heart attack victims have no problem with cholesterol. Besides that, cholesterol and other lipid problems are first and best treated by addressing lifestyle issues. This is one of the few claims in medicine that is not controversial: No drug can duplicate the benefits of a healthy lifestyle. KEY INSIGHT

Endothelial dysfunction and reduced nitric oxide are underrated as a cause of atherosclerosis. Nitric oxide is a potent vasodilator. It works similarly to nitroglycerine, the medicine that people take to relieve chest pain caused by constricted arteries in the heart. Nitric oxide may be the body’s best defense against atherosclerosis and clot

formation. Most of the root causes of the Aging Syndrome are harmful to endothelial cells over time, which means they impair the ability to produce nitric oxide. The opposite happens when we improve our root causes—a healthier endothelium that produces more nitric oxide. Measuring Atherosclerosis One of the biggest challenges of atherosclerosis is measuring it. The only sure method is to insert a catheter with a viewing device into a blood vessel in the leg or arm, guide it to the artery of choice, inject a contrast dye into the artery, and then observe images of blood flowing through the artery on an X-ray. This procedure detects obstacles and plaque, but it is invasive, costly, and risky. It is used exclusively to diagnose the extent of heart disease and to determine appropriate treatment. Less invasive techniques are being evaluated, but nothing else yet provides a valid measure of atherosclerosis throughout the body. An ultrasound of the carotid arteries in the neck can show atherosclerosis in these arteries, but that is not necessarily indicative of any others. Fortunately, for the Aging Syndrome, we don’t need to measure the extent of our atherosclerosis. Remember that it’s not a question of whether we have it or not. We most certainly do have it. In fact, we would probably be surprised by the extent of it. The important thing is to accept that we have it, know that it can cause serious problems

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before it ever causes symptoms, and do the best we can right now to control it. That means improving every root cause, managing every megacause condition, and taking medications as prescribed by our doctor.

Hypertension Blood pressure is the force of blood against the artery walls. It is highest when the heart contracts (systolic pressure) and lowest when the heart relaxes between beats (diastolic pressure). Traditionally, blood pressure is considered “high” (i.e., hypertension) when the higher pressure is at least 140 millimeters of mercury (mm Hg) or the lower pressure is at least 90 mm Hg. A new category, “pre-hypertension,” is a systolic pressure between 120 and 139 or a diastolic pressure between 80 and 89. This new category stems from reseach showing that the risks of high blood pressure increase long before the diagnostic threshold is reached. This challenges the diagnostic delusion—that we don’t have to worry about our blood pressure until it reaches 140/90. It’s another example of the fallacy of categorizing. Is there a difference between a systolic pressure of 139 and one of 140, or a diastolic pressure of 89 and one of 90? Of course not, but they are different categories. Categories are established mainly for prescribing drugs. Blood pressure drugs are approved for use only with a reading of 140/90 or higher. Interestingly, trials are under way (spon-

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sored by pharmaceutical companies) to establish the efficacy of drug therapy for people who have pre-hypertension even though lifestyle approaches are far more effective at this level, not to mention safer and free. Blood pressure numbers are arbitrary anyway. The only numbers that really count are 110 and 70. That’s the optimal level—risk increases progressively as pressure rises above this level. The higher the level, the greater the risk, but any increase can be damaging to blood vessel walls. Hypertension is unique among the megacause conditions for two reasons: 1. It has been recognized the longest (more than 100 years). 2. We know the least about its mechanism. In fact, we are remarkably ignorant about prioritizing the top five to ten leading contributors to the process. But, hypertension is like the other megacauses in two ways: most of us are going to get it, and lifestyle changes are very effective at reversing it for much of the disease process. The Age Effect One of the most interesting statistics about hypertension is how its incidence increases with age—from about one-third at age 50, to about half by 60, and to twothirds by 70.

18–34

35–44

45–54

55–64

Age

Ages 45–54: men 36%, women 35%

31% 16%

75



4 –7 65

4 –6 55

–5

4

6%

45

10

4

Causes of Hypertension There are times when hypertension is the result of another medical condition, but this happens in fewer than one out of ten cases. For the rest, most experts believe that there is no single factor, but rather a variety of factors. Blood pressure is determined mainly by resistance in the smaller arteries and arterioles. These vessels have a relatively thick muscular wall that contracts and relaxes to adjust blood flow and pressure. They dilate when more blood is needed or when the pressure increases; they constrict when blood is needed elsewhere or when the pressure drops. The dilation and constriction are controlled mainly by our autonomic nervous system, the part of our nervous system that operates subconsciously to regulate our body systems. Pressure-sensing nerve cells throughout our circulatory system constantly monitor the pressure in our arteries. When the pressure gets too high or too low, a series of events is triggered that either

48%

50

–4

The burden on African Americans is especially concerning. They develop hypertension earlier, have higher levels at any age, and have higher rates of strokes, heart attacks, and kidney disease as a result.

65%

4

Ages 75+: men 67%, women 82%

78%

–3

Ages 65–74: men 62%, women 73%

18

Ages 55–64: men 48%, women 54%

100

Prevalence of Hypertension (%)

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35

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Age Figure 12.1  I ncrease in hypertension with age. Source: Nation l Health and Nutrition Examination Survey.

lowers or raises blood pressure. These events mainly involve the release of different hormones that interact with the endothelium. However, when the endothelium is not functioning properly, the artery does not adjust as it should, especially when the pressure is high and the endothelium needs to dilate. Nitric oxide production is reduced, and the artery remains in its default condition, which is slightly constricted. This causes blood pressure to gradually rise. Other factors can also increase blood pressure. Anything that overstimulates

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Why Do African Americans More Often Have High Blood Pressure? One in three African Americans has hypertension versus one in five people overall. To make matters worse, the disease process is accelerated: Blacks are nearly twice as likely as whites to suffer a fatal stroke, one and a half times as likely to die from heart disease, and four times as likely to have kidney failure. Black men, in particular, are hard hit by hypertension—a death rate nearly three times the national average. The reason may lie in genes. Three out of four African Americans are sensitive to salt versus one in three whites. This means that salt causes them to retain sodium, which increases blood volume, which in turn increases blood pressure. This cycle may be a survival adaptation in hot, dry climates because it conserves water, but it is a handicap in other climates. The good news is that African Americans respond very well to a diet that is low in sodium and fat and high in fruits, vegetables, and fiber.

the sympathetic branch of the autonomic nervous system (the blood pressure– increasing side) can do it. Changes in hormones released from the adrenal glands can affect the volume of blood in our system, which also affects blood pressure. But, the endothelium of these smaller arteries seems to be ground zero. Many of the same factors that accelerate atherosclerosis also increase blood pressure through their impact on the endothelium. The important thing is that these are the factors we can manage to lower our blood pressure. A New Way of Thinking about Hypertension Our blood pressure provides a crude estimate of how well our arteries are able to dilate—the lower the blood pressure, the greater the dilating capacity. Blood pres-

sure also turns out to be a pretty good indicator of fat tissue status. Blood pressure goes up directly with fat accumulation. KEY INSIGHT

Blood pressure is one of the best indicators of the status of the Aging Syndrome. Measuring blood pressure seems simple enough, but entire books have been written about it. Many factors affect our blood pressure from moment to moment. Many of us experience “white-coat hypertension”—our blood pressure goes up when the measurement is taken in the doctor’s office. This is a great example of how stress and emotions affect blood pressure. Other factors also contribute to subtle variations in pressure throughout the day. Only with

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Mistaken Assumptions

Facts

It is normal for blood pressure to increase with age.

Blood pressure does not increase because of age but because the behaviors and exposures that contribute to it have been going on longer.

I know my blood pressure is OK because I feel fine.

There are no symptoms of increasing blood pressure until it is quite advanced. But all the time, artery damage is increasing and the heart is working harder than it should.

Taking medication is the best way for me to control high blood pressure.

Medication is the usual treatment, but it not enough in at least half of people with increased blood pressure. Losing weight, exercising, eating healthy, and managing stress are often more effective.

Blood pressure needs to be checked only once or twice a year.

Blood pressure should be checked often because it is constantly changing.

As long as a blood pressure reading is lower than 140/90, it’s OK.

The optimal level is 110/70. Risk increases at any level above this. Elevated blood pressure is serious long before it is labeled “high.”

High blood pressure is an isolated condition.

High blood pressure is a key indicator of the Aging Syndrome—an important part of a process that accelerates disease processes and leads to many other problems.

repeated measurements in various settings can we really get a feel for what our usual range of blood pressure is. Most pharmacies, including those in supermarkets, have machines that you can use free of charge. Or, you can buy a basic blood pressure measuring unit for less than $50 and use it at home whenever you want. It is unacceptable that one in three people who have hypertension don’t know it, when testing is so simple and readily available.

KEY INSIGHT

A single measurement is never enough to know your “usual” blood pressure. One of the striking things about hypertension is that two out of three people who are aware of it do not have it under control. About four out of five of them depend on medication to control it, but fewer than half attain adequate control

Chapter 12: Constricted Circulation 

with drugs. And, adequate only means a reading below 140/90, which is far from optimal. KEY INSIGHT

It is difficult to get blood pressure down to an optimal level with medication alone. Because hypertension is so common with increasing age, it represents a huge market for the pharmaceutical industry. Hence, we have an enormous amount of research and promotion of drug therapy but very little regarding lifestyle interventions. We do know, however, that blood pressure is exquisitely sensitive to lifestyle changes, which are actually more effective than drug therapy, especially before blood pressure gets too high. KEY INSIGHT

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Hypertension makes the heart work harder. Pumping blood through stiff arteries is like using resistance when you’re doing an exercise. But, resistance in exercise is healthy because it’s temporary. You work against the resistance, tire yourself out, then relax and recover. The recovery period is vital because that is when positive adaptations occur. With high blood pressure, the heart doesn’t get a chance to relax. The main pumping chamber—the left ventricle—becomes enlarged in an unhealthy fashion. It requires more oxygen and is unable to recover completely between beats. Hypertension can go on for many years, even decades, as it slowly strains the heart, damages arteries and organs, and accelerates several life-threatening disease processes. That’s why hypertension is called the silent killer. KEY INSIGHT

Almost everyone can lower blood pressure through exercise and fat reduction.

High blood pressure is especially hard on the heart.

The Big Picture Root Causes of Constricted Circulation Root cause behaviors and exposures dra- blood thicker, hastening atherosclerosis. They trigger inflammation in arteries, inmatically affect the endothelial cells that line blood vessels. They all contribute to crease blood pressure, and disrupt the damendothelial damage and inhibit nitric oxide age repair process. Nearly every root cause production, thus impairing the vessels’ abil- can do this independently; think of the imity to dilate. These behaviors and exposures pact when they occur simultaneously. also cause oxidative stress and make the Sounds like “aging” but it isn’t.

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» Physical disuse—Disuse results in poorer blood flow and loss of unused

capillaries; impairs dilating ability, resulting in arteries becoming stiffer and less able to adapt to changing needs for blood flow; contributes to higher blood pressure and thickening of the blood, which promote plaque buildup.

» Poor diet and nutrition—Highly processed foods can increase blood glucose and blood lipid levels causing an increase in oxidative stress, releasing free radicals that contribute to atherosclerosis, stiffening arteries, and thickening blood; trans fats and saturated fats make platelets stickier and more likely to form plaque; too much sodium and red meat and too little potassium can increase blood pressure.

» Stress—Chronically elevated stress hormones cause an increase in blood pressure,

can injure the endothelium, impair dilation, accelerate atherosclerosis, make the blood thicker and stickier; they also contribute to an unhealthy lipid profile—more cholesterol produced by the liver, a higher ratio of bad to good cholesterol.

» Excessive alcohol—Increases the stickiness of the blood and stimulates plaque

formation; a byproduct of alcohol increases the binding of immune cells to the blood vessel wall, increases blood pressure, and makes arteries stiffer by impairing nitric oxide production.

» Negative attitude and emotions—Cause substances to be released that contribute

to endothelial damage, preventing them from dilating normally; cause the blood to get stickier by activating platelets (laughter has the opposite effect); contribute to higher blood pressure.

» Secondhand smoke—Chemicals absorbed into the blood from secondhand smoke

injure the endothelium, causing inflammation and plaque development; impair dilating, stiffening arteries; increase blood pressure; and activate platelets, which make the blood thicker and stickier, more likely to clot.

» Environmental exposures—A number of environmental toxins have been linked to increasing blood pressure and accelerating atherosclerosis and clot formation; the inflammatory response to any foreign substance in the blood disrupts the endothelium and triggers inflammation and atherosclerosis.

» Medications and herbs—Many medications, including over-the-counter drugs, can

increase blood pressure; some herbal supplements, especially for weight loss, can too.

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» Genes—Genes influence the development of endothelial problems, changes in

blood vessel walls, and the rate of developing atherosclerosis; the manner in which genes are expressed affects the response to every root cause (e.g., an increased sensitivity to salt that leads to high blood pressure). Interactions with the Other Megacauses

Metabolic Madness

» Chronically elevated blood sugar causes glucose to attach to capillary walls, which impairs the exchange of oxygen and nutrients.

» Insulin resistance, the associated increased insulin level, and the metabolic syn-

drome all can increase blood pressure, accelerate atherosclerosis, and contribute to endothelial dysfunction and stiffening of arteries; insulin resistance and endothelial dysfunction are directly related—if one worsens, so does the other.

» When both diabetes and the metabolic syndrome are present, significant

atherosclerosis is likely (about a nine in ten chance); with the metabolic syndrome alone, three out of four had significant atherosclerosis.

» Most diabetics die from complications related to atherosclerosis. » The arteries of children who have the metabolic syndrome appear much older than their age.

» Atherosclerosis is accelerated when hypertension is combined with diabetes (over hypertension alone).

» Endothelial dysfunction and impaired clot breakdown are increasingly seen as central features of the metabolic syndrome.

» Nitric oxide responsiveness and production are reduced in people who have the metabolic syndrome and diabetes.

» Excess fat causes increased resistance to blood flow—3 to 4 extra miles of blood

vessels for each pound of fat; blood pressure increases to overcome this resistance.

» Obesity worsens most risk factors for atherosclerosis and cardiovascular disease

(e.g., hypertension, insulin resistance, glucose intolerance, hypertriglyceridemia, reduced HDL cholesterol, and low levels of adiponectin).

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» Obesity increases the likelihood of advanced atherosclerosis even if no other risk

factors are present, largely due to endothelial dysfunction and reductions in nitric oxide production.

Insidious Inflammation

» Inflammation is one of the main drivers of atherosclerosis, especially when combined with diabetes.

» The inflammatory response initiates plaque development; chronic irritation causes persistent inflammation.

» Inflammation causes an increase in the permeability of the vessel wall, allowing both good and bad substances to infiltrate.

» Inflammation leads to thicker, stickier blood and an environment more conducive to clot formation.

» Chronic bacterial infections of the gums are associated with inflammation of the vessel wall.

Relationship to Disease and Death root cause effects. And, they interact in Atherosclerosis and hypertension both their effects on the endothelium and the play key roles in disease and death. They vessel walls to slowly but surely constrict are independent processes, but they usuthe flow of blood. ally occur simultaneously and share many Atherosclerosis

» Atherosclerosis is the single most important cause of death and disease, heart attacks, and strokes.

» Atherosclerosis can lead to disability not only by triggering heart attacks and

strokes but also by contributing to frailty, weakness, and unplanned weight loss.

» It contributes to cognitive decline and dementia; Alzheimer’s disease is rare in people who do not have significant atherosclerosis.

» Silent strokes are a sign of advanced atherosclerosis (they double the risk for dementia). » Atherosclerosis can contribute to every disease process and damage to any organ when the associated arteries are affected.

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Hypertension

» Hypertension is the major cause of heart failure, vascular disease, kidney failure, and strokes.

» Hypertension reduces life expectancy by about five years compared to “normal” blood pressure.

» Every 20-point increase in systolic pressure above 115 or 10-point increase in

diastolic pressure above 75 doubles the risk of dying from a stroke or heart attack.

» Hypertension overworks the heart, leading to left ventricular hypertrophy and

congestive heart failure (CHF); it makes the prognosis with heart disease worse.

» Two out of three people who have heart attacks and three out of four who have strokes and CHF have high blood pressure.

» When hypertension is combined with diabetes, the risk of cardiovascular events is even higher.

» Hypertension reduces blood flow in many parts of the brain; it may increase the risk of dementia.

» Arterial stiffness is associated with most “aging”-related loss of function, especially physical and mental performance.

Our new mindset Constricted circulation is the great accelerator of the Aging Syndrome. The process is progressive but not inevitable. Constricted circulation is about 80% the result of our habits, behaviors, and exposures—in other words, the root causes of the Aging Syndrome. Root causes contribute to constricted circulation in numerous ways, but most important is damage to the endothelium. Constricted circulation is highly responsive to changes in the root causes. Plaque buildup can be reduced, blood pressure can be lowered, endothelial function can be improved, nitric oxide production can be increased, and arteries can become more flexible. The more we do and the sooner we do it, the more power we have to improve our circulation. The cost of waiting for a diagnosis is, at the very least, a loss of reserve capacity, but it may also be a serious life-changing event.

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CHAPTER

13 Metabolic Madness The Clash between Fat and Muscle Middle age is when your age starts to show around your middle. —Bob Hope

What does the word metabolism mean to you? Most would say something like: how fast our motor runs or how fast we burn calories. We would also probably say that metabolism slows with age and that it causes us to put on another pound or two with each passing year. Like most other issues related to increasing age, there is a shred of truth to this, but it’s only a small piece of the puzzle. Changes in the composition of our body (i.e., proportion of fat versus muscle) actually contribute more to metabolism than metabolism contributes to changes in body weight. You could probably guess that any slowing in metabolism has a lot more to do with the Aging Syndrome than with any innate aging process. Metabolism is actually incredibly complex, so let’s begin with a simple definition: Metabolism: All of the chemical processes going on in the body This sounds simple, until you realize that our body contains about 50 trillion cells, and each of these cells has many chemical reactions going on simultaneously. Metabolism is the combination of all of this. Overall, it is a balance between

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anabolic (building up) and catabolic (breaking down) reactions. Anabolic reactions use energy to build and repair cells, proteins, and molecules. Catabolic reactions break down larger substances (larger molecules, ingested food, or body tissues if needed) into simpler molecules. When this happens, energy is released to power body functions as well as to perform mental and physical work. With older age, the balance shifts steadily to the catabolic side. The result is frailty, which is less an effect of aging than lack of stimulation, as we saw in Chapter 7. Specific proteins, called enzymes, coordinate the chemical reactions in our various body systems to keep us healthy. This is where genes play an important role. Genes provide the DNA blueprints for building the enzymes as well as every other protein in our body. If a gene has a slight defect, the structure of the enzyme produced may be a little off as well. The result is that the reactions that the enzyme is involved in may not occur as efficiently as they normally would. Hormones also play key roles by regulating the activity of enzymes. Changes in hormones can activate or de-activate specific enzymes. Many factors influence hormones—this is one of the keys to disease processes in the Aging Syndrome. We will be especially concerned with the hormone insulin, which helps control our blood sugar level. You can see that there is a whole lot more

to metabolism than simply how fast we burn calories. Metabolic madness is about a set of abnormalities in metabolism that occur primarily as a result of two root causes: physical disuse (inactivity) and poor dietary habits (overconsumption). Metabolic madness is rapidly becoming a major force in the Aging Syndrome simply because these two root causes are so common. About two out of three Americans are overfat and not active enough to remain healthy. The inevitable result—expanding fat cells and shrinking muscle cells—opens the door to metabolic madness. Expanding fat cells become more active, secreting a number of hormone-like substances that play havoc with metabolism. Shrinking muscle cells become less metabolically active and increasingly resistant to the key hormone, insulin. Metabolic madness is best recognized by its most obvious component, obesity, and its primary disease outcome, type 2 diabetes. But another component, the metabolic syndrome, is rapidly taking center stage. It is the bridge that connects obesity, inactivity, insulin, and diabetes. Genes are involved, but there is no question that muscle and fat cells are the major players in this megacause. Our discussion will follow the two paths shown in Figure 13.1—first through fat cells to obesity and then through muscle cells to insulin resistance.

Chapter 13: Metabolic Madness 

Overconsumption

Physical disuse

Expanding fat cells

Atrophy of muscle cells Genes

Obesity and insulin resistance Genes Obesity and insulin resistance Metabolic syndrome Type 2 diabetes Multiple chronic diseases Complications Disability and death Figure 13.1  Origins of Metabolic Madness.

The Cost of Expanding Fat Cells Obesity is an enormous problem, and it’s getting worse. It is now the second leading cause of preventable death in the United States as well as a key factor in 80% of cases of type 2 diabetes and 70% of cases of

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cardiovascular disease. Unfortunately, few important health topics are more misunderstood than obesity. Most of our confusion about obesity stems from two incorrect beliefs. The first is the emphasis on diet. Obesity and type 2 diabetes are both routinely blamed on diet when physical inactivity is a far more important cause. The second mistaken belief is that body weight is a valid indicator of body fat. How often do we hear, “I lost seven pounds in the first week on my new diet”? Would the enthusiasm be the same if the person said, “I lost seven pounds of water in the first week on my new diet”? When we change the composition of our diet, especially reducing carbohydrates, we start breaking down our reserves of carbohydrate energy (glycogen) because glucose is our body’s preferred energy source. Water is released in this process. But the weight loss is only temporary because we store only a limited amount of glycogen. We just can’t accept the fact that the seven pounds is water loss that will be restored when we replenish our glycogen stores. We need to lose fat, not water. An entire industry is built on sustaining the confusion about weight loss. We spend billions of dollars on diet and weight loss solutions, and the industry is working hard to make sure that this continues. It would be a disaster for these enterprises if we stopped believing that diet, genes, and metabolism are the main

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Mistaken Assumptions

Facts

As we age, our metabolism slows down.

Our metabolism slows as our muscle cells shrink from disuse.

Problems with metabolism Problems with metabolism occur as fat accumulates, not create a tendency toward fat before. accumulation. “Aging” contributes to obesity.

There is no evidence that aging makes us fat. But, there is overwhelming evidence that excess fat contributes to the Aging Syndrome.

We are born with a certain metabolic rate that is unchangeable.

Three factors affect our metabolic rate: genes, body composition, and activity level. We can control how our genes are expressed, our body composition, and our activity level, so we can influence our metabolic rate.

Diet is both the major cause of and the best cure for obesity.

Diet is neither the cause nor the cure. We would be much better off if we replaced our obsession with diet with a greater interest in physical activity.

causes of obesity, and that the answer is just finding the right diet.

A New Way of Thinking about Fat Accumulation KEY INSIGHT

Obesity and overweight are about fat, not weight. This sounds simple, so why is it overlooked so often? The problem is that we can’t easily measure fat. If we could, we may not have such an obsession with “weight” loss diets. Body weight alone can be used to monitor your weight once you’ve reached your goal weight, but it is a poor way to

monitor fat loss. It can’t differentiate a loss due to fat, water, or muscle. The best definition of obesity is excessive fat. But how much is excessive? There are two ways to answer this question. The first is simply: more than necessary. Unfortunately, we “need” far less fat than our distant ancestors did. The second answer is: any amount that is associated with an increased risk to health. The news is no better here—less fat generally means lower risk. Science has yet to determine how much fat we can tolerate, or how much our risk is increased with a little excess fat. But, here’s the key point: Less is better. One caveat: Some studies suggest that mortality is actually higher at very low BMIs. This ap-

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How to Measure Fat We have two simple ways to estimate fat: body mass index (BMI) and waist circumference (WC). BMI is the ratio of weight to height; it accounts for differences in weight due to differences in height. WC uses a simple cloth tape to measure the largest distance around the middle, usually at the belly button. WC is more important because it provides an estimate of the riskiest type of fat—belly fat. There are a number of other ways to measure fat—skin fold measurements, underwater weighing, and bioelectrical impedance—but all have limitations and are not readily available.

pears to be more a reflection of the studies’ inclusion of people who are frail due to advanced disease. As disease processes advance, the balance between anabolic and catabolic processes shifts steadily to the catabolic, or breaking down, side, which leads to frailty and a lower BMI. Our understanding of fat cells has changed dramatically in recent years. We used to think they were all simple energy storage depots that expanded and contracted with the balance of our caloric in-

take and expenditure. We now know that there is a big difference between fat cells in our limbs and butt and those in our upper torso. And, there is a big difference between fat that is just under the skin and fat that lies deeper in our abdominal cavity. It is this internal belly fat that is most likely to lead to metabolic madness. As these fat cells enlarge, they begin to release a number of hormone-like substances, called cytokines (Table 13.1), which disrupt metabolism in many different ways.

Table 13.1  Effect of Expanding Belly (Central) Fat Cells on Cytokine Production Increased levels

 Leptin—results in a loss of appetite control and inability to experience feelings of satiety  Resistin—increases insulin resistance, may stimulate glucose output from the liver  Interleukin 6—increases insulin resistance, contributes to atherosclerosis  Free fatty acids—contributes to insulin resistance by reducing the use of glucose  Plasminogen activator inhibitor-1—inhibits breakdown of clots, contributes to atherosclerosis

 Tumor necrosis factor-alpha—increases insulin resistance, contributes to atherosclerosis Decreased levels

 Adiponectin—is inversely associated with insulin resistance and inflammation

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KEY INSIGHT

Not all fat cells are the same. Those in the mid-section (belly) are the most troublesome because they contribute more to metabolic madness. The complete story of how these internal belly fat cells affect our metabolism is still unfolding. These cells could actually turn out to be the most metabolically active tissue in our body. All of the cytokines discovered so far except one, adiponectin, are produced in greater quantities as belly fat expands. And, they all seem to be associated with inflammation, insulin resistance,

atherosclerosis, and endothelial dysfunction (stiffening arteries). In other words, they contribute to all three megacauses that accelerate the Aging Syndrome. Adiponectin is the lone “good” cytokine. It has the opposite effect—improving all aspects of metabolic madness— and is associated with less heart disease, diabetes, inflammation, and even cancer. We want more of it, but levels of adiponectin decrease as belly fat increases. The good news is that adiponectin levels increase when we become more active and more fit and lose fat. Central, or internal, belly fat is more difficult to measure than fat on the outside

Mistaken Assumptions

Facts

Body weight provides a reasonable estimate of fat.

Body weight is a poor indicator of fat. A better indicator is the combination of body mass index (BMI) and waist circumference (WC).

All fat is the same.

Fat in the limbs and butt is less harmful than fat in the belly; fat that is deeper in the torso surrounding the internal organs is the most harmful. These fat cells become like endocrine tumors as they enlarge, releasing chemicals that cause metabolic madness.

Fat cells are passive energy storage sites.

Belly fat cells are far from passive. They become increasingly dynamic as they enlarge.

Body mass index (BMI) is a good indicator of health risks.

Waist circumference (WC) is a better indicator of health risks. It explains most obesity-related health risks.

We have little control over where We cannot control where we get fat, but we can fat accumulates in our body. control how fat we get.

Chapter 13: Metabolic Madness 

of the body, which can be estimated by skin fold measurements. This involves an instrument that measures the amount of skin you can pinch at various locations on the body. Waist circumference (WC) is a reasonable indicator of central fat because the waistline increases as these fat cells expand. That’s why WC has become our most useful measurement of fatness. And, this is also why the apple shape (large belly) is a more serious health concern than the pear shape (larger hips). KEY INSIGHT

The larger the waistline, the greater the problem with metabolic madness.

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Our genes affect how our fat cells respond as they expand. Some people can be overweight, even obese, and have few problems. Others with less fat can have more belly fat cells. In general, however, the larger the waistline, the more likely there is to be a problem. A waist circumference of 40 inches in men and 35 in women is one of the criteria for diagnosing the metabolic syndrome.

Why We’re Fat—We Fought the Law and the Law Won How many times have you heard people pondering their weight gain: “I can’t understand it,” “It must be my metabolism,” “It’s

What is The Average Waist Circumference of Adult Americans? The average waist circumference of U.S. adults has increased continuously during the past 15 years. Over half of U.S. adults are considered abdominally obese (men ≥ 40 inches, women ≥ 35 inches). The National Health and Nutrition Examination Survey shows that between 1988 and 2004, the age-adjusted mean WC increased from 37.8 inches to 39.5 inches in men and from 35 inches to 37 inches in women, and the age-adjusted prevalence of abdominal obesity increased from 29% to 42% among men and from 47% to 61% among women.

Waist Circumference (inches) 1960–1962 1988–1994 1999–2000 2003–2004

Men Women 35 30.3 37.8 35 39 36.3 39.5 37

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my hormones,” “I hate this aging, can’t keep the weight off,” “I’m not doing anything different and I still gain,” and so on. The cause of excess fat is simple—more calories consumed than expended. Like everything else in the universe, our body is subject to the first law of thermodynamics—energy cannot be created or destroyed, only transformed from one form into another. In other words, when we consume more calories (energy) than we use (transform) in all metabolic activities, the excess is stored (transformed) as fat. The excess is simply the result of consuming too much or expending too little. However, our obsession with diet and metabolism makes us believe that we get fatter because we’re eating the wrong things and our metabolism is slowing down because we’re getting older. We overlook the biggest factor: physical disuse. KEY INSIGHT

Excess fat reflects physical disuse more than diet. Our level of fat is one of the best indicators of our degree of physical disuse. Most of us start becoming less active at about age 15. By the time we’re 50, the average person’s energy expenditure from physical activity is about half of what it was at age 15. At the same time, in our obsessions with what we eat, we often overlook how much we eat. The volume of food consumed by adult Americans has increased

by about 20% in women and 10% in men in the last 30 years. In terms of fat accumulation, it doesn’t matter where the calories come from. Not that what we eat is not important. The nutrients we have to work with depend entirely on the quality of food we consume. But in terms of fat accumulation, it’s all about caloric balance. A calorie is simply a measure of energy, and every calorie is the same amount of energy. The gradual decline in physical activity without a matching decrease in calories consumed results in a slow but steady accumulation of fat. This may suggest a change in metabolism due to aging, but a problem with metabolism is almost never the cause of obesity. Even if it were, it would not change the basics of fat loss—increase physical activity and adjust eating habits. In the end, activity is more important as both a cause and a cure for obesity. And, it is the most important predictor of long-term success in maintaining a healthy weight. An important reason for this is that a certain level of physical activity is necessary for our appetite control systems. Inactivity disables this system and actually increases our appetite. It’s why cattle and sheep are put in feedlots—they’re less active so their appetite increases; they eat more and gain weight faster. KEY INSIGHT

A problem with metabolism is almost never the cause of obesity.

Chapter 13: Metabolic Madness 

This is another example of one of our favorite themes—that nature is working against us in today’s lifestyle. Our distant ancestors who were the best at storing energy were more likely to survive famines and to reproduce successfully. Nature pushed us in the direction of eating as much as we can (especially fat, the richest source of calories), to conserve as much energy as possible by avoiding unnecessary physical activity, and to build our fat stores. For these folks it was survival of the fattest and the fittest. However, fattest is a relative term. The fattest hunter-gatherers were probably more like the fit of today. KEY INSIGHT

Natural selection favors obesity.

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The Cost of Atrophying (Shrinking) Muscle Adding a few inches around the middle may be the hallmark of metabolic madness, but equally important is the atrophy of muscle. As muscle adapts to disuse, muscle cells go in the opposite direction as fat cells—from being very metabolically active to almost shutting down. Muscle is the most adaptable tissue in the body, which can be a blessing or a curse when it comes to metabolism. A muscle that is used more develops its metabolic “machinery” and its capacity to transform calories into energy. In our bodies, muscle is the biggest user of sugar (glucose), but when muscles are not used, adaptations go in the opposite direction—shrinking and shutting down their metabolic “machinery” (Table 13.2). The

Table 13.2  Adaptations in Muscle Cells That Contribute to Metabolic Madness

 Muscle cells shrink.  Some capillaries in the cell dry up.  Nerve fibers that depend on these capillaries die.  The number of insulin receptors on the cell surface decreases.  The number of enzymes involved in making energy decreases.  The amount of stored glucose (glycogen) decreases.  The number of mitochondria (metabolic factories) decreases.  There are fewer glucose transporters inside the cell (they carry glucose from receptors on the cell surface to mitochondria).

 The capacity for producing energy and performing work decreases.  Metabolism (calories used) slows.

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key adaptation to disuse is increasing resistance to the hormone insulin.

The Key Role of Insulin Keeping the level of blood sugar (glucose) fairly constant is one of the highest priorities of our metabolism because our brain depends on a steady supply of glucose for energy. When blood sugar gets too low, we become dizzy, confused, disoriented, and tired. This can be a serious problem. For thousands of generations, our distant ancestors were constantly active, usually without a regular food supply. They didn’t have to worry much about their blood sugar level getting too high. As a result, we have evolved several mechanisms to increase our blood sugar level when it drops too low. Our liver is a storehouse and manufacturing center of glucose, and we have a number of hormones (glucagon, epinephrine, growth hormone, cortisol) that trigger the liver to release glucose into the blood when the level gets low. The liver can also make glucose out of fats and proteins. Our body will break down muscle, if necessary, to produce glucose. KEY INSIGHT

Protecting against a low level of blood sugar is a higher priority than lowering a high level of blood sugar. On the other hand, we have only one biological mechanism—the hormone in-

sulin—to lower the level of blood sugar when it gets too high. This is the crux of the metabolic syndrome. When we are regularly consuming too many calories and burning too few, we overwork our pancreas, which is our only source of insulin. It keeps producing extra insulin in an attempt to keep our blood sugar level in the normal range, and eventually it becomes exhausted. When our blood sugar level remains abnormally high (a fasting level of 100 mg/dL), it’s not life threatening, but it can do a lot of damage. It makes the blood “sticky,” which is especially bad for the capillaries that feed individual cells. Capillaries are only one cell thick, so they get “gummed up” easily when there is too much sugar in the blood. The result is that the cells become starved for oxygen and nutrients. This can damage every cell in our body. It’s why poorly controlled diabetes eventually causes so many problems. Diabetic complications result from the loss of capillary circulation. KEY INSIGHT

A high blood sugar level may not be life threatening, but it damages cells. Glucose essentially gets a free pass into cells of the brain, heart, and liver, but it requires insulin to get into muscle and fat cells. Muscle accounts for most (75%) of the work that insulin does to lower the

Chapter 13: Metabolic Madness 

level of blood sugar. Individual muscle cells must, however, be able to control the amount of glucose they allow in because their need for fuel varies so much. They can use up to 100 times as much fuel during strenuous activity as at rest. Each muscle cell controls its glucose intake through its response to insulin. KEY INSIGHT

Muscle cells are the key to how well insulin controls our level of blood sugar. When our blood sugar level rises after a meal, the pancreas releases insulin into the blood. Insulin travels through the blood and attaches to special receptors on the surface of muscle cells (and to a lesser degree on fat cells). This triggers a series of reactions inside the cell that opens a “door” and brings a special transporter protein to the receptor. The glucose molecule attaches to the transporter and is

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taken into the cell, where it is either transformed into a storage form (glycogen) or taken to a mitochondria where it goes through a series of enzyme-controlled reactions that produce the energy currency of the body, called ATP. Muscle cells that are used regularly get bigger and store more glycogen. They have more insulin receptors, glucose transporters, enzymes, and mitochondria. This is the metabolic machinery that we mentioned earlier. Muscle cells prefer glucose for energy because glucose breaks down easily and a certain amount of it can be stored right in the cell. Muscle tissue that is used frequently becomes very sensitive to insulin. The insulin receptors on the surface of these muscle cells become like magnets for insulin in order to pull glucose out of the blood to meet the energy needs of the cell. During strenuous exercise, the doors for glucose can actually open even without insulin. Maintaining

Mistaken Assumptions

Facts

Overweight is the main cause of blood sugar problems.

Insulin resistance in muscles is at least as big a cause of blood sugar problems.

Problems with blood sugar are The age effect falls apart when we consider activity inevitable with increasing age. levels. When activity and fitness are maintained at older ages, there is little change in glucose tolerance. Insulin sensitivity decreases with age.

Older folks, up to at least 80, who exercise regularly have similar insulin sensitivity as active people in their 20s.

Medication is the best way to lower blood sugar levels.

Increasing physical activity, with some exercise for all muscle groups, is the best way to keep blood sugar in line.

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insulin sensitivity is our goal; it stops metabolic madness in its tracks. If our distant ancestors’ main challenge was getting enough food, our main challenge today is getting enough physical activity to keep our muscle cells sensitive to insulin.

How Insulin Resistance Develops When muscle cells are not used for even a few days, adaptations occur in the metabolic machinery of the cell. Insulin does not attach to receptors as readily, and glucose stays in the blood longer. This is insulin resistance—muscle cells becoming resistant to insulin in the blood because they don’t need glucose. Their stores are full and they are not being used so they don’t need to produce energy. It’s the opposite of insulin sensitivity. KEY INSIGHT

Insulin resistance develops when muscle cells are not used enough. As the pancreas responds by secreting more insulin to overcome the resistance, two problems result. First, the level of insulin becomes abnormally high, which is necessary to keep the blood sugar level from rising too high. But, a high insulin level contributes to a number of metabolic abnormalities, including those that become the metabolic syndrome—fat accumulation in the belly, rising levels of triglycerides, depressed amounts

of good cholesterol, and rising blood pressure (Table 13.3). Second, the pancreas eventually wears out, and its production of insulin begins to drop. At this point the blood sugar level rises and remains elevated, symptoms develop, and glucose intolerance or type 2 diabetes is diagnosed as if it has just occurred. KEY INSIGHT

Expanding fat cells also contribute to insulin resistance.

Glucose (carbohydrates) and fatty acids (fat) are our primary sources of energy. Between meals, the liver releases glucose and fat cells release fatty acids into our blood to supply this energy. But, following a meal, as glucose levels rise and insulin is released into the blood, the increase in insulin also slows the release of fatty acids from fat cells. Your body is saying, “Let’s use the glucose and save the fat for later.” When insulin resistance develops, glucose that is not taken up by muscle cells gets pushed into fat cells. Fat cells expand, and as they expand, they release more fatty acids. Your body is now thinking, “Hey, we’ve got too much fat; let’s use it.” But, the fat-burning pathways in muscle cells have been shut down along with the glucose-burning pathways. So, only a limited amount of fat can be used, and the level of fatty acids in the blood remains

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Table 13.3  The Metabolic Effects of Too Much Insulin in the Blood

 Increases fat accumulation  Increases triglycerides (released from the liver)  Reduces HDL (good) cholesterol  Does not increase LDL (bad) cholesterol, but its composition changes to become more promoting of atherosclerosis

 Increases stickiness of the blood (increases risk of clot formation)  Increases leptin production (contributes to weight gain)  Increases uric acid production  Reduces endothelial function (contributes to loss of elasticity in arteries)  Increases sympathetic nervous system stimulation (increases release of glucose and fatty acids from liver)

 Increases blood pressure elevated. This depresses the use of glucose even more. We end up with blood that is clogged with excess glucose, fatty acids, and insulin. This results in even more insulin resistance and leads directly to the metabolic syndrome and diabetes.

The Metabolic Syndrome The metabolic syndrome is a group of related metabolic abnormalities that are triggered by expanding fat cells and shrinking muscle cells (Table 13.4). It is an epidemic that parallels the trends in overweight and inactivity. Overall, about one in three adults have the metabolic syndrome, and over age 60 the proportion increases to nearly half. It is being seen more frequently in adolescents—more than a third of overweight

adolescents have the metabolic syndrome compared to only one in 100 who are not overweight. The underlying cause is insulin resistance, and the best independent predictor is waist circumference. We don’t hear much about the metabolic syndrome from our doctors for the same reason that overweight and obesity are seldom addressed—the optimal treatment is a change in eating and activity habits. Insurance plans don’t reimburse such interventions, and doctors don’t believe their patients will make the changes anyway. So, doctors end up prescribing a combination of medications for the individual conditions as they are diagnosed. This seldom results in adequate control. A decade from now the metabolic syndrome is sure to be a major topic of discussion in

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Table 13.4  The Metabolic Syndrome—Criteria for Diagnosis

 Central obesity (WC ≥ 40 inches in men, ≥ 35 inches in women)  Fasting blood sugar level higher than 100 mg/dL  Blood pressure 130/85 or higher  Blood triglyceride level 150 mg/dL or higher  HDL (good) cholesterol lower than 40 mg/dL for men, lower than 50 mg/dL for women People who have three or more of these conditions meet the diagnostic criteria for the metabolic syndrome.

doctors’ offices. It is a growing epidemic that is reaching younger and younger ages, and it is a direct path to diabetes, heart disease, premature death, and excessive

medical costs. It’s the elephant sitting in the middle of the room that we can ignore for only so long.

The Big Picture Root Causes of Metabolic Madness Many interactions between root causes and disease processes occur through effects on metabolism. Obviously we’ve seen the impact of inactivity (physical disuse) and overeating (diet). Metabolic madness is

difficult to avoid with these two root cause behaviors. And, of course, we’re fighting genes that promote fat storage and insulin resistance the entire way. Here’s a summary of the root cause effects:

» Physical disuse—This is the key factor. Atrophy of muscle cells diminishes metabolic capacity and causes insulin resistance to develop; contributes to expanding fat cells and throws appetite control mechanisms out of whack.

» Poor diet and nutrition—Overeating contributes to expanding fat cells; too much fat contributes to increased fatty acid levels and insulin resistance; too many refined carbohydrates increases blood sugar levels and aggravates insulin resistance; contributes to worsening blood lipid profile.

» Stress—Chronically elevated stress hormone levels stimulate appetite, promote

belly fat, and contribute to insulin resistance by causing increases in both glucose and fatty acids released from the liver.

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What’s the Big Deal About the Metabolic Syndrome?     

It means your genes make you very sensitive to a sedentary lifestyle. It is a sign of a disease process that could drastically impair your future quality of life. It raises the urgency to make changes in eating and exercise. Diabetes is almost inevitable if changes are not made. Without lifestyle changes, the inevitable result will be multiple-drug therapy, with all of the side effects.

» Excessive alcohol—Alcohol consumption changes metabolism; less fat is used for energy and more is stored in fat cells; this increases triglycerides in the blood and leads to poorer control of blood sugar.

» Negative attitude and emotions—Negative thoughts and feelings, whether acute or chronic, contribute to increased belly fat, insulin resistance, increased triglycerides, and lower good cholesterol.

» Secondhand smoke—Smoke contributes to insulin resistance and the metabolic

syndrome by inactivating certain enzymes and by having an unfavorable effect on blood lipids.

» Environmental exposures—Various environmental toxins can impair the control of blood sugar and increase belly fat and insulin resistance.

» Medications and herbs—Several medications contribute to weight gain; others can worsen the control of blood sugar or cause changes in blood lipids. Interactions with the Other Megacauses Constricted Circulation

» Most of the long-term damage from metabolic madness is to the circulation, especially the impact of chronic high levels of blood sugar on the capillaries.

» Insulin resistance, increased insulin levels, and the metabolic syndrome all increase blood pressure (doubles the likelihood of hypertension).

» The metabolic syndrome (insulin resistance, hyperinsulinemia, elevated blood

glucose, lipid abnormalities) accelerates atherosclerosis and endothelial dysfunction (loss of elasticity in arteries).

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» Both abdominal fat accumulation and insulin resistance cause changes in blood

lipids that contribute to atherosclerosis—a drop in good (HDL) cholesterol, an increase in triglycerides, and a change in the makeup of bad (LDL) cholesterol to a more harmful type.

Insidious Inflammation

» The cytokines produced by expanding belly fat cells are a major source of inflammation. Most obese folks are in a state of chronic inflammation.

Relationship to Disease and Death cascade of changes that have far-reaching Metabolic madness is like a snowball rolleffects on all body systems and accelerate ing downhill. The changes in carbohydrate most disease processes. and fat metabolism that occur with central obesity and insulin resistance begin a Obesity

» Obesity doubles the risk of dying in the next 10 years and increases the risk of serious adverse events from cardiovascular disease and diabetes compared to normal weight.

» BMI and WC are directly related to the risk for diabetes—higher numbers mean greater risk; at middle age, weight gain and increased waist size are the key risk factors for diabetes; 90% of type 2 diabetics are overweight.

» Obesity increases the risk for osteoarthritis of the knee, gall bladder disease, most cancers, obstructive sleep apnea, and depression in women.

» It is the best single predictor of hypertension. » Obesity is the strongest factor in disability and functional impairment. Insulin Resistance and the Metabolic Syndrome

» Healthy people who are the most insulin resistant experience the most accelerated disease processes over the next decade. The most insulin sensitive experience the least acceleration of most chronic diseases.

» The risk of developing diabetes is five times higher; the risks of heart attack and

stroke are two to three times higher with the metabolic syndrome than without;

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once the condition progresses to diabetes, the risk is five times higher (75% of diabetics die from heart disease).

» The risks and adverse consequences of elevated blood glucose occur at much lower levels than the threshold of diabetes; a chronically elevated level is toxic to all cells and contributes to all disease processes by damaging capillaries.

» Progression to diabetes is associated with many serious disease processes besides

heart disease and stroke, including diseases of the nerves, kidneys, brain (dementia, Alzheimer’s disease), eyes (retinopathy, cataracts, glaucoma), and feet (nerve and blood vessel damage), infections of the skin and mouth, and osteoporosis. Our new mindset

When activity and fitness levels are maintained, there is little change in insulin action with increasing age. The challenge is to maintain our muscle mass because muscles that are not used become resistant to insulin, the heart of metabolic madness. Metabolic madness is completely reversible by adopting a lifestyle that is more in line with how our body is designed to function. That means, first and foremost, becoming more physically active but also eating wisely (less and more nutritious food), controlling our response to stress, and so on. In other words, metabolic madness responds very well to self-managing the Aging Syndrome.

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CHAPTER

14 Insidious Inflammation The Silent Storm of the Aging Syndrome Life is pleasant. Death is peaceful. It’s the transition that’s troublesome. —Isaac Asimov

When was the last time you experienced some inflammation? You’re probably thinking back to the last time you strained a muscle, sprained an ankle, or had an infection or some other acute illness. And, you would be correct about the inflammation part. Any time you have an infection, injury, or illness, you certainly have inflammation. But you would probably be wrong about the “last time” part. We are usually aware of only obvious inflammation, like the redness and swelling in a sprained ankle or a sore throat. The reality is that we have inflammation going on in many parts of our body right now that we are not aware of. First, a couple of definitions: Inflammation: A nonspecific, reactive process by which white blood cells and other inflammatory substances protect tissues from further damage from irritation, injury, or infection Insidious: Slowly and subtly harmful or destructive

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Inflammation is part of our immune system. Its role is to defend us against germs, viruses, and other threats to our body. Inflammation controls the damage from injuries and begins the healing process. It can occur anywhere. Catch a cold, sprain an ankle, overdo an activity, and our immune system triggers an inflammatory reaction to begin healing and restoring balance. The pain, swelling, redness, and heat tell us that inflammation is occurring. This kind of inflammation is good. It kills pathogens and repairs damage. It’s how our body is designed to work. It forces us to rest. It makes us more resilient. Without inflammation, we would be in big trouble. The immune system is incredibly complex and, like most biological processes, is far from completely understood. Many different types of cells, substances, and organs are involved. Nerves and hormones play a role as well. Immune cells and nerves detect abnormalities and initiate the response. Asthma, being an inflammatory disease, is a great example. An inflammatory reaction can be triggered by inhaled allergens that come in contact with immune cells or by emotional stress that stimulates nerve fibers. Genes largely determine our sensitivities, but just about any provocation has the potential to set off an inflammatory response. The response is always the same because inflammation involves substances

that are already present in the blood and in cells, substances whose purpose is to respond when an irritation or abnormal substance is detected. White blood cells (WBC), of which there are several types, orchestrate the responses:

» The inflammatory response begins

when injured or irritated cells release chemicals that cause nearby blood vessels to dilate; this increases blood flow to the area and accounts for the redness and heat. The purpose is to get more immune cells to the site, along with nutrients to help repair the damage.

» Capillaries become more permeable; they leak water and protein into the injured area, which causes swelling and helps flush out toxins.

» Local nerves are stimulated; this increases sensitivity to pain and further relaxes blood vessels to augment blood flow.

» Chemicals released attract WBC to

the site (the type of WBC depends on the type of pathogen present); they migrate into the tissue, where they attack pathogens and consume dead cells to prevent the spread of the irritation and promote the repair of damaged tissues.

» Other substances (cytokines)

are released into the blood to

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communicate with other immune cells; they provoke a variety of system-wide responses. When the threat is neutralized, antiinflammatory compounds take over to shut down the inflammation and continue the healing process.

The Rise of Inflammation As a Megacause Recall our criteria for a megacause:

» Is extremely common; affects virtually everyone

» Affects many disease processes,

including nearly every body system

» Is responsible for substantial disability and death

» Has a reasonably well-defined

process of beginning and progressing

Inflammation is the newest megacause only because its role in disease processes has been ignored for so long. Medicine has long recognized the problems of an overactive immune system—autoimmune diseases, allergies, sensitivities. But only in the last decade have scientists begun to understand the full breadth of its impact. This understanding comes from research into the effects of dozens of inflammationpromoting substances, called cytokines, that are produced in response to inflammatory stimuli. Cytokines are released into

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the bloodstream where they promote inflammation. Just about any tissue or organ can become inflamed. Any time you see -itis on the end of diagnosis, you know it involves inflammation. But, remember that the inflammation was there long before the diagnosis was made. That’s why the real issue is chronic inflammation. The weak link with inflammation has always been the lack of a simple, valid marker of the developing process. There are markers of inflammation, but few guidelines for how to interpret them and use them in planning treatment. At this point, many doctors tend to dismiss chronic inflammation. We can’t see it like we can see obesity or monitor it like we can monitor blood pressure. Inflammation is more like atherosclerosis in this respect, but we don’t have the volume of research that we do with atherosclerosis or even insulin resistance. But, that situation is changing. A protein in the blood called C-reactive protein (CRP) is being increasingly accepted as a marker of chronic inflammation. Levels of CRP are elevated when inflammation is present anywhere in the body, and research has confirmed the impact of an elevated CRP level as an independent risk factor for heart attacks and strokes. It may actually explain much of the risk that is not explained by conventional risk factors, which includes nearly half of the cases. In Chapters 12 and 13, we saw the

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connections with the other two megacauses. In constricted circulation, inflammation in the arteries begins the process of atherosclerosis, and then makes plaques more likely to rupture and form clots. In metabolic madness, expanding fat cells in the abdominal region become prolific producers of inflammatory cytokines that not only wreak havoc with metabolism and lead to the metabolic syndrome but also influence disease processes all over the body. Inflammation may actually be a link between most of our chronic disease processes. Autoimmune diseases, such as rheumatoid arthritis, type 1 diabetes, lupus, and multiple sclerosis, are primarily caused by out-of-control inflammation. But, evidence is mounting that many other chronic diseases, such as heart disease, stroke, Alzheimer’s, type 2 diabetes, osteoarthritis, asthma, and some cancers, are at least partly caused by inflammation. And, a role is emerging in many other common conditions, such as obesity, depression, and chronic fatigue. If all of this is not enough, chronic inflammation is associated with an earlier death from any cause.

When Inflammation Goes Wrong When inflammation occurs, there are four possible results: 1. The threat is removed, inflammation resolves, and the tissue is restored

to its normal state—this is what we want to happen.

2. Scar tissue forms, with collagen replacing normal tissue—this is what usually happens when there is extensive damage.

3. An abscess (cavity) forms containing the debris of dead cells, bacteria, and white blood cells (pus)—this occurs with only certain types of infection. 4. The inflammatory stimulus persists, and the inflammation becomes chronic—this is what we don’t want to happen.

In a normal healthy body, inflammation ebbs and flows. Threats challenge us and we shift to a more inflammatory state; the threat is removed, and anti-inflammation forces take over to heal the damage. The key is how efficient the process is—how quickly the threat is resolved and balance is restored. Problems occur when the threat is not completely resolved and the inflammatory process does not completely shut off. When this happens, substances that promote inflammation continue to be released into the bloodstream, resulting in chronic, lowgrade inflammation. This kind of inflammation can, over time, become established in blood vessels as well as muscles, joints, organs, and other tissues. This is why we call it “insidious” inflammation. We don’t know if or where this inflammation is happening, and we don’t realize that it is feeding disease

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How Can We Measure Inflammation? Currently, the best measure of inflammation is a protein in our blood called C-reactive protein, or CRP. It is produced by the liver in response to inflammation. It can tell you that you have inflammation somewhere in your body, but it can’t tell you where. A more sensitive CRP test, called high-sensitivity CRP (hs-CRP), can help define the risk for heart disease. A high hs-CRP level is increasingly seen as a risk factor for heart disease.

 If your hs-CRP level is lower than 1.0 mg/L, that’s good.  If it’s between 1.0 and 3.0 mg/L, that’s about average.  If it’s higher than 3.0 mg/L, your risk for cardiovascular disease is high. And, if your hs-CRP level is higher than 3.0 mg/L, your inflammation is probably accelerating other disease processes too.

processes. This kind of inflammation is bad for the Aging Syndrome. Chronic inflammation is our concern for several important reasons:

» It is self-perpetuating. » It can last for years without us knowing it is happening.

» It is sustained by habitual behaviors

irritation and inflammation. The area becomes a battleground of pro- and antiinflammation forces, with tissue destruction and repair going on simultaneously. The ultimate result is more scar tissue replacing healthy, functioning tissues and declining reserve capacity, in other words, another source of “aging.”

and exposures.

Getting Stuck in the “On” Position

healthy tissues.

Our immune system evolved to handle acute infections and prevent damage from injuries in young bodies so they could reproduce more successfully. Over thousands of generations, such threats were relatively infrequent, although pretty serious when they did happen. Our immune system was never designed to protect us from a multitude of chronic, low-level infections and inflammatory triggers in our middle age

» It results in scar tissue replacing » It is part of every degenerative disease process.

Chronic inflammation results in WBCs accumulating in the irritated tissues; they continue to do their job, attacking irritants and consuming damaged and dead cells, but in the process they produce free radicals that perpetuate the cycle of

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and older years. That’s what we face today—a steady stream of minor threats that trigger an inflammatory reaction in our body because they are not “normal.” Think about how much the environment has changed just since our grandparents’ day. Even the sun is more dangerous today. We’re inundated with chemicals and other substances that are not natural to our body. They’re in our food, our water, the air we breathe, the materials our homes are built and furnished with, the products we use, and our workplaces. Think about the difference in the type of stress we face today, how under-active and over-fat we are, how our attitudes and emotions become dominated by fear and negativity, and how we so easily turn to medications or alcohol. All of these factors set us up for inflammation. And, if that’s not enough, we also have more subclinical infections and more chronic conditions such as high blood pressure, high cholesterol, high blood sugar, and insulin resistance that promote inflammation. KEY INSIGHT

Our immune system is not designed to respond to so many concurrent, albeit relatively insignificant, abnormal conditions. With so many subtle inflammatory reactions being regularly triggered, our immune response never completely shuts

off (Table 14.1). We remain in a proinflammatory state. The area of inflammation becomes a battleground of destruction and repair. Both processes are going on simultaneously, which costs energy and creates oxidative stress in cells. Our healing forces weaken with time if nothing changes.

The Age Effect The immune system typically changes somewhat with age, although there is considerable variability in the degree of change:

» All immune cells experience some decline in function.

» The number of functioning T cells (a type of white blood cell) decreases.

» More T cells become specialized to

specific threats; fewer remain that are not specialized (that is, available for new threats).

» The ability to distinguish between

normal and abnormal cells and substances declines.

» Pro-inflammatory factors increase and fewer anti-inflammation substances are produced.

We typically experience a greater burden of chronic subclinical infections as we get older (of which we’re usually not aware). The best example is cytomegalo-

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Table 14.1  What Can Provoke Inflammation? Commonly accepted inflammatory triggers

Under-recognized inflammatory triggers

 Infections (e.g., bacteria, viruses, fungi)  Injuries  Allergens  Sunburn  Excessive X-rays and radioactive

 Overactivity (too much or too hard)  Underactivity (too fat)  Common foods (e.g., highly processed,

materials

 

Corrosive chemicals Extremes of heat and cold

high sugar content, white flour, artificial ingredients, trans fats, vegetable oils, excessive animal fat)

 Excessive alcohol consumption  Exposure to the 80,000 chemicals on the market

 Exposure to heavy metals (e.g., lead, mercury, cadmium)

 Fumes in homes and workplaces  Air pollution  Some medications  Stress  Pessimism  Harmful emotions (e.g., anger, fear, anxiety)

 Loneliness

virus (CMV)—a herpes virus that infects about half of all adults in the United States. CMV is easily transmitted to developing fetuses, so it is increasingly common in children as well. It causes few problems, at least in healthy people, but it consistently elicits an inflammatory response. Lowgrade gum infections, H. pylori infections in the stomach lining, and Lyme disease are other common infections. More than

a quarter of all autopsies reveal chronic infections that were unknown in life. What is the real effect of these changes? On the positive side, we have a larger immunological memory bank—that is, a greater number of specialized T cells. If we encounter the same virus or bacterial infection again, we’ll be better at responding to it. That’s why adults get sick less often than children. On the negative

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side, we become less efficient at responding to new challenges. More of our immune system capacity is committed to fighting chronic low-grade infections and defending against old threats. We’re less able to hold off latent viruses, keep autoimmune diseases at bay, prevent the growth of cancer cells, and repair damaged tissues. Some recurrent inflammatory responses get stuck on at a low level. This all contributes to a growing problem of chronic inflammation and immune system exhaustion. Chronic inflammation is so common with increasing age that it is sometimes called “inflammaging.” The implication is that inflammation and aging are inseparable; in other words, inflammation is part of the mystery of aging. The key question is how much of our chronic inflammation could be eliminated by changing our pro-inflammatory root causes, controlling our megacause conditions, and treating our chronic infections. Age is important but, once again, only as an estimate of the time over which pro-inflammatory factors have been triggering chronic inflammation. More time means more widespread inflammation, overuse of the immune response, and greater depletion of the immune system. Aging is not driven by inflammation, just as inflammation is not driven by aging, at least for the most part. As in every body system, there is some irreversible decline in immune function with increasing age. But, as in every other

system, it is insignificant when compared to the impact of disuse and the other root causes that become more critical factors with increasing age. The connection with aging is made far too casually. We know the downside of that assumption. We don’t realize how much our root causes affect something as subtle as inflammation. The real connection between inflammation and getting old is the role inflammation plays in the Aging Syndrome.

A New Way of Thinking about Insidious Inflammation The connections between inflammation, pro-inflammatory substances (cytokines), immune function, the root causes, and disease processes are one of the most complex mysteries in the medical sciences. The complexity is in the biochemistry, which, once again, we don’t have to deal with. For us, the simple part is the powerful part. First, a few mistaken assumptions: We’ve long viewed inflammation as an isolated occurrence, resulting from a specific disease, infection, or injury. However, as we learn more about the process and how cells interact with one another, we now know that inflammation can no longer be addressed as an isolated problem. It is a whole-body issue. Unfortunately, diagnoses are made only when symptoms get bad enough to warrant a trip to the doctor. Then, inflammation is treated as an isolated condition—dermatologists treat

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Mistaken Assumptions

Facts

Inflammation is bad. We need to stop it as soon as possible.

Short-term inflammation is an important part of healing. It needs to run its course.

Inflammation is temporary; it lasts a few days and then it’s over.

Inflammation should be temporary, but it becomes chronic when the infection or irritation is not resolved.

Medication is the best treatment for inflammation.

Medication can improve symptoms and cure some bacterial infections, but not chronic inflammation. The only way to resolve chronic inflammation is to eliminate the trigger that is causing it.

Aging weakens the immune system.

The immune system becomes weak from exhaustion due to years of overactivation resulting from chronic inflammation.

inflammation of the skin, gastroenterologists treat inflammation of the lining of the stomach, dentists treat inflammation of the gums, and on and on. Chronic inflammation can result in subtle chronic symptoms—fatigue, aches and pains, stiffness, just not feeling up to par, and so on. We’ve been programmed to think that these symptoms are caused by “aging,” but we should be associating these symptoms with the Aging Syndrome. This brings us to a key point in our new thinking about inflammation: It can affect the entire body. KEY INSIGHT

Inflammation in one part of the body can lead to, or aggravate, inflammation in other parts of the body.

This process is nowhere more evident than in the case of gingivitis, inflammation of the gums. Probably half of all adults have gingivitis, and it becomes increasingly common with older age. This is another example of a “disease of aging” that has been incorrectly labeled. Gum disease begins in childhood and advances over the course of a lifetime unless steps are taken to control it. Eventually, the “aging” of the disease process leads the dentist to make the diagnosis. Unfortunately, during all this time leading up to the diagnosis, inflammation of the gums has probably been contributing to inflammation in other parts of the body. This is why dentists have become much more serious about treating gum disease. Gingivitis may be the poster child for chronic inflammation because it is so

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common and so easily observed. If only other areas of inflammation could be so easily evaluated. Gingivitis may prove to be a predictor of more extensive chronic inflammation because it is clearly related to inflammation of the arteries and is a risk factor for heart disease. The same bacteria are found in both areas, but we’re not sure that they spread from the gums to the arteries. We do know, however, that gingivitis may be just the tip of the inflammation iceberg. And, we know that when blood vessels become chronically inflamed, the risk for insidious inflammation increases. Chronic blood vessel inflammation seems to be a common link between our major chronic diseases—heart disease, diabetes, stroke, and obesity.

KEY INSIGHT

The extent of gingivitis (gum inflammation) may be an indicator of other internal inflammation. Most common chronic diseases involve increasing inflammation with older age—that is, with the aging of the disease process. And, with declining immune efficiency, the disease processes themselves contribute to the cycle of inflammation (Figure 14.1). KEY INSIGHT

When inflammation is present, disease processes accelerate.

Negative root causes Inflammatory reaction Accelerating disease processes

Declining immune efficiency

Figure 14.1  The Cycle of Inflammation

Persisting negative behaviors/exposures

Chronic inflammation

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KEY INSIGHT

Negative root cause behaviors and exposures promote inflammation. The root causes of the Aging Syndrome are the key to chronic inflammation because of their potential to trigger ongoing inflammatory reactions. This is how chronic inflammation gets established— recurring exposures. Indoor air pollution is a great example. Homes and workplaces are getting tighter, thereby exposing people to more potential toxins, and it is an ongoing exposure. The inflammatory reaction continues as long as the trigger is present. KEY INSIGHT

The interaction of root causes increases the likelihood of chronic inflammation. Think of someone who is abdominally obese, inactive, has a stressful job, lives in a new home with poor air exchange, works in a setting where he is exposed to a variety of chemicals, eats a diet of mostly packaged and processed food, commutes to work with a smoker, drinks a little too much alcohol to relax, and has high blood pressure and high cholesterol. Every one of these conditions is pro-inflammatory; the more present, the more chronic the inflammation, the more rapidly the immune system will be exhausted, and the more rapidly we grow old. The good news is that most of

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this inflammation is reversible when we reduce or eliminate the underlying triggers. Chronic inflammation is of the diagnosis delusion—that it’s not a problem until it becomes a diagnosed condition. We fail to realize that chronic inflammation can simmer for years under the radar. The vague symptoms get attributed to “aging”—inflammation in cells and tissues feeds disease processes. Eventually the immune system becomes exhausted, disease processes become symptomatic, or an event occurs that results in a diagnosis. KEY INSIGHT

Chronic inflammation can exist for years under the radar. The key to controlling chronic inflammation is balancing the pro- and anti-inflammation mechanisms, but this balance is tenuous. We produce many anti-inflammation and anti-oxidant substances whose job it is to shut down inflammation and instigate tissue rebuilding. Centenarians and older folks who thrive in old age generally have two things in common with regard to inflammation: First, they have less chronic inflammation, hence a lower burden of inflammation. Second, they have quite strong anti-inflammation mechanisms. These two features enable them to overcome at least part of the age-related decline in immune efficiency.

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KEY INSIGHT

The key to controlling chronic inflammation is maintaining the balance between pro- and anti-inflammation forces in our bodies.

Inflammatory processes can easily run amok when inflammatory stimuli continue. Just about everything we eat, drink, breathe, think, feel, and do can affect the balance of inflammatory substances pro-

duced in our body. Negative root cause behaviors and exposures set the stage for inflammation; healthy root causes promote anti-inflammation mechanisms. As we get older, we’ve got to do all we can to control our pro-inflammatory stimuli and strengthen our anti-inflammation forces. The focus is not on a specific enemy, but on strengthening our body’s innate healing mechanisms through a way of life that also happens to be the best plan for selfmanaging the Aging Syndrome.

Mistaken Assumptions

Facts

Inflammation is limited to the area in which the injury or infection occurs.

Inflammation in one part of the body can lead to, or aggravate, inflammation in other parts of the body.

The symptoms of inflammation are mainly pain, swelling, redness, and heat.

These are the symptoms of acute inflammation. Chronic inflammation results in symptoms that we don’t connect to inflammation—fatigue, aches, stiffness, general pain, just not feeling well.

Inflammation is caused by outside forces that we have little control over.

There are many subtle triggers of chronic inflammation that are part of our daily life, but we can control many of them.

With no obvious injury or infection, there is no inflammation.

Subtle tissue irritation and low-level infections are going on all the time and trigger inflammation.

Chronic inflammation is a minor factor in disease processes.

Chronic inflammation accelerates disease processes more than we think; for example, it is more important than high cholesterol for heart disease.

Inflammation drives the aging process.

Chronic inflammation drives the Aging Syndrome.

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The Big Picture Root Causes of Insidious Inflammation The root causes of the Aging Syndrome shift the balance of pro- and anti-inflammatory influences toward inflammation. Why? Simply because they represent factors in our lives that are foreign to the way our body has evolved to function. The root

causes put stress on our cells (resulting in free radicals being formed), which causes inflammatory reactions. And, because they are part of our lifestyle, these reactions are repeated on a regular basis.

» Physical disuse—Loss of muscle and expanding fat cells promote inflammation

through an increase in cytokines and oxidative stress; weakness, immobility, and stiffness increase the risk of strains, injuries, and overexertion, which trigger additional inflammation.

» Poor diet—The body sees foods that have been abnormally changed as foreign invaders, which triggers inflammation.

» Processed foods that contain artificial ingredients and added refined sugar, trans fats and partially hydrogenated oils, heat-processed foods (pasteurized, dried, smoked, fried, or grilled).

» Changing balance of omega-6 to omega-3 fatty acids (ratio was less than 3:1 early in the 20th century, today it is closer to 20:1, largely due to the introduction of refined vegetable oils).

» Stress—The stress response causes the release of pro-inflammatory substances (cytokines) to deal with possible injury; unresolved stress promotes chronic inflammation through continued release of cytokines.

» Secondhand smoke and other air contaminants—Trigger inflammatory reactions in airways, resulting in chronic inflammation of the respiratory tract if ongoing.

» Environment—Exposure to chemicals causes inflammatory reactions. Includes in-

door pollutants such as synthetic fibers, latex, glues, adhesives, plastics, air fresheners, and cleaning products; outdoor pollutants such as pesticides, heavy metals, air pollution, smog, smoke, and dust.

» Negative emotions—Trigger the release of pro-inflammatory cytokines, which contribute to a state of chronic inflammation.

» Excessive alcohol—Promotes inflammation in the gastrointestinal tract.

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» Genes—Genetic variations affect the inflammatory response and robustness of the

immune system; root causes affect the way inflammatory genes are expressed, which ultimately determines the ability to respond to threats and resist disease processes. Interactions with the Other Megacauses

Metabolic Madness

» Abdominal obesity is an inflammatory state; this is one of the reasons it is associated with so many disease problems.

» Excess belly fat is a prime source of pro-inflammatory cytokines that result in chronic inflammation.

» The metabolic syndrome is associated with chronic inflammation, related to both fat accumulation and insulin resistance.

» One of the substances released during chronic inflammation is tumor necrosis factor (TNF); it makes cells even more resistant to insulin and contributes to the disease process leading to type 2 diabetes.

» The development of complications from diabetes trigger additional inflammation. Constricted Circulation

» Inflammation and atherosclerosis are closely related; root causes damage the delicate endothelium of blood vessels, triggering inflammatory reactions that begin plaque formation.

» Immune system cells orchestrate the atherosclerosis process, recruiting cells to respond to foreign substances in vessel walls and repairing the damage.

» Inflammation ultimately determines the risk for plaque rupture and clot formation

and predicts (via the CRP level) the progression of atherosclerosis and hypertension.

Relationship to Disease and Death Inflammation is increasingly linked to The initial manifestation of virtually evfrailty, functional decline, and disability at ery disease known to man is inflammation in cells. When you’re sick with a cold or older ages. Disease processes have different flu and feel wiped out, it’s due mainly to kinds of relationships with inflammation the system-wide inflammatory reaction. through the effect on the immune system:

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» For autoimmune diseases, it is the main cause; these include rheumatoid arthritis, lupus, multiple sclerosis, emphysema, and type 1 diabetes.

» Some diseases are caused by unresolved infections, such as ulcers and gingivitis. » Chronic infections have been found to increase the risk for some cancers, including bladder, stomach, esophageal, colon, and liver cancer.

» Some diseases are caused by severe inflammatory reactions; these include asthma, allergies, migraines, and irritable bowel syndrome.

» Chronic inflammation is increasingly linked to the onset and course of many chronic diseases, including atherosclerosis, heart disease, strokes, type 2 diabetes, chronic obstructive pulmonary disease (COPD), Alzheimer’s disease, dementia, osteoporosis, and osteoarthritis.

The higher the CRP level (more inflammation), the greater the risk of mortality and morbidity from these conditions. Inflammation makes plaques more unstable, increasing the risk of rupture and resulting in clots that cause heart attacks and strokes. Our new mindset When inflammation becomes chronic, it can overwhelm our anti-inflammation defenses and spread throughout the bloodstream to other cells and tissues. This accelerates virtually every disease process and, of course, the Aging Syndrome. We face an increasing burden of inflammation and infection as we get older because disease processes are advancing and root causes are becoming more proinflammatory. If we continue along the same path, insidious inflammation will weaken and deplete our immune system, making us more susceptible to disease processes and old before our time.

Next, we will look at the individual root causes. The goal is to learn a little more about each of them before we get to the Personal Plan in Part III, where the

focus will be on thinking and acting differently with regard to each of these behaviors and exposures.

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CHAPTER

15 The Root Causes Understanding the Little Things That Make Us Old I am daily making myself what I am. —Robert Thurman

You don’t have to worry so much about the megacauses if you take care of the root causes. The root causes, taken together, really are ground zero when it comes to the Aging Syndrome. This chapter provides an overview of each root cause. The objective is to understand the consequences of ignoring them. This is the foundation for Part III, which presents the Personal Plan for thinking about and selfmanaging each of these factors in your life. We’ll take them in the order of their overall rating in Chapter 10: 1. Physical disuse

6. Excessive alcohol

2. Mental disuse

7. Tobacco and secondhand smoke

3. Poor diet and nutrition

8. Environment

4. Stress

9. Medications and herbs

5. Negative attitude and emotions

10. Genes

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1. Physical Disuse Physical disuse is the simplest, most powerful root cause. We see the impact of disuse all around us—the increasing number of overweight folks and the frail, weakened elderly. What it comes down to is this: How we use our body determines how it functions and how fast it grows old. We have a body that is designed for activity. Problems develop when it is not used enough, and these problems look an awful lot like “aging.” Most of us overestimate how active we are. It’s because we’re tired so much of the time, and we associate being tired with being busy and being busy with being active. How active are you really? There are two simple indications of whether you have a problem with disuse. First is your fat stores. Excessive body fat is the clearest sign of disuse. Two out of three of us are overfat. Second is the number of steps you take on most days of the week. You can use a pedometer clipped to your pants or belt to count your steps. A healthy number is 10,000 steps a day, but U.S. adults average only about 6500 (inactive is considered fewer than 6000). And, the number goes down with weight gain and increasing age. Only one in four men and one in ten women achieve the goal of 10,000 steps on most days. In our lifestyle, few of us can take that many steps without adding some planned walking. Our hunter-gatherer

ancestors are estimated to have averaged between 12,000 and 24,000 steps per day. In the current-day Amish population, who have a traditional agricultural lifestyle, men average more than 18,000 steps a day and women more than 14,000. Excess fat is the obvious outcome, but there is much more to disuse. Adaptations occur in every body system as a result of too little movement as well as how we use our body in daily life. Physical disuse contributes to all three megacauses and accelerates nearly every disease process. For us, the focus is on the megacauses because if we change these conditions, we slow the effects of the Aging Syndrome. Our daily activities account for the vast majority of our body use and most of our energy expenditure. So, our general activity level plays a key role in both weight control and daily functioning. A simple example is posture. The stooped-over, shouldersdrooping, head-forward posture of a frail elderly person is a posture of weakness, usually the result of weakening and stiffening muscles of the upper torso. Similarly, if we never breathe deeply, as we do when we exercise vigorously, our rib cage stiffens, our respiratory muscles weaken, and the alveoli deep in our lungs dry up from nonuse. And, our lung capacity decreases. The same thing applies to walking, sitting, getting out of a chair, climbing stairs, lifting, bending—all the activities we do in daily life. Our habitual patterns of using

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our body cause adaptations, good and bad. If we are mindless about these patterns of movement, the usual result is weakness and stiffness. Changing our patterns of use and becoming more active in daily life are the keys to reversing disuse. How Physical Disuse Harms Physical disuse and mental disuse are the top-rated root causes because muscle and brain cells are particularly responsive to use since they are not replaced regularly as are most other cells. They depend on use for circulation, nourishment, oxygenation, and waste removal. Disuse leads to the breakdown of cellular components, inefficient repair, and poorer functioning. It contributes to poor

circulation and weakening of the heart, muscles, tendons, and bones. Elasticity declines as connective tissue infiltrates normal tissues, leading to increased blood pressure and muscle, back, and joint problems. The Age Effect We can get away with disuse for years because of our resilience and reserve capacity. But, after about age 50, disuse starts to catch up with us. The adaptations seem to occur faster and become more difficult to reverse. The evolutionary drive to rest seems to get stronger, and the intrinsic aging process, though a minor factor, continues to chip away at our abilities and capacities. The cycle of disuse is selfperpetuating (Figure 15.1). Weight gain,

Declining use Accelerated disease

Increasing injuries

Declining fitness (strength and stamina)

Expanding fat cells/ shrinking muscle cells

Poorer performance Increasing fatigue Increasing stiffness Figure 15.1  The Cycle of Disuse.

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fatigue, declining strength, increasing stiffness, poor performance, and minor injuries all contribute to even greater disuse. And, they confirm our expectations of aging. Age alone is never the obstacle we think it is. Nearly every adaptation to disuse improves with increased use at any age. Even nursing home residents in their 90s experience dramatic increases in strength and mobility when they start exercising. It is never too late. Needs do change, however, with increasing age. Strength and flexibility take on greater urgency as weakness and stiffness become bigger threats to quality of life. Still, relatively few older adults engage in any strengthening exercise—fewer than one in four between ages 45 and 64, one in five between 65 and 74, and one in seven over 75. Bottom Line Strong and consistent evidence shows that inactivity and poor fitness are associated with earlier death, more chronic disease, and poorer functioning. In other words, our degree of physical disuse largely determines our susceptibility to the Aging Syndrome. We just don’t realize how much our daily life has changed in only a couple of generations. We don’t think about the hours spent sitting—watching TV, using the computer, watching movies, playing video games, sitting at work, sitting in the car, and so on. We can easily get through the day with little physi-

cal activity. It’s easier to sit and fall out of shape than to get up and be active. Remember, we’re hard-wired to prefer rest over activity. To overcome disuse requires a new way of thinking about how we use our body—an attitude that embraces opportunities to be active. If we don’t adopt a “more active” mentality, then the harmful adaptations will continue and actually accelerate with age. Impact of Physical Disuse on the Megacauses Constricted Circulation  Physical disuse removes the key stimulus for blood circulation to our muscles and brain. It results in poorer blood flow and loss of capillaries that are not used. Physical activity is the key stimulus to open up blood vessels, so it is vital for maintaining their elasticity. Disuse impairs their ability to dilate, resulting in arteries becoming stiffer and less able to adapt to changing needs for optimal blood flow. This increases blood pressure. Disuse also contributes to a thickening of the blood, accelerating the process of atherosclerosis. Metabolic Madness  Muscle cells that are not used become resistant to insulin; blood sugar levels rise, causing an increase in insulin secretion; high levels of insulin cause additional metabolic problems (e.g., fat accumulation and lipid changes). Fat accumulation, especially in the belly,

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Other “Aging” Effects of Physical Disuse Slower metabolism  Metabolic factories in muscle cells are shut down when not regularly used; for each pound of muscle lost, about 40 fewer calories are burned per day. Declining strength  Muscles shrink, which results in declines in maximum strength as well as endurance. Declining mobility  The walking gait becomes restricted and slower. Lower lung function  All measures diminish. Lower aerobic capacity  Aerobic capacity declines twice as fast in sedentary people. Greater fatigue  Energy production is reduced, and activities require more effort. Poorer balance  Muscle weakness and loss of mobility lead to falls and stumbles. Low back pain, stooped posture  Muscles supporting the spine weaken and stiffen. Joints  Weakness leads to joint instability, pain, and increased risk of injury. Nervous system  Increased sympathetic nervous system activity contributes to disease.

The Big Picture— Death and Disease from Physical Disuse Mortality  Physical disuse is the second leading cause of preventable death (about 250,000 per year); lower fitness, lower activity, muscular weakness, lower vital capacity, and slower walking speed are all associated with earlier death. Cardiovascular  The heart becomes weaker and less efficient; a sedentary lifestyle doubles the risk for heart disease. Type 2 diabetes  The risk of diabetes is inversely related to activity and fitness levels—lower levels of each increase the risk; time in sedentary activities and larger waist size increase the risk. Osteoporosis  Osteoporosis leads to weaker, softer, more brittle bones; lower levels of activity and strength double the risk of fractures. Cancer  The risk is increased for several types, including colon, breast, and prostate. Other disease  There is increased risk for gallstones, depression, anxiety, and erectile dysfunction.

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causes these fat cells to become increasingly active—releasing a variety of hormone-like substances, called cytokines, that contribute to inflammation, insulin resistance, diabetes, and hypertension. Disuse also disrupts our appetite control mechanisms, which results in overeating and more weight gain. Insidious Inflammation  The cytokines released into the blood by expanding abdominal fat cells contribute to chronic inflammation all over the body. Frailty and injuries from disuse also result in inflammation. Disuse leads to a lower capacity for physical exertion, and overdoing it causes inflammation. The threshold for inflammation is lowered. On the other hand, mild to moderate activity stimulates the release of substances that reduce inflammation.

nerve cells in the brain. The pathway is strengthened as we repeat the thought, practice the skill, or study the new material. Neural pathways become easier to follow, like a well-used trail in the woods. The task or skill becomes easier, the memory stronger. On the other hand, with declining mental activity, we use fewer pathways in our brain. Lesser used pathways become slow and “overgrown.” Neural networks shrink and become weaker. It takes longer for nerve impulses to get through. The result is slower processing, fading memories, and poorer coordination—a slow decline in our mental abilities due to the degeneration of neural pathways. It affects every mental function we do not use; it impairs our quality of life and skews our attitude about growing older.

2. Mental Disuse

How Mental Disuse Harms

The brain scan of a person who is playing a new game for the first time shows high levels of brain activity. If the person practices the game for a month and the scan is repeated, it will show significantly less activity, indicating improved mental efficiency—the brain is accomplishing the same task with less work. This is identical to what happens with physical training: As we adapt, we can do the same work with less effort. Our brain is constantly being re-wired. Every new experience uses a specific pathway between

Mental disuse is as impressive an example of “use it or lose it” as physical disuse. A keyboard or string musician has a much larger motor cortex than a nonmusician (i.e., the part of the brain that controls hand and finger movement) just as a right-handed professional tennis player has a much larger and stronger right forearm than someone who doesn’t play tennis. It’s simple adaptation to use in both cases. And, the mirror image is adaptation to disuse—smaller, weaker, declining function. Adaptations to mental disuse

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occur in neurons (brain cells) and neural networks—neurons shrink, networks become less dense, connections (synapses) degenerate. The neurotransmitters that pass impulses between neurons decrease and become less sensitive to receptors. The result is that cognitive functioning slows and mental capacity is reduced. We tend to underestimate mental disuse because we’re not as aware of its effects. We can’t see and feel the atrophy of our mind the way we can see and feel the atrophy of our body. The effects are subtle and difficult to measure. They happen gradually as we get older, which makes them a perfect scapegoat for aging. But, when symptoms such as forgetfulness, confusion, and speaking difficulties become severe enough, they get labeled dementia. Can using our brain more actually protect against these mental diseases? The answer is becoming increasingly clear: yes, even against the most feared dementia, Alzheimer’s disease. Mental disuse is rated very high in its impact on the Aging Syndrome because of its relationship to mental functioning. A high quality of life requires sound mental functioning. Mental disuse does not contribute directly to the megacauses the way the other root causes do, but it provides a great example of the interactions among root causes, megacauses, and the Aging Syndrome. Without a vibrant brain, it is difficult to change our thinking

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about aging, to understand the interactions in the Aging Syndrome, and to become a proficient self-manager of our root cause behaviors and exposures. The Age Effect At middle age, we may react a bit slower and take a little longer to learn new things, but we have experience on our side. We even get better at some things—integrating information, sorting out what is useful from what is not, deciding what to focus on, and knowing how to study and learn. Younger brains can memorize and recite information faster, but at older ages we are better at deciding what to memorize. A modest decline in reaction time, processing speed, and memory has been attributed to cognitive “aging.” But, how much of this decline is due to the real, mysterious aging process? Remember that the changes have to be consistent (because aging is universal) and not reversible with lifestyle changes. The answer is the same one we have found every time we try to quantify the effects of aging—some, but much less than you think. There is tremendous variability in the decline in mental functioning with increasing age, and research over the last 30 years has shown that virtually all of the mental problems attributed to aging can be overcome with appropriate training. So, once again, use trumps aging as a cause.

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A Simple Example An older person recalls 6 items on a memory test, while a young college student recalls 8, a significant performance advantage of 25%. Then both go through identical memory training. Both will improve and, percentage-wise, to a similar degree. The student will still have a 25% advantage, but now there are18 items recalled by the older person versus 24 by the student. When we compare the trained older person with the untrained student, however, we get a completely different picture—18 items for the trained older person versus 8 for the untrained student. It’s an impressive difference that far overrides any effect of aging.

The rate of cognitive decline is slower at any age in those who remain mentally active versus those who do not. The problem is that, as we get older, we simply use our brain less. We retire, we quit writing, studying, analyzing, recalling information, interacting with others, solving problems, trying new things, and so on. We go to fewer social events and give up more activities. All of these changes result in declining stimulation of specific neural networks in our brain. These networks thrive on use at any age. They do not get worn out from overuse, but rather they wither away from lack of use. When lack of use coincides with older age, it’s called aging. Bottom Line Think about how you use your brain. When was the last time you did a complex calculation, wrote an essay, memorized a poem, did long division, read a nonfiction book, took a class, learned a new skill, did a crossword puzzle? It’s not that we don’t do these

things because we can’t do them; rather, we can’t do them because we’ve quit doing them. If we don’t do anything different, our brain will atrophy from disuse. On the other hand, we can embrace a variety of activities and activate more neural networks in our brain and improve its functioning. Use it or lose it—it really is that simple. Impact on the Aging Syndrome Mental disuse is a unique root cause. It doesn’t cause specific biochemical effects that directly contribute to the megacauses. The impact is on the efficiency of mental processing. Our brain is the key to how effectively we develop the wisdom to know what “aging” is and is not, to distinguish what we can control from what we cannot, to be able to accept what we cannot control, to process our mistaken assumptions and form new beliefs, to consciously self-manage the change process, and so on. There is a lot of mental work to do in managing the Aging Syndrome. The

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The Big Picture— Death and Disease from Mental Disuse Mortality  The rate is increased in people who have mild cognitive impairment. Dementia and Alzheimer’s disease (AD)  More time spent in non–mentally stimulating activities increases the risk of developing AD; mild cognitive impairment triples the risk for AD compared to those without cognitive impairment. Disability  Mental disuse is a major factor in the development of disability and loss of independence.

better our mental functioning, the easier this process is. Reversing mental disuse is part of it, but so is controlling the megacause conditions because they can impair brain function and disrupt our ability to manage the Aging Syndrome. Impact of the Megacauses on Mental Functioning Constricted Circulation  Optimal mental functioning requires elastic arteries with minimal atherosclerosis. Constricted circulation causes a decline in functioning due to an oxygen deficiency as a result of impaired blood flow. High blood pressure can also harm mental functioning. It has been linked to memory problems and damage to the part of neurons (axons) that transmits impulses throughout the brain and central nervous system. Metabolic Madness  High blood sugar levels impair memory by depressing the function of the hippocampus. They can

even lead to atrophy of this part of the brain, which plays a key role in consolidating information from short-term to long-term memory. Diabetes is associated with declining cognitive performance. Insidious Inflammation  Chronic inflammation contributes to cognitive deterioration as well as developing dementia.

3. Poor Diet and Nutrition Diet is easily our most misunderstood root cause for both good and bad reasons. The good reasons have to do with the incredible complexity of the science of nutrition (think biochemistry). There is still a lot we don’t understand. Consider how our understanding of fat cells has changed in the last decade or how our understanding of appetite control is evolving. The bad reasons for our poor understanding also stem from this complexity because it opens the door to the promotion of half-truths and sales of products and programs to people

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who don’t need them. This is similar to what is going on in the anti-aging industry, which is thriving on the mystery of the aging process. In either case, complexity opens the door to charlatans, including legitimate scientists who sometimes become blinded by a possible pot of gold at the end of their research. They can take a select group of studies that seem to support a new theory, develop a program or product based on it, give it to a group of people knowing that some will respond favorably simply because of a placebo effect, and then use these people to promote the product or program. Many diet “experts” deliberately make nutrition seem more complex than it needs to be in order to sell their program as a solution. Glance through the diet section of your favorite bookstore. There seems to be no shortage of breakthroughs for curing disease or enhancing health, performance, longevity, or weight loss. Could they all be true? What should we believe? To make matters worse, it seems that every week a new study contradicts something that we thought was true. Our goal is to simplify. We’ll begin with five basic truths about diet and nutrition: 1. Diet is about nutrition, not weight or fat loss. It’s about how we provide our body with the energy and nutrients it needs to function optimally. Fat loss is about energy balance.

2. We are not what we eat, but what we eat provides the raw materials. How we use these raw materials depends on our genes, disease processes, lifestyle, and how we eat.

3. There are no magic foods or supplements. The only magic “diet” formula is moderation, balance, and a variety of whole foods—you can’t put that in a pill. 4. We can’t depend on government guidelines. They don’t do enough to distinguish the quality of foods within each food group.

5. We should be wary of the latest diet breakthrough or claims made based on a single study; they make a good headline but may have little relevance to real life. Be wary of claims based on animal studies; they may not apply to humans. Wait until randomized, controlled studies have been carried out in people. How Poor Diet and Nutrition Harm Over the last 40 years, the link between diet and disease has grown stronger and stronger. The situation is primarily a matter of too much food, but it’s also about too many unhealthy foods and too few healthy foods (Table 15.1). The term empty calories is appropriate when we consider the nutrient value of many of the foods on our

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Table 15.1  The Sad State of Current Eating Patterns Consuming Too Little* Whole grains

Only about 1 in 25 gets the recommended three or more servings per day.

Fruits

Only 1 in 10 consumes the recommended four or more servings per day.

Vegetables

Only 1 in 10 meets the recommendation of five or more servings per day.

Nuts, seeds, and legumes

About 1 in 7 gets the recommended four or more servings per day.

Consuming Too Much† Sugar-sweetened beverages

More than half consume at least 36 ounces per week.

Sweets and bakery desserts

About 2 out of 3 consume at least 25 servings per week.

High-fructose corn syrup

Not available until 1960s, it now provides 20% of carbohydrates and 10% of calories for the average person.

Bad fats

Ratio of bad fats to good fats (omega-6:omega-3 fats) should be 2:1 to 3:1 but is currently 15:1 to 17:1 due to the increase in refined vegetable oils and the decrease in fish, wild game, nuts, seeds, and green, leafy vegetables.

Sodium

Most of us consume 15 times what we need (75% comes from processed foods).

Total caloric intake

Between 1971 and 2004, caloric intake increased by 22% in women and 10% in men. The increase is largely attributed to more starches, refined grains, and sugars.

*There are some ethnic and racial differences; for example, Mexican Americans, on average, consume more whole grains and legumes but fewer vegetables. †Again, there are racial and ethnic differences: Blacks and Mexican Americans, on average, consume more sugar-sweetened beverages, and Mexican Americans typically consume fewer sweets. Source: National Health and Nutrition Examination Survey.

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supermarket shelves. The trend of mass producing food in factory farms, feedlots, warehouses, and processing plants raises new concerns about the quality and the impact of ingredients added to packaged, processed, and manufactured foods. All of these factors play a role in the development of megacauses and the acceleration of chronic disease processes. Over hundreds of thousands of years, our body adapted to limited calories and a diet high in fruits, vegetables, lean meats, and seafood. These adaptations included:

» A strong drive to eat whenever we can

» A strong proficiency at storing energy as fat to guard against starvation

» A preference for fat because of its high energy content

» A desire for carbohydrates because

they make us feel good and increase brain serotonin levels (the “happy” neurotransmitter) There were no unhealthy carbohydrates or fats. The challenge was simply getting enough calories. It has all changed in the last hundred years. We’re now overwhelmed with unhealthy food products—processed foods high in sodium, unhealthy fats, little fiber, and added sugar and artificial chemicals. And, this is not our only problem with diet. We have also adopted many unhealthy eating habits.

The Age Effect With increasing age, the need for some nutrients (calcium, vitamin D, protein) increases at the same time that appetite may begin to diminish. This happens at a time when many people are being put on prescription medications, which can contribute to appetite and digestive problems. It becomes all the more important to focus on higher-quality foods and to maintain good digestive health. Bottom Line Diet is often overrated as a cause of weight problems, performance problems, and chronic disease. There is, however, no question that eating healthy is an essential part of managing the Aging Syndrome. The good news is that, in this case, it is simpler than you think. We are not recommending individual foods or supplements or any special diet. The essentials of a healthy diet are simple—a variety of whole foods: fruits and vegetables, whole grains, legumes, nuts and seeds, lean protein, eggs, and lower-fat dairy as well as fewer processed, packaged foods with added sugar, flavorings, preservatives, colors, and so on. This part is straightforward and quite frankly not very interesting. What is interesting, however, is why we eat the way we do even when we know we shouldn’t. The biggest challenge is simply eating too much—recall the impressive results of

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The Big Picture— Death and Disease from Poor Diet and Nutrition Mortality  The mortality rate is higher in people who consume more meat and fewer fruits and vegetables. Heart disease and stroke  The risk increases with greater intake of trans fats, saturated fats, red meat and processed meat, high-fat dairy, fried foods, starchy foods, and high-glycemic-load foods (refined carbs). It also increases with a low intake of good fats, fiber, whole grains, fruits, and vegetables. Type 2 diabetes  The risk increases with an excessive intake of starchy foods, highglycemic-load foods (i.e., refined grains and starches), sugar-sweetened and diet beverages, and red and processed meats and too little fiber (especially cruciferous and yellow vegetables). Cancer  Overall, a third of cancers are related to food in some way; the risk increases with intake of starchy foods (pancreatic in women), red and processed meat (colorectal, prostate, breast, lung, esophageal), soda (pancreatic), excessive dairy —too much calcium (prostate), and seared meat (prostate); low intake of fruits and vegetables (most types); and increasing evidence of the role of food contaminants, such as toxins in food. Osteoporosis  The risk increases with red meat and excessive protein intake (pulls calcium from bones). Diverticulitis  The risk increases with low fiber intake. Autoimmune disease (lupus, eczema, and rheumatoid arthritis)  The risk increases with inadequate intake of good fats. Endometriosis  A higher intake of trans fats increases the risk.

the caloric restriction research. Diet and eating are two very different things. A lot of attention is paid to the food and too little to the eating. In the Personal Plan, we’ll outline a new way of thinking about eating—not only what, but when, why, and how much we eat.

Impact of Poor Diet and Nutrition on the Megacauses Constricted Circulation  A highly processed, calorie-dense, nutrient-depleted diet causes spikes in blood glucose and blood lipids that increase oxidative stress and trigger the release of free radicals that

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contribute to atherosclerosis, stiffening arteries, and thickening blood. Atherosclerosis is promoted by trans fats and an excessive intake of saturated fats; these types of fats make platelets stickier and more likely to form plaque. Blood pressure may be increased by an excessive intake of sodium and red meat and too little potassium; increased fructose has also been associated with an increase in blood pressure. Metabolic Madness  Diet contributes to metabolic madness in several ways— fat accumulation, lipid changes, insulin resistance, and glucose intolerance. Body fat increases with an excessive intake of sugar-sweetened beverages, refined grains, starchy foods, and low-fiber intake; highfructose corn syrup may block the brain’s ability to tell us when we’re full and hence contributes to overeating. Consuming too many trans fats and saturated fats increases bad cholesterol, and trans fats also decrease good cholesterol, as does eating too many simple sugars and too few good fats (omega-3). Insulin resistance and the metabolic syndrome are promoted by consuming too many refined grains and sugar-sweetened drinks, overeating, and taking in a high total carbohydrate load. Insidious Inflammation  The highly processed, calorie-dense diet that increases oxidative stress and the associated free radicals contributes to inflammation. Several eating habits—overeating; taking

in too much sugar, sugar-sweetened soft drinks, diet soft drinks, refined grains, and trans fats; and not eating enough good fats—also promote inflammation. And, heat-processed foods (pasteurized, dried, smoked, fried, or grilled) produce toxins that result in inflammation.

4. Stress When was the last time you felt some stress? We all experience stress at times— before an interview or a presentation, when we’re late, stuck in traffic, treated rudely, facing a deadline, going to the doctor, when the car breaks down, when we’re criticized for something or make a mistake, and so on. Stress is part of our daily life. It’s unavoidable. It can even be a good thing in some situations—it can help us focus and perform our best. And, in emergencies, it gives us strength and abilities we never knew we had. The response to stress is always the same. It is hard-wired into our DNA as a survival mechanism—a powerful biological response triggered by our brain the instant we sense a threat. Our sympathetic nervous system takes over and sends a signal to our adrenal glands to pump out adrenaline and then cortisol. These hormones cause a surge of energy to prepare us for action. This is a great system when we have to fight off an enemy or flee a tiger . . . or lift a car off someone trapped underneath. However, it’s a physical reac-

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tion that is designed to be brief. As soon as the fight, flight, interview, or presentation is over, the stress response is turned off. We relax. Our body returns to its normal state, and we relax . . . at least that’s how it’s supposed to work. Stress was once infrequent. It was mainly about big things, true fight-orflight situations. The stress response worked perfectly. Today, we can’t get away from stress. It’s mostly about little things that we often have little control over. The stress response wasn’t designed for petty arguments, rudeness, waiting in line, job pressures, financial problems, traffic jams, relationship problems, and the like. There is usually no immediate resolution to these issues. Our brain doesn’t know when the threat is over. How Stress Harms Problems occur when the stress response is not turned off. Our adrenal glands continue to pump out stress hormones and cause stored energy to be released into our bloodstream. This causes blood pressure, blood sugar, and blood fat levels all to remain elevated and our blood to remain thicker so that it can clot quickly in the event of injury. The immune system is depressed, the stomach is upset, and nervousness and anxiety persist. It causes wear and tear on organ systems and aggravates every disease process. Stress has another harmful effect—how it affects

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the other root causes. It can make us act mindlessly. This may mean we drink more alcohol, use drugs, overuse medications, overeat, eat junk food, or fall into more passive activities, like watching TV. It affects our attitude and our emotions— we’re more negative and pessimistic, more reactive and prone to anger, and more often in a bad mood. The Age Effect The types of stressors may change, but the response does not change. We let go of some things that used to bother us, but we have new things to worry about—advancing disease, new diagnoses, more frequent doctor visits, and more limitations in abilities. As we get older, it takes less perceived stress to trigger the response and to keep it activated. Smaller stressors take greater tolls because our reserve capacity is declining. Stress feeds disease processes and can make symptoms, such as pain, worse. Interactions with the other root causes are magnified by stress and become more pronounced with older age. And, as usual, we attribute it all to aging. Bottom Line If you hold a light object out in front of you for a minute or two, it’s no big deal. But keep holding it. After several minutes, it gets heavier; after 15 minutes, you may feel a twinge in your shoulder, an ache in your arm. The longer you hold it,

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The Big Picture—Death and Disease from Stress Cardiovascular damage  This is the most serious risk; a sudden increase in blood pressure can trigger angina, arrhythmias, heart attacks, and strokes in people who have atherosclerosis; job stress after a heart attack increases the likelihood of the disease recurring. Digestive problems  Digestive problems are common with chronic stress—it can irritate the lining of the intestines; increase the risk for irritable bowel syndrome, colitis, and peptic ulcer disease; increase gastric acid secretions, which can inflame the esophagus; and contribute to diarrhea, nausea, cramps, and bloating. Cognitive deficits  Stress contributes to the atrophy of neurons and neural networks in the brain, especially the memory center—the hippocampus; it leads to deficits in learning and memory. Asthma/allergies  Stress can trigger attacks and flare-ups of autoimmune diseases; stress makes asthma more difficult to control. Can worsen many disease processes  Stress may exacerbate these conditions: high blood pressure, diabetes, depression, anxiety, headaches, low back pain, osteoporosis, gum disease, erectile dysfunction, skin conditions, addiction problems, autoimmune diseases, chronic pain, and insomnia; stress also undermines efforts to change behaviors.

the heavier it becomes. So it is with stress. The longer you keep it inside, the greater the burden becomes. We may not be able to escape our stressors, but we can change how we respond to them. We can set the object down. We control our interpretation of every stressor we face, and we control the emotions we feel when we experience them. We can change our brain’s response. This involves a new way of thinking about stress and a strategy for responding to it in a healthy way. We’ll present it to you in the Personal Plan.

Impact of Stress on the Megacauses Constricted Circulation  Chronically elevated stress hormones damage arteries, cause them to become less elastic, and make the blood become thicker and stickier—all of these promote atherosclerosis. Stress hormones cause an increase in blood pressure, which can also injure the lining of blood vessels, accelerating atherosclerosis. Metabolic Madness  A chronically elevated cortisol level stimulates the appetite

Chapter 15: The Root Causes 

and promotes fat to be deposited in the belly. It signals the liver to release glucose and fatty acids into the blood, and muscle to break down protein to make more glucose. It causes excess insulin to be secreted by the pancreas, and insulin resistance to develop in muscles that don’t need more glucose. Stress contributes to a more atherogenic lipid profile—more cholesterol produced by the liver and a higher ratio of bad to good cholesterol. Insidious Inflammation  Stress hormones stimulate the production of proinflammatory cytokines that aggravate inflammation all over the body, especially in the colon. They suppress the immune system, increasing the risk of infections, prolonging infections and increasing the vulnerability to disease processes.

5. Negative Attitude and Emotions Your mind can be your biggest ally or your greatest adversary in how you age. It has to do with how you think. The person you are is shaped by your patterns of thought that stem from your assumptions and beliefs. They shape your expectations and attitudes. Your attitudes, in turn, largely determine your behaviors, and your behaviors shape how you age. Essentially, we are all the product of our thought patterns. As Ghandi said, “What we think, we become.” We saw a great example of this in the last

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root cause, stress. We can change the impact of stress by simply changing how we think about it. The same is true with “aging.” Thinking that “aging” is inevitable and unchangeable creates expectations of decline and limitations, and then acceptance of them when they happen. This root cause is about how our attitude and thought patterns set the stage for how we act and what we accept as we get older. Our feelings and emotions, good and bad, are products of our thoughts. We think first, then we feel. Emotions have a powerful impact on the Aging Syndrome—as ally or adversary. Positive and negative emotions have opposite effects on the chemicals released by our brain. Positive emotions produce higher levels of feel-good chemicals, like serotonin and dopamine, while negative emotions depress these hormones. Research is showing stronger and stronger connections between attitudes and emotions and chronic disease and longevity. How Negative Attitudes and Emotions Harm Our brain communicates with every cell in our body through the chemicals it produces. Every thought we have produces chemicals that can affect the functioning of every cell and body system. For example, the fear of a heart attack can bring on chest pain even when there is no heart disease; the belief that toxins are pres-

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ent in a building can make us sick even if there are none. We have mentioned how powerful the placebo effect is, and it is merely a result of our beliefs. The consistent, strong response that people have to placebos is a bane of the pharmaceutical industry. One-third of people who receive a placebo, believing it is the real drug, get better even though there is nothing in the pill. The drug manufacturers have to beat this number to prove the effectiveness of a drug. Some people also experience side effects with placebos when told that side effects are possible. It’s all the power of our thoughts and beliefs. They can be friend or foe. A great deal of evidence shows that negative emotions (pessimism, loneliness, anger, fear, anxiety, etc.) accelerate the aging of disease processes while positive emotions (optimism, hope, gratefulness, joy, calmness, etc.) slow disease processes and speed recovery. The same relationship occurs with physical functioning, frailty, and wear and tear on the body—worse with negativity, better in the presence of positive feelings. A pessimistic attitude lowers expectations, which becomes an obstacle to positive change. Those who expect to slow down with increasing age become less active as they get older, and they do slow down; those who expect to be less involved in social events stay home more; those who

expect their mental processes to slow down do less to challenge their brain. A negative outlook focuses on limitations, while a positive outlook recognizes possibilities (Figure 15.2). The Age Effect As we get older, we tend to become a little more resistant to change, a little more closed-minded, and somewhat less outgoing in our social interactions. It’s easier not to get involved. On the other hand, most of us also become more conscientious, easier to get along with, and less aggressive. The balance of these tendencies is generally favorable to the Aging Syndrome, with two exceptions. First, we’ve got to be open to changing negative thought patterns and mistaken assumptions and beliefs. Second, we’ve got to make a conscious effort to be socially involved, including doing volunteer work for organizations and causes we believe in. As we get older, our attitude about getting older becomes increasingly important. It’s easy to become pessimistic when we start to feel more aches and pains, have more injuries, have to give up some activities, get more diagnoses and have to take more medications, and so forth. Pessimism is the default state of our psyche, just as disuse is the default state of our body. It’s the easy way—simply accept that there is nothing we can do about

Chapter 15: The Root Causes 

Mistaken assumptions Erroneous beliefs Negative thoughts Negative attitudes Harmful emotions Unhealthy behaviors Poor self-efficacy Worsening root causes Accelerated megacauses Accelerated Aging Syndrome Disability and disease-related events Pessimism and lower expectations Figure 15.2  Effects of Negative Thinking.

it, and then we don’t have to do anything. Optimism requires effort. It means taking an active role—seeing problems as challenges and opportunities to get better. It means raising expectations for the road ahead.

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Bottom Line We live in a time of uncertainty. Since 9/11 and the downturn in the economy, pessimism and fear have grown; it’s tougher to remain optimistic. The broadening negativity is becoming an increasingly important factor in the Aging Syndrome. We’ve got to turn to one of the fundamental rules for self-managing the syndrome—accept what we have no control over and change what we can control. One thing we can control is our thought patterns. We can change how we think about what happens to us. We can focus on positive things like gratitude and forgiveness, and this can change our attitude. To undo negative thoughts and emotions requires becoming aware of them as they happen, then consciously interrupting them and replacing them with a positive spin. A positive thought changes our emotional response, and it changes our brain chemistry in a healthy way. There is an impressive body of evidence showing how positive attitudes and emotions, especially optimism, can improve disease outcomes and increase longevity. Impact of Negative Attitude and Emotions on the Megacauses Constricted Circulation  Negative emotions compound the effects of chronic stress, causing the release of chemicals that are harmful to the heart and blood vessels.

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The Big Picture—Death and Disease from Negative Attitude and Emotions Mortality  Mounting evidence links isolation, lack of support, and negative emotions to higher mortality rates. Cardiovascular disease  There is a direct relationship between negative emotions and cardiovascular disease (i.e., more negative emotions, more disease); these emotions include anxiety, anger, hostility, worry, pessimism, and depression. Respiratory  Negative emotions can cause tightening of the airways, leading to declining lung function—a hallmark of “aging.” Depression  Pessimism and loneliness are major contributing factors. Dementia and Alzheimer’s disease  Social isolation in old age increases the risk. Mental functioning  Increasing isolation leads to declining memory and mental functioning; the smaller the social network, the more rapid the decline. Cancer  Higher rates of cancer are observed in pessimistic versus optimistic people. Other disease processes  Many studies have shown that negative people get sick more and recover slower when they do get sick; a negative attitude accelerates many disease processes, including osteoporosis, arthritis, type 2 diabetes, periodontal disease, and autoimmune diseases.

Negative emotions promote atherosclerosis by contributing to damage to the endothelium of blood vessels; they also cause the blood to get stickier by activating platelets (laughter has the opposite effect). Many negative emotions also contribute to an increase in blood pressure. Metabolic Madness  Negative emotions (depression, anger—in men, hostility, and pessimism) have been linked to an increased risk of developing the metabolic

syndrome—fat accumulation, especially in the belly, insulin resistance, higher fasting insulin and serum triglyceride levels, and lower good (HDL) cholesterol. Insidious Inflammation  Negative emotions, especially hostility, are associated with a dampening of the immune response, which contributes to a state of chronic inflammation. Negative emotions stimulate the production of pro-inflammatory cytokines that cause and sustain inflammation.

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Infections and wounds take longer to heal, leading to even more pro-inflammatory cytokines.

6. Excessive Alcohol

en

+30

W om

+20

en

+10

M

Percent change in mortality risk

Alcohol is an enigma in our society. On one hand, it is accepted as a part of social events and celebrations. And, it even has some real health benefits. On the other hand, the news is littered with tragedies related to alcohol. Most of us know someone or some family that has experienced the devastation that alcohol abuse can have on mind and body. The simple truth is that no drug is more abused or more embraced. So, what is the impact of alcohol on the Aging Syndrome? Is it a toxin, a remedy, or something in between?

0 –10 –20 –30 0

1

2

3

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Drinks per day Figure 15.3  Effect of Alcohol Consumption on Risk of Mortality from Cardiovascular Disease.

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How Excessive Alcohol Harms Alcohol is a great example of a hormetic substance—a small amount has a positive effect, but beyond a small amount, the harm increases in direct proportion to the amount consumed. We mentioned it in regard to calorie restriction. Figure 15.3 shows the classic hormetic response. The risk for heart disease decreases as we go from no alcohol consumption to a little alcohol, but as consumption rises, the risk for heart disease increases sharply. A small amount of alcohol makes the blood a little less sticky and the blood vessels a little more elastic. And, a small amount can improve cholesterol levels and perhaps even enhance insulin sensitivity a little. However, all of the positive effects are quickly reversed as consumption increases. And, alcohol is toxic to nerve cells in the brain at any level. The Age Effect As we get older, we generally have less tolerance for alcohol because of changes in our body composition—a lower water content and a higher fat content. These factors increase the concentration of alcohol. There is also a reduction in the liver’s ability to break down alcohol, so it takes longer to get it out of our system. Excess consumption can result in quicker and longer-lasting intoxication, reversal of the positive effects on the heart, and more damage to organs like the liver,

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The Big Picture—Death and Disease from Excessive Alcohol Mortality  Alcohol is responsible for about 100,000 deaths a year in the United States from a variety of causes. Dementia  Alcohol is toxic to brain cells in dose-dependent fashion; it impairs receptors on the brain cells, which impairs brain function and interrupts many body processes; it increases the risk for dementia. Cardiovascular disease  Consistent heavy consumption weakens the left ventricle of the heart (the main pumping chamber) and increases the risk for arrhythmias, heart disease, and stroke. Liver disease  Alcohol impairs the ability of the liver to regenerate; it is the leading cause of liver-related mortality—cirrhosis and cancer. Osteoporosis  Excessive alcohol can reduce bone density by impairing calcium metabolism. Cancer  The risk is increased for several types of cancer, including breast, mouth, pharynx, larynx, esophagus, and colon. Insomnia and sleep apnea  Alcohol interferes with sleep quality and increases the risk for sleep apnea. Disabilities  Alcohol increases the risk of driving-related accidents, falls, injuries, and so on.

pancreas, and kidney. Women are more susceptible to the harmful effects of alcohol at any age due to their smaller body mass. So, women have lower limits to begin with, and these limits become even lower with older age. Bottom Line The optimal dose of alcohol is about one drink per day for most people, two for larger men. This amount of alcohol can re-

duce the risk of dying from heart disease by about 25%. That said, we all respond to alcohol a little differently in how we metabolize it, how it affects our behavior, and how it affects our health. Size, gender, genes, emotions, disease, food, and so on all play a role. The one consistent thing about alcohol is that its negative effects increase with increased consumption. Ob viously more frequent heavy consumption is worse than occasional heavy con-

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sumption. With alcohol, it’s easy to slip over the edge from health promoting to disease promoting. In the Personal Plan, we’ll provide some strategies and rules to keep you in the health-promoting zone. Impact of Excessive Alcohol on the Megacauses Constricted Circulation  Too much alcohol increases the stickiness of the blood, partly because of an increase in serum adhesion molecule levels. Alcohol consumption stimulates plaque formation—a byproduct of alcohol increases the binding of immune cells to the blood vessel wall, which begins the process of atherosclerosis. Excessive alcohol also increases blood pressure and makes arteries stiffer by impairing their ability to dilate (disrupts endothelial cell function and nitric oxide production). Metabolic Madness  Excessive alcohol changes our metabolism; ethanol is used first and fatty acid oxidation is reduced, which contributes to an accumulation of fat. Too much alcohol has a negative effect on blood lipid levels—an increase in triglycerides and a decrease in good (HDL) cholesterol. Excessive alcohol also reduces blood glucose control, accelerating the progression toward diabetes. Insidious Inflammation  A little alcohol actually reduces inflammation, but excessive use increases inflammation and suppresses the immune system, resulting in more in-

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fections, especially in the lungs. Chronic excessive use results in chronic inflammation of the gastrointestinal system and the pancreas; it damages mucosa, increases the risk of bleeding and scar tissue formation, and impairs the absorption of nutrients.

7. Secondhand Smoke Why are we discussing secondhand smoke and not actual smoking? For anyone who smokes, smoking is clearly the number one root cause. Yet another message to smokers about the dangers of smoking is not necessary—they know the risk they’re taking and if they really wanted to quit, there is plenty of support to help them, beginning with their doctor. Even insurance companies reimburse smoking cessation interventions. This root cause is for the rest of us who most likely don’t realize the risks of breathing secondhand smoke (SHS), the smoke from a burning cigarette or from someone’s exhaled smoke. SHS contains hundreds of chemicals, including about 50 known carcinogens. For nonsmokers, it’s nearly as bad as smoking in terms of chemicals absorbed into the blood. How Secondhand Smoke Harms When we breathe air contaminated with SHS, the airborne chemicals move through our bronchial system and into our lungs, where they are absorbed into our bloodstream and carried through our blood

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The Big Picture— Death and Disease from Secondhand Smoke Mortality  SHS is responsible for at least 46,000 deaths from cardiovascular disease and 3400 deaths from lung cancer every year. Heart disease  SHS increases the risk by 30%; it increases irregular heart rhythms and damage if a heart attack does occur. Lung cancer  SHS increases the risk by 20%–30% (living with smoker) and also raises the risk for breast and nasal sinus cancer. Respiratory diseases  The risks are increased for COPD (obstructive lung disease), asthma, chronic bronchitis, and nasal allergies—living with a smoker doubles the risk for wheezing and other asthma-related symptoms. Skin  Long-term exposure to SHS ages the skin (e.g., premature wrinkling and thinning).

vessels to every cell in our body. SHS has a much greater effect on our blood vessels than you would expect based on the doses of toxins received by passive versus active smokers. Our blood vessels are extremely sensitive to tobacco smoke. It doesn’t take much to harm them. The effect is immediate—within 30 minutes arteries in the heart are constricted nearly to the same degree as in a habitual smoker. And, with a daily one-hour exposure, markers of blood vessel function are reduced to nearly the levels of smokers. SHS exposure contributes to accelerated “aging” in several ways. It slows tissue repair by impairing fibroblasts (cells that control repair processes) and by causing an increase in stress hormones. It causes chronic fatigue by increasing carbon mon-

oxide and reducing oxygen in the blood. And, it contributes to stiffness through the buildup of connective tissue, scarring, and fibrosis. The Age Effect As we get older and the Aging Syndrome advances, the reserve capacities of our lungs and cardiovascular system are gradually diminishing. This increases the impact of breathing SHS. The effects on blood vessels last longer. Young children are extremely vulnerable because their respiratory system is not fully developed and is more sensitive. Young people regularly exposed to SHS have been shown to have only 25% of the normal elasticity in their arteries; after a year without SHS, they

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Acute effects (first 30 mins) Clot formation (platelet activation)

96%

Damage to endothelium

45%

Reduction in dilating ability

Active smoking effect

91%

Chronic effects Risk for heart disease

40%

Atherosclerosis (carotid IMT)

41% 80%

Inflammation Reduced HDL (good cholesterol)

73% 57%

Depleted antioxidants (vitamin C) 25

50

75

100

Secondhand smoke as a percentage of active smoking effect Figure 15.4  Comparison of Effects of Secondhand Smoke and Active Smoking. Source: Barnoya and Glantz, “Cardiovascular Effects of Secondhand Smoke,” Circulation 2005.

were still only 60% of normal. For older folks, the effect is even more persistent. Bottom Line SHS is more damaging than we think. It’s easy to feel the irritation in our respiratory system, but we can’t feel the effect in our blood vessels, which is more serious. The good news is that the situation is improving. Restrictions on indoor smoking are resulting in fewer of us being exposed to SHS. In the early 1990s, there were few restrictions on indoor smoking and most of us were exposed to it. By 2002, restrictions were becoming increasingly common and the number of people ex-

posed to SHS had been cut in half (but still 43%). The trend continues, but millions of us are still exposed to secondhand smoke. Homes are the bastion of smokers, where exposure and resistance to change are greatest. We all need to help smokers quit, not just for their own health but also for everyone who shares the indoor air where they smoke, especially children, the elderly, and anyone who has respiratory sensitivities or cardiovascular disease. Impact of Secondhand Smoke on the Megacauses Constricted Circulation  SHS causes arteries to tighten and to remain constricted; it impairs their ability to dilate.

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This increases blood pressure, reduces blood flow, decreases the levels of oxygen and nutrients delivered to cells, and increases stress on the heart. It promotes atherosclerosis; chemicals that are absorbed into the blood from SHS injure the delicate lining of arteries (endothelium), which stimulates the repair process, that is, plaque development. SHS also activates platelets in the blood, which makes the blood thicker and stickier, more likely to clot and develop atherosclerosis. Metabolic Madness  SHS plays a secondary role in metabolic madness, but it does contribute to insulin resistance. It inactivates enzymes involved in energy metabolism, and it has a negative effect on lipids—lowering good cholesterol (HDL) and raising bad (LDL). A measure of SHS exposure (serum cotinine) has been directly related to risk for metabolic syndrome. Insidious Inflammation  The damage to blood vessel walls and the entire respiratory tract triggers a low-grade systemic inflammatory response, followed by scar tissue formation. It stimulates a release of inflammatory cytokines and an increase in free radicals as a result of oxidative stress. Alveoli, the fragile air sacs of the lungs where oxygen and carbon dioxide are exchanged, become impaired. They absorb less oxygen, so the amount of oxygen delivered to every cell in the body is

reduced. SHS also depresses the immune system and reduces the capacity to fight infections.

8. Environmental Exposures How can “environmental exposures” qualify as a root cause? The other causes seem to have very real and direct effects on the Aging Syndrome. What does the environment do to us? It is a different type of root cause. Its effects are more subtle, less flashy, tougher to pinpoint. Its impact may take many years to be felt. But, the consequences are as great, if not greater, than those of many other root causes. If you’re thinking that the environment is a problem only for someone who works in a chemical factory or a coal mine, think again. It is a growing problem for all of us. We’re all aware of the big issues—oil spills, acid rain, toxic wastes, air and water pollution, deforestation, climate change, and so on. We’re less aware of the air quality inside our homes and workplaces— what’s happening as buildings become tighter and more synthetic materials and products are used, not only in construction but also in furnishings and everyday items. We’re unaware of the chemicals in the water coming out of our tap or in the food we consume, the radon seeping up from the ground below us, the electromagnetic radiation that surrounds us, or the noise that we’ve grown accustomed to. This is what we’re talking about with

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this root cause. Environmental exposures can threaten our health and accelerate the Aging Syndrome, but we diminish their importance because they’re less obvious, and difficult to measure. They take longer to cause problems, and they’re often the other guy’s problem. And, there always seems to be someone telling us that there is no need to be concerned, that the problem is exaggerated by the eco-Nazis. These issues are complicated. Paranoia and fear can sometimes be as bad as the hazards themselves, but, on the other hand, how many times have we been told that something is safe, only to find out years later that it wasn’t? The answer is to learn about the issues, control what you can control in your own environment, and build your capacity to resist the rest by managing all of your other root causes as well. How Environmental Exposures Harm The environment is a complex root cause because there are so many questions. Everyone’s exposure is somewhat different, and everyone’s response varies with unique genes, reserves, and disease processes. The health effects may not be known for many years, and then how do you prove the cause? Is a cancer that develops 15 years down the road a big deal? Of course it is, but what began the process that ultimately led to the cancer developing to the point of being

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diagnosed? Many factors are involved— where you live, the building you live in, the traffic on your street, your indoor environment, the climate you live in, the work you do, your water supply, the foods you eat, your childhood exposures, and so on. Environmental factors interact. The more different toxins you are exposed to, the higher the dosages, and the longer the exposure, the greater the potential harm. Airborne pollutants are the most common potentially harmful exposure for most of us. They enter the respiratory tract as volatile gases, liquid droplets, or minute particles. The immediate response is usually an activation of the sympathetic nervous system (stress response)—increasing heart rate, blood pressure, breathing rate, platelet activation, and so on. The immune system responds by initiating an inflammatory response. Toxins that reach the blood—through the lungs, digestive tract, or skin—cause the same inflammatory response along blood vessel walls. This sets off a cascade of oxidative stress mechanisms, release of free radicals, damage to DNA, and stimulation of further inflammation and atherosclerosis in the vessel wall. Every abnormal exposure triggers a response. If the exposure is ongoing, the inflammation, scarring, and atherosclerosis become chronic. The result is often felt as fatigue, headaches, and shortness of breath . . . and it has nothing to do with “aging.”

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KEY INSIGHT

The same pollutant released indoors will result in many times the exposure as when it is released outdoors, and the exposure lasts much longer. That’s why we must pay greater attention to indoor environments. The Age Effect Just as with secondhand smoke, sensitivity to environmental toxins increases with age in proportion to the depletion of reserve capacities (especially in the respiratory, cardiovascular, and immune systems). With older age, detoxification systems are less robust due to interactions between long-term exposures and chronic disease processes. Lower levels of toxins become greater threats. Respiratory or cardiovascular problems make us particularly vulnerable to toxins in the air. More advanced disease processes increase susceptibility; for example, someone with advanced atherosclerosis may experience angina in response to a relatively low level of smog. Bottom Line We tend to minimize environmental hazards because they’re not always obvious. We feel that if these hazards are going to cause any problems, the trouble will be many years away, so why worry now? We have to guard against this mindset for

two reasons. First, environmental hazards do affect disease processes and the rate at which the Aging Syndrome makes us old right now. Second, we have a responsibility to give our children and future generations the best environment possible. Unfortunately, there are more questions than answers regarding environmental exposures. The list is dizzying. We are using so many more chemicals in our world today than we did 50 years ago. We are exposed to so many more potential hazards. Which chemicals are safe and which are not? We can’t possibly research every one. When industrysupported research concludes that there is no problem, can we really be confident that it is true? So, with all this uncertainty, what can we do? At first glance, it may seem like not much. But we can actually do far more than we realize. We don’t have to become radical environmentalists, but rather informed consumers and advocates. We can learn more about potential environmental hazards and get involved in local issues. We can pay more attention to our indoor environments, our water, and our food. This is where our exposures are more intense and chronic. Reducing these pollutants and toxins has a positive effect on all three megacauses. The old adage “Think globally, act locally” applies to the Aging Syndrome as well as the planet. If we act in our own homes, workplaces, and com-

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The Big Picture—Death and Disease from Environmental Exposures Mortality  About 64,000 people die prematurely every year from breathing bad air. People who have chronic lung or heart disease are at the greatest risk. Living in polluted cities is estimated to lower life expectancy by one to two years. Carbon monoxide poisoning causes 800 to 1000 deaths per year. Respiratory disease  Air pollution reduces lung function; exacerbates asthma, chronic bronchitis, emphysema, and COPD; makes respiratory infections worse; and affects pulmonary development in children. Exposure to cadmium in hazardous wastes accelerates lung diseases. Cancer  Environmental factors increase the risk of many types of cancer—excess sun exposure (skin), asbestos, benzene, arsenic and vinyl chloride (different types), inhaled radon (lung), air pollution (lung), volatile organic compounds (leukemia, brain), chlorinated water, nitrates in water (gastrointestinal tract, bladder), arsenic in water (bladder, skin, lungs), permanent hair dyes (bladder), bisphenol A from plastics (breast), chemicals in some pesticides—for example, 2,4-D, DDT (breast, prostate, non-Hodgkin’s lymphoma). Cardiovascular disease  The risk increases as air pollution gets worse. Risk also increases with chronic exposure to arsenic, lead, BPA, and a high noise level. Risk increases with multiple exposures and with advanced disease. Eye disease  Cataract risk increases with exposure to UV rays (thinning ozone). Kidney disease  The risk increases with exposure to toxic metals (e.g., arsenic, lead, mercury, cadmium). Liver disease  Exposure to arsenic, BPA, and lead increases the risk. Nervous system disorders  The risk increases with exposure to arsenic, pesticides, VOCs, and lead. Osteoporosis  Exposure to lead and cadmium increases the risk. Skin  Exposure to UV radiation increases the premature aging of the skin—it can make the skin become thick, wrinkled, and leathery.

munities first, we can slow down the Aging Syndrome. In the Personal Plan we’ll provide a strategy for tackling the poten-

tial hazards that we can control and that have the greatest potential impact on the Aging Syndrome.

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Impact of Environmental Exposures on the Megacauses Constricted Circulation  Outdoor air pollution (i.e., smog) increases blood pressure and the thickness of the blood, accelerating atherosclerosis and constricting blood vessels. Many other toxins (e.g., polyaromatic hydrocarbons, aldehydes, arsenic, and lead) have also been linked to increasing blood pressure, accelerating atherosclerosis, and clot formation. The inflammatory response to any foreign substance in the blood disrupts the endothelium, causes vessels to lose elasticity, and triggers atherosclerosis. Metabolic Madness  Several environmental toxins, including arsenic in drinking water, bisphenol A (BPA) in plastics, and nitrogen dioxide in air pollution, increase the risk for metabolic problems that lead to diabetes. BPA interferes with hormones, promoting fat accumulation and insulin resistance, and it inhibits the release of adiponectin from fat cells (the “good” cytokine that increases insulin sensitivity and reduces inflammation). Animal studies show that particulate air pollution can increase blood glucose levels, abdominal fat, and insulin resistance, especially in association with high-fat diets. Insidious Inflammation  Any abnormal substance in the blood can trigger inflammation in arterial walls. This includes any pollutant or toxin that is breathed in, consumed,

or absorbed. Particles in the air, mostly from traffic (smog), as well as dust and fumes can all injure the lining of the respiratory tract— the finer the particle, the deeper the injury. This injury causes inflammation; with continued exposure, the inflammation can become chronic. Inflammation enables pollutants to get past the protective mucosa to trigger allergic responses. Air pollution also reduces the lungs’ ability to defend against viruses and bacteria, which makes respiratory infections worse.

9. Medications and Herbs The next time you see an advertisement for a drug on TV, listen carefully to the end when the announcer’s voice changes to a low, rapid drone as he rattles off the list of possible side effects. It’s usually a sobering list, ranging from mild symptoms to severe consequences. Medications are effective and necessary for treating many serious conditions. In fact, they are life saving for some—antibiotics for serious bacterial infections, insulin for type 1 diabetes, and thyroid hormone for hypothyroidism. The problem is that medications have also become the treatment of choice for milder diseases when the balance of benefits to risks is much less impressive, and for the treatment of chronic disease when lifestyle changes would be more effective. It’s easier, and much more efficient, for doctors to write a prescription that is covered

Number of prescriptions

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Total prescriptions

30

31.6

Unique prescriptions 21.6

20

10

9.3 2.2 18–44

4.7 45–64

6.3

65–74

Age group Figure 15.5  Increasing Use of Medications with Age. Source: 2006 Medical Expenditure Panel Survey.

by insurance than to counsel a patient on lifestyle changes when such counseling is not reimbursed. It’s yet another part of the diagnosis delusion—when a diagnosis is made, the latest drug therapy is usually considered the best medicine. We’re using more and more medications. Between 1997 and 2007, the number of prescriptions increased 72%, to nearly 4 billion in 2007, an average of 12.6 per year for every person in the United States. Use increases with age (Figure 15.5). Two in five seniors (age 65+) were placed on five or more different prescription medications in 2006, and one in three received at least eight. In addition, older adults use twice as many over-the-counter medications as prescription drugs. Prescribing cascades are becoming increasingly common—

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prescribing a new drug to treat an unrecognized adverse effect of another drug. All of this is why medication interactions and side effects are likely to become an increasingly important root cause as we get older. Medications and herbs are another unique root cause because we don’t have a very good understanding of their harmful effects. There are no widely accepted or standardized methods to measure their safety, few studies to fall back on. Herbs are not regulated by anyone, and drugs, once on the market, have little oversight, especially in relation to interactions. This is not unlike the situation with environmental toxins: We’re told that approved drugs are safe, except for the long list of potential short-term problems. But no one knows the long-term effects, the interactions, or the effects in people who have other disease processes. Doctors face a huge challenge in keeping up with the latest information about medications. Most of their information comes from pharmaceutical reps whose sole purpose is to get them to prescribe more of their products. It’s not about the patient; it’s about the product. In some cases the side effects are worse than the ailment being treated. How Medications and Herbs Harm Medications and herbal therapies contribute to the Aging Syndrome both directly and indirectly. There are two types of direct

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e nc ra ea Cl Side-effects increase

Us e

effects: one obvious but unusual and the other vague but common. The first includes serious adverse effects that result in disease-related events, hospitalizations, and deaths. These effects occur mostly at older ages with advanced disease processes associated with depleted strength and capacity. However, there are exceptions—deaths and cardiovascular complications have occurred in young, relatively healthy people as a result of herbal therapies for weight loss (ephedra), arthritis drugs (Vioxx), and diabetes drugs (Avandia). The second type of direct effect consists of “mild” side effects that are quite common but difficult to link to a specific medication because they are an interaction effect, or they are confused with “aging,” or they are thought to be the result of another disease or lifestyle factor. An important, but under-appreciated side effect is just feeling lousy, which undermines our attempts to change behaviors. Fatigue is the most frequent drug side effect, but nausea, weakness, dizziness, headaches, and cloudy thinking are also quite common. These side effects do not make you feel like exercising, eating healthier, or doing mentally stimulating activities. The unfortunate thing is that we often accept feeling this way as the price we have to pay to stay healthy. The indirect effect is through our belief in medications as the sole answer to our chronic disease problems. This attitude diverts our attention away from the

Medication use and clearance

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Age Figure 15.6  Interaction of Increasing Use and Increasing Clearance. As medication use increases and clearance of medication decreases with age, the probability of sideeffects increases.

real underlying issues, such as unhealthy eating, inactivity, uncontrolled stress, excessive alcohol use, negativity, unhealthy emotions, exposure to environmental toxins, and so on. The Age Effect As we get older, changes in body composition (decreased water content, increased fat content, and decreased muscle), reduced kidney function, reduced liver size and blood flow, changes in receptor sensitivity, and an increase in chronic conditions result in medications staying in our system longer. We gradually become more sensitive to them. As we take an increasing number of drugs and herbs, the likeli-

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The Big Picture—Death and Disease from Medications and Herbs Mortality  Nearly 100,000 Americans die each year from adverse effects of prescription medications; the exact number is not known because few autopsies are performed. Medication-related complications are a growing area of preventable medical errors. Four of the top six medications that cause deaths are opioid painkillers (oxycodone, fentanyl, morphine, and methadone); acetaminophen (part of Vicodin) is also in the top six. The only non-painkiller is the antipsychotic drug clozapine. Serious adverse effects  More than a million patients are admitted to U.S. hospitals or treated in emergency rooms annually because of a bad reaction to a medication; the number of medication-related complications requiring emergency treatment is increasing each year, especially in the 65+ age group—this accounts for up to one in five ER visits and one in three hospital admissions. Liver damage  Liver toxicity may be the most frequent adverse reaction to herbal products; some are safe at low doses, but toxic at high doses. The liver is also the target of damage from several medications, including popular cholesterol and blood pressure drugs as well as acetaminophen. Kidney disease  The risk increases with the number of medications used because most are cleared through the kidneys. Osteoporosis  The risk of fracture seems to be increased with proton pump inhibitors (PPIs) for stomach problems. Sexual dysfunction and libido  Several medications, such as antidepressants, antihistamines, and blood pressure drugs, contribute to these problems.

hood of side effects increases. When the number of drugs we are taking reaches eight or more, the probability of some adverse effects approaches 100%. .

Bottom Line Most of us do not anticipate the degree to which we will be using medications,

and most of us are not very savvy about avoiding trouble with them. The potential adverse effects increase with the number used and with increasing age. The best way to minimize the potential harm is to minimize our dependence on medications. This, we know by now, is best accomplished by self-managing our root

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causes and disease processes. If we ignore them, we will inevitably be taking increasing numbers and dosages of medications. Medication use should not be a major root cause of the Aging Syndrome, but it is, and the trends suggest that it will become an even bigger cause. Impact of Medications and Herbs on the Megacauses Constricted Circulation  Several medications can increase blood pressure, including cough and cold medicines, some antidepressants in combination with alcohol, and some cancer drugs. Some herbal products can also increase blood pressure, including ma-huang (ephedra), ginseng, licorice, St. John’s wort, and yohimbine. Metabolic Madness  Weight gain is a common consequence of many drugs, including some but not all diabetes drugs, blood pressure drugs (notably ace inhibiters and diuretics), antihistamines, thyroid drugs, sleep aids, steroids (prednisone), antidepressants, and migraine drugs. Glucose and lipid metabolism and blood glucose control are impaired by antipsychotics, beta blockers, and diuretics. Some herbs can also cause an increase in blood glucose levels (e.g., St. John’s wort, licorice, and ma-huang or ephedra). Insidious Inflammation  The class of blood pressure drugs called angiotensin II antagonists promote inflammation, while

some of the atypical antipsychotic drugs (Risperdal, Zyprexa, Seroquel, Geodon, Abilify, and Invega) are known to suppress the immune system.

10. Genes When we rated the root causes, genes were at the bottom. How can this be when genes play a role in virtually every health problem we develop as we grow older? We don’t discount heredity, but we rate it low for two important reasons. First, genes are oversold as a cause of “aging,” or getting old. The best research, including the well-respected MacArthur Studies of Successful Aging, has consistently overturned the myth that we are at the mercy of our genes. These studies clearly show that lifestyle has a much greater impact than genes. Studies of identical twins show us that genes are responsible for only about 20% of individual longevity. With the exception of a few rare genetic diseases, genes seldom cause diseases, disabilities, or changes in function. Instead, they operate as the setup man, making us vulnerable to conditions that undermine our health as we grow older. The second reason genes rank so low in the list of root causes is that, other than being aware of our inherited risks, we can’t do much about our genes—that is, our actual DNA. Some day, maybe, but not today. We can, however, do a lot about the impact of our genes simply by changing the other root causes.

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Person B (genotype B)

Phenotype B (expressed genes)

A

Phenotype A (expressed genes)

Disease susceptibility pe

Root cause behaviors and exposures

Phenotype

Ph en ot y

Person A (genotype A)

Root causes

Disease incidence

Genotype

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eB

typ eno h P

Age

Figure 15.7  Interaction Between Genes, Root Causes, and Disease Processes.

How Genes Harm Our genes affect our potential for everything—how fast we can run, our ability to do math or to play a musical instrument, how easily we gain or lose weight, and the probability that we will develop diabetes, high blood pressure, cancer, or any other chronic health condition. We all have varying degrees of vulnerability to every disease process and every root cause, based on slight variations in our genes. Each of us has a certain number of abnormal genes that result in minor changes in the proteins they produce. These slightly different proteins may have no effect at all, or they may alter a biochemical pathway that affects the likelihood of developing a disease, or the rate at which it progresses. Acceleration or deceleration of disease processes depends on the interactions among our genes and our root causes. Genes allow some people to get away with more bad habits than others. Remember our old friend, Jeanne Calment, who lived to 122 despite being a regular

smoker for many years. She had genes that somehow protected her from the ravages of tobacco smoke. Other smokers develop lung cancer in their 40s because their genes made them vulnerable to one or more of the many carcinogens in tobacco smoke. The same can be said for other conditions and diseases. We’ve all heard of people who did all the right things and still had a heart attack at age 40. On the other hand, we know of people who smoked, drank, ate poorly, and did not exercise and lived to a ripe old age. Most of us are somewhere in between. The key point is that our genes respond to changes in biochemical factors and environmental stimuli. Specific genes can be turned on or off by these signals. Genes that are turned on are said to be “expressed.” The set of genes that we are born with is called our genotype. The set of genes that are expressed is our phenotype. It’s the phenotype that is important in the development of disease and the course of the Aging Syndrome. Our phenotype

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How Can We Know Our Genetic Risks? The best indication of our own particular genetic Achilles heel is our parents—what diseases they developed and at what age. The younger they were when they were diagnosed, the stronger our genetic risk. This knowledge may be the most powerful medicine available to us because it gives us a glimpse into the future and allows us to change our lifestyle now to reduce potentially harmful influences of our genes as we age. Do you know your family history? Nearly everyone (96%) knows that it’s important, but only one in three of us have ever tried to gather and write down our family’s health history.

changes with our environment and with changes in our root causes. Positive root cause behaviors and exposures can result in a longevity phenotype, while negative root causes contribute to a more vulnerable phenotype—an “aging” phenotype. Ultimately, we are not destined to develop a disease if we have a positive family history for it or a particular gene variant, but if we expose ourselves to an environment that promotes the disease, then our probability of developing that disease increases dramatically. For example, certain gene variations create the following relationships:

» We will put on fat in our abdominal region if we consume too many calories.

» Our blood pressure will go up if we consume too much salt.

» Our bad cholesterol level will go up if we eat too much saturated fat.

» We will develop insulin resistance if we become too sedentary or too fat.

» We will develop lung disease if we are exposed to tobacco smoke.

The list could go on and on. In virtually every case, our genes can protect, promote, or have no effect on the condition we are exposed to. We could have a defective gene that sets us up for high blood pressure, but it may have no effect at all if we eat healthy and stay active. The “ifs” are huge when it comes to genes. The Age Effect Genes become more important the older we get. Remember that natural selection is about the survival of the species, not the individual. It has little to do with longevity and everything to do with reproducing. We have a strong sex drive from the mid-teens through our 20s because those are our prime reproductive years. Genes are probably not going to be much help as we

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get older. Therefore, as we age, we’ve got to minimize their potential harm by controlling how they are expressed. This situation changes as we age. Some genes become less active, others more active. Some genes that have been turned off for years may get turned on. This switching on and off of genes is a fundamental part of adaptation, the interaction between genes and environment. At any age, the most important factor in how genes get expressed is day-today habits and exposures—in other words, root causes. For example, exercise turns on genes in muscle cells that produce enzymes that enable energy to be produced more efficiently; disuse turns off these same genes. Thus, managing our genes is just one more reason it becomes increasingly important to minimize negative root causes and maximize positive root causes as we get older. Bottom Line We inherit genes from our parents, but we can also inherit lifestyle tendencies and attitudes. When diseases “run in families,” is it because of genes or a shared lifestyle? The answer is usually both, but lifestyle is what we can change. There is still a lot we don’t understand about genes, but one thing we are quite certain of is that there is no magic clock “aging” gene as researchers once fantasized about. The Human Genome Project certainly moved our understanding ahead, but it also opened the door to the much more complex world of how genes

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function. The more we learn, the more we realize that many genes are involved in the changes that occur with “aging.” Technology now allows scientists to scan the genes of large numbers of people, identify variations, and associate them with particular diseases. It makes for interesting news stories—“Alzheimer’s Gene Found,” but what do these relationships really mean? Some day we may be able to repair defective genes, but that is many years away. What would you do right now if your gene scan showed a variant that is associated with a particular disease? You would do everything at your disposal to reduce the chance of this gene being expressed. You would reduce your negative root cause behaviors and exposures because they can trigger the expression of harmful variants of genes. You would also attempt to strengthen your immune system and build your reserve capacities. But, you don’t need a gene scan. Just know your family history, and you can self-manage your root causes as if your genes put you at risk; then you will be doing as much as possible to make sure that these genes do not get expressed. Managing the Aging Syndrome is about the present. It is about what is possible right now. Impact of Genes on the Megacauses Constricted Circulation  Variants in cardiovascular genes interact with root causes—physical disuse, poor diet and

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The Big Picture—Death and Disease from Genes Mortality  Siblings of centenarians are four times as likely to live into their 90s as the rest of us, but how much of it is genes? Twin studies suggest that genes account for about 20% of differences in longevity. Cardiovascular disease  Having a father who died of heart disease before age 55 doubles the risk of cardiovascular disease for men. If both parents died early (mother