The Metabolic Ghetto: An Evolutionary Perspective on Nutrition, Power Relations and Chronic Disease 9780511972959

Table of contents :
Preface page ix
1 Introduction 1
Part I The Physiology of Chronic Disease 21
2 Models of Chronic Disease 23
3 Links Between Nutrition and Ill-Health 43
4 The Developmental Origins of Disease 64
5 Life-Course Models of Chronic Disease Aetiology 83
6 Social, Ethnic and Geographical Variability 106
Part II An Evolutionary Perspective on Human Metabolism 127
7 Life History Theory 129
8 Ancestral Environments 149
9 The Evolution of Human Adaptability 167
10 Sensitivity in Early Life 189
11 The Evolutionary Biology of Inequality 213
12 The Metabolic Ghetto 233
Part III A Historical Perspective on Human Nutrition 253
13 The Emergence of Agriculture 255
14 Trade, Capitalism and Imperialism 275
15 Hierarchy, Growth and Metabolism 295
16 The Emergence of Consumerism 317
17 The Political Economy of Nutrition 339
18 The Dual Burden of Malnutrition 359
Part IV Power, Nutrition and Society 381
19 A Series of Games 383
20 A Question of Agency 406
21 Epilogue 431
Notes 437
References 482
Index 602

Citation preview

The Metabolic Ghetto An Evolutionary Perspective on Nutrition, Power Relations and Chronic Disease JONATHAN C. K. WELLS UCL Institute of Child Health, London

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University Printing House, Cambridge CB2 8BS, United Kingdom Cambridge University Press is part of the University of Cambridge. It furthers the University’s mission by disseminating knowledge in the pursuit of education, learning and research at the highest international levels of excellence. www.cambridge.org Information on this title: www.cambridge.org/9781107009479 © J.C.K. Wells 2016 This publication is in copyright. Subject to statutory exception and to the provisions of relevant collective licensing agreements, no reproduction of any part may take place without the written permission of Cambridge University Press. First published 2016 Printed in the United Kingdom by TJ International Ltd. Padstow Cornwall A catalogue record for this publication is available from the British Library Library of Congress Cataloging-in-Publication data Wells, Jonathan C. K., author. The metabolic ghetto : an evolutionary perspective on nutrition, power relations, and chronic disease / Jonathan Wells. Cambridge, United Kingdom ; New York : Cambridge University Press, 2016. | Includes index. LCCN 2016015463 | ISBN 9781107009479 | MESH: Chronic Disease | Nutrition Disorders | Power (Psychology) | Socioeconomic Factors LCC RC108 | NLM WT 500 | DDC 616/.044–dc23 LC record available at https://lccn.loc.gov/2016015463 ISBN 978-1-107-00947-9 Hardback Cambridge University Press has no responsibility for the persistence or accuracy of URLs for external or third-party internet websites referred to in this publication, and does not guarantee that any content on such websites is, or will remain, accurate or appropriate.

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For Akanksha

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The Metabolic Ghetto An Evolutionary Perspective on Nutrition, Power Relations and Chronic Disease Chronic diseases have rapidly become the leading global cause of morbidity and mortality, yet there is poor understanding of this transition, or why particular social and ethnic groups are especially susceptible. In this book, Wells adopts a multidisciplinary approach to human nutrition, emphasizing how power relations shape the physiological pathways to obesity, diabetes, hypertension and cardiovascular disease. Part I reviews the physiological basis of chronic diseases, presenting a ‘capacity–load’ model that integrates the nutritional contributions of developmental experience and adult lifestyle. Part II presents an evolutionary perspective on the sensitivity of human metabolism to ecological stresses, highlighting how social hierarchy impacts metabolism on an intergenerational timescale. Part III reviews how nutrition has changed over time, as societies evolved and coalesced towards a single global economic system. Part IV integrates these physiological, evolutionary and politico-economic perspectives in a unifying framework, to deepen our understanding of the societal basis of metabolic ill-health. Jonathan C. K. Wells is Professor of Anthropology and Paediatric Nutrition at UCL Institute of Child Health and a leading international researcher in the field of paediatric nutrition. His empirical research focuses on human growth, body composition and metabolism, and is complemented by the development of evolutionary perspectives on these topics. He has contributed extensively to the scientific literature and is the author of The Evolutionary Biology of Human Body Fatness: Thrift and Control (Cambridge University Press, 2010).

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Contents

Preface 1

Introduction

page ix 1

Part I The Physiology of Chronic Disease

21

2

Models of Chronic Disease

23

3

Links Between Nutrition and Ill-Health

43

4

The Developmental Origins of Disease

64

5

Life-Course Models of Chronic Disease Aetiology

83

6

Social, Ethnic and Geographical Variability

Part II An Evolutionary Perspective on Human Metabolism

106 127

7

Life History Theory

129

8

Ancestral Environments

149

9

The Evolution of Human Adaptability

167

10

Sensitivity in Early Life

189

11

The Evolutionary Biology of Inequality

213

12

The Metabolic Ghetto

233

Part III A Historical Perspective on Human Nutrition

253

13

255

The Emergence of Agriculture

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viii

Contents

14

Trade, Capitalism and Imperialism

275

15

Hierarchy, Growth and Metabolism

295

16

The Emergence of Consumerism

317

17

The Political Economy of Nutrition

339

18

The Dual Burden of Malnutrition

359

Part IV Power, Nutrition and Society

381

19

A Series of Games

383

20

A Question of Agency

406

21

Epilogue

431

Notes References Index

437 482 602

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Preface

It is twenty five years ago this summer since I gave my word to the old lady Sarma. This has brought a twofold happiness: first, because of the fact that I actually kept my word, something which could easily be understood by anyone who had managed to do so for even half the time; and secondly, because I can at last tell the story which I have had to keep secret all this time. Leonid Borodin – The Year of Miracle and Grief

It is thirty years ago this summer since I climbed Mont Blanc, the highest mountain in Western Europe, though the route was not technically challenging. I remember an immense landscape emerging as the day began to dawn, the lights of a huge distant city still visible in the fading darkness to the north. Groups of head-torches winked on the snow slopes. The final path led up a knife-edge ridge, offering the undesirable choice of falling into France on one side or Italy on the other. From the summit, waves of mountain ridges rolled away in every direction, their crests picked out by the rising sun. It was cold but surprisingly gentle on the top of Europe that day. I have often been reminded of that event while working on this book. There was the same sense of taking on something that might prove beyond me, but that was worth trying anyway. With hindsight, planning ten chapters and finishing with twenty indicates many false summits. There was the same lure that if one went further and higher than usual, one might be rewarded with a bigger view. And the same challenge of unpredictable terrain: piles of books and papers have regularly avalanched. My aim is to offer a multidisciplinary account of how power relations impact health through the medium of nutrition. To this end, I have brought together physiological, evolutionary, anthropological, historical, political and economic perspectives. This allows me to develop a societal perspective on how chronic non-communicable diseases have become the leading global cause of illness and premature death even as undernutrition remains widespread, while both forms of ill-health are unevenly socially distributed. This approach is necessary because biomedical scientists pay inadequate attention to power relations when developing models of disease, while social scientists rarely extend their political analyses to the physiological traits that are fundamental to health. Furthermore, few have addressed the reasons why humans are prone to hierarchical societies, or how the nutrition–power relationship changes as societies themselves evolve. Of course, the idea that a single book could do justice to such an enormous topic is ridiculous. I have known from the start that I cannot succeed, but only attempt to fail less badly. The reader must judge whether I fall into France or Italy.

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Preface

Trying to address both detail and the big picture is daunting. In Invisible Cities, the novelist Italo Calvino depicted the Venetian explorer Marco Polo describing a bridge, ‘stone by stone’, to Kublai Khan, the blind ageing Emperor of the Tartars: ‘But which is the stone that supports the bridge?’ Kublai Khan asks. ‘The bridge is not supported by one stone or another,’ Marco answers, ‘but by the line of the arch that they form.’ Kublai Khan remains silent, reflecting. Then he adds: ‘Why do you speak to me of the stones? It is only the arch that matters to me.’ Polo answers: ‘Without stones there is no arch.’1

This is my dilemma. Many of the best novels – including those of Calvino – are short, but scientific arguments must be backed with evidence. I need both stones and arch, and in particular I want to show how different perspectives – adjacent stones – can be linked together. This will not be a short book. Scientific progress has been likened to the growth of a snowball rolling down a mountainside, with its ever-increasing surface area representing ‘the unknown’.2 To develop a genuinely multidisciplinary perspective, one must not only engage with multiple rapidly expanding literatures but also embrace differences in terminology, concepts and styles of enquiry, all the while keeping a unifying aim in mind. I learned early on that novelists have unique expertise in this area, for they often build astoundingly complex worlds while weaving a clear narrative through them. It is particularly helpful that biologists and novelists share interest in the way that environments shape experience through the course of life. A novel such as Boris Pasternak’s Dr Zhivago reminds us that while it is difficult to understand Zhivago’s experiences outside their historical setting, it is also difficult to interpret broader events without seeing them through the experience of individuals. What is missing from our scientific understanding of malnutrition and its health penalties is this kind of dynamic perspective. A disease such as diabetes emerges through both societal transformation and the life-course experience of an individual. Unfortunately, the early-life ‘secret’ of undernutrition may eventually reveal itself in the form of adult ill-health. Conceptually, therefore, novelists have addressed many of the issues I have grappled with, and they have done so rather more elegantly. Above all, novelists surely have a deeper understanding of the meaning of food than scientists. We can recast this book, therefore, as an effort to set the stories transcribed within our bodies in their broader societal context. As an undergraduate student in social anthropology at the University of Cambridge, I was encouraged by Keith Hart to read fiction as well as the conventional ethnographic literature. When I moved on to research in nutrition, I found that novels provided a unique unifying lens. Body composition, my specialist interest, may be likened to a physical ‘memory’ of past events. Our physical condition today reflects our cumulative nutritional experience.3 The fundamental relationship between society and metabolism transcends fiction. In Aldous Huxley’s Brave New World, for example, mass-consumption was elevated to the raison d’être of society, with the drug soma used to reduce consciousness of the prevailing emptiness. ‘Self-indulgence up to the very limits imposed by hygiene and

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Preface

xi

economics. Otherwise the wheels stop turning.’4 In the modern era, what scientists have failed to understand is the deeper politico-economic basis of both extremes of malnutrition. In Nineteen Eighty-Four, George Orwell offered a darker perspective: this time, that a perpetual state of war would justify extreme levels of control over individuals, a scenario achieved by the ‘surveillance state’.5 It is intriguing, first, that both of these societies were characterized by profound social hierarchy, and second, that life is steadily converging on fiction. Consumer society has indeed strengthened its metabolic grip in recent decades, while diverse forms of digital media subject us to covert observation and manipulation, concealed in the guise of endless consumer choice. And these traits are fundamentally connected, for processed foods and mobile phones are just two of many ‘gifts’ to society from the military–industrial complex. The role of nutrition in disciplining populations is no mere fictional scenario. Of course, where there is power there is also resistance, and human biology shows many layers of resilience against nutritional stress. My previous book explored how our body fat provides an overarching ‘energy insurance scheme’ while also fuelling functions such as growth, reproduction and immune defence.6 In the present book, I will pay particular attention to the role of the mother in buffering her offspring against ecological stress. In the thirteenth century, the Persian poet Jelaluddin Rumi described what the unborn baby might miss on account of such protection.7 Suppose one said to the fetus: ‘Outside is a beautiful world With mountains and oceans, Patchwork fields and fragrant orchards, A sky illuminated by the sun, Or the moon and countless stars. Bathed by breezes, Gardens host banquets and weddings. Why stay in your confining misery?’ But the fetus would not listen: ‘You are absurd and deceitful. I know only darkness. Outside the world has no scent or colour’.

If the fetus is oblivious of orchards and weddings, it is also substantially protected from the ravages of war and starvation. But such buffering is only partial, and if the mother herself is malnourished, then her ‘protection’ itself manifests as nutritional stress for the fetus. Historically, chronic undernutrition maintained control over those at the bottom of social hierarchies, and because it takes generations to resolve, it comes to represent a ‘metabolic ghetto’. This phrase is intended to highlight the ‘grip’ that hierarchies exert over nutrition and metabolism. Unfortunately, undernutrition is not the only such ghetto. Consumer society may seem the epitome of free choice, but it too has co-opted our metabolism for economic gain. In the modern era, entire populations are pushed to ‘over-consume’, generating another metabolically perturbed niche of obesity that may likewise take generations to resolve. Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:40:52, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959

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Preface

We have no hope of dealing with the global epidemics of diabetes and cardiovascular disease if we do not address the fundamental ways in which nutrition is used to discipline human behaviour. Why do we submit to such coercion? Carlos Gamerro offered an answer in his novel, An Open Secret.8 ‘The perfect crime is precisely the one committed in the sight of everyone – because then there are no witnesses, only accomplices.’ If malnutrition persists in ‘liberal democratic’ countries, it is because there is rather less liberty and democracy than we pretend. Nutrition is both a key locus of our collective disempowerment and a means for concealing its full magnitude. To participate in consumer society is to ‘consent’, and nicotine, sugar, caffeine and addictive digital technologies play a key role in manufacturing that consent. This book owes much to my family, who have always encouraged me to explore the world and to follow my interests. My academic career has enabled me to read diverse literatures and to participate in research studies with many wonderful colleagues across Europe, South America, Africa and Asia, giving me empirical experience of what I am trying to make sense of. I am particularly grateful to Mario Cortina-Borja, Carlos Grijalva-Eternod, David Leon, Emma Pomeroy, David Osrin, Graham Rook, Aubrey Sheiham, Meghan Shirley, Mario Siervo, Jay Stock, Julie Wallace and Elizabeth Wells for discussions and critique of selected chapters. Despite their support, specialists will no doubt find many errors in this book, or point to literature of which I am ignorant. My hope is that, though the facts must inevitably become outdated, the broader concepts will remain valid. I am extremely grateful for the support and patience of my editor, Katrina Halliday, at Cambridge University Press, and for the meticulous work of Victoria Parrin, Velmurugan Inbasigamoni, Richard Hallas and colleagues on the manuscript. Above all, my greatest support has come from Akanksha, who has read every chapter, made sure I kept women at the heart of the arguments, joined in the research efforts and periodically enticed me back to the mountains to regain the energy to write. May we always return to mountains and oceans, patchwork fields and fragrant orchards, and when day is done gaze up at countless stars. . .

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1

Introduction

I remembered the bombs, the incendiaries and the scattered bodies, and it occurred to me that living might be the price, not the reward of survival Stratis Haviaras – The Heroic Age

If the ever-obliging Martians agreed to review the current state of human nutrition, they would be forced to report a crisis. Although humans are numerous (around 7.3 billion), geographically widespread and able to live on average for about 68 years, almost half of those alive are either undernourished or overweight. Around 1 billion lack access to adequate food, and undernutrition is the primary reason why in some countries up to one child in five dies before five years of age. At the other extreme, roughly 2.1 billion are now overweight, with around 800 million adults clinically obese.1 In turn, excess weight is the strongest marker of a global epidemic of degenerative diseases and premature adult mortality. The Martians would probably consider malnutrition, encompassing both extremes of body weight, a defining characteristic of our species. The Martians would immediately recognize that, with minimal exception, humans practice agriculture rather than foraging for wild resources. But they could be forgiven if they reached another conclusion: that this system farms not only crops and animals, but also humans themselves, and is geared towards producing not only food but also power and wealth, all of which end up highly unevenly distributed. This, then, is a book about human nutrition and health. But if you are expecting a discussion of what foods make a healthy diet, how much physical activity should be undertaken each day or what is the ideal body weight, you will be disappointed. Such a book would presuppose that if we knew these ideals, all could readily adopt them. This book looks at nutrition and health from the reverse perspective: I want to address how our hierarchical societies undermine healthy living. I use the term ‘nutrition’ throughout this book very broadly, referring not only to food intake but also to physical activity patterns and the condition of the body in terms of its growth, composition and ability to resist infectious diseases. I want to understand why our nutritional status plays such an important role in the unequal distribution of illhealth. I will direct most attention to ‘chronic diseases’, such as obesity, diabetes, hypertension, cardiovascular disease and stroke, but I will also address undernutrition. These two types of malnutrition may both be considered ‘metabolic syndromes’ – one where the body receives inadequate nutritional fuel, and the other where it is unable to accommodate excess circulating fuel.

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2

Introduction

Table 1.1. The United Nations Millennium Development Goals 1. Eradicate extreme poverty and hunger 2. Achieve universal primary education 3. Promote gender equality and empower women 4. Reduce child mortality 5. Improve maternal health 6. Combat HIV/AIDS, malaria and other diseases 7. Ensure environmental sustainability 8. Global partnership for development

My primary thesis is that the relationship between nutrition and health is deeply embedded in power relations, and that it always has been. Only if we understand this broader scenario can we assess how contemporary capitalism shapes our health through the medium of nutrition. Indeed, we will not fully understand the nature of capitalism until we look inside the body. Human malnutrition is increasingly recognized as a global problem. In 2000, the United Nations established eight ‘Millennium Development Goals’, intended to mobilize unprecedented national and institutional effort to combat poverty and illhealth (Table 1.1).2 Nutrition clearly transcends these goals, yet one could also argue that it is explicitly acknowledged only in the first of them, and has thus been rendered relatively invisible. Chronic diseases are absent from these goals, despite being closely associated with poverty, unhealthy lifestyles and unsustainable use of environmental resources. Even if we do acknowledge the importance of nutrition for health, do we know what must be done to resolve malnutrition? A vast amount of scientific and policy research has been conducted. Over 2 million scientific articles have been published on the topic of cardiovascular disease alone, though far fewer on undernutrition. Despite this effort, chronic undernutrition remains widespread in most global regions, while the numbers affected by obesity and chronic diseases are rapidly increasing worldwide. Looking beyond obvious and immediate causes such as unhealthy diets and living conditions, the last decade has seen particular emphasis on the ‘social determinants’ of ill-health and premature mortality.3 This approach, initially developed to address highincome countries, recognizes that the primary factors predisposing to common forms of ill-health cluster unequally across social hierarchies. Substantial research has shown that the influence of hierarchical position on health is mediated by the stress response, which in turn is shaped by socio-environmental factors such as access to healthcare and employment, the quality of the working environment and the magnitude of community social support. Exposure to adverse conditions in early life is particularly important, generating lifelong health penalties. This approach also acknowledges the mediating role of nutrition: those lower in social hierarchies have poorer diets and less opportunity for leisure-time physical activity, while exposure to harsh economic and social conditions drives high use of alcohol, drugs and tobacco. In high-income countries, therefore, obesity and chronic diseases cluster among the poorer groups.

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Introduction

3

This paradigm offers a valuable lens through which to focus on contemporary health inequalities in countries such as the UK. For example, London is often described as a collection of small villages, but despite being close together as the crow flies these localities differ remarkably in their quality of life. A recent study found that travelling east from Westminster to Canning Town on the Underground, the decline in male life expectancy between these two boroughs is equivalent to a fall of 0.75 years for each station passed on the way.4 Male life expectancy at birth is 77.7 years in Westminster, but 71.6 years just a few miles away in Canning Town. Female life expectancy declines from 84.2 to 80.6 years over the same distance: half a year per station. This social gradient within a single city is merely a local manifestation of a broader national pattern. In England overall, the poorest groups live for 10 years less on average than the most affluent.5 Moreover, they are more likely to suffer from chronic diseases and acquire them at younger ages, so that they experience 20 fewer years of healthy life on average than the most affluent.6 Social hierarchies thus have profound implications for health and longevity. Despite the strengths of the ‘social determinants’ paradigm, it leaves several crucial questions unanswered at a global level. First, why are humans so prone to hierarchical societies in the first place? Second, whatever the role of psychosocial stress, why should hierarchies leave such profound imprints in nutritional aspects of health? And third, why do social gradients in health in low- and middle-income countries show striking differences from those in high-income countries? In low- and middle-income countries, lower socio-hierarchical position is undoubtedly associated with poor health, in particular mediated by undernutrition. But in these countries, obesity and chronic diseases remain commoner among the more affluent sections of society, though that does not mean they are entirely absent from poorer groups.7 In other words, being higher in the hierarchy in these countries elevates risk of the same diseases that are most common in groups lower in the hierarchy in high-income countries. Clearly, these diseases have no uniform association in humans with wealth, or with socio-hierarchical position. There is something more complex going on, and that is the kernel of this book. My question is very simple: in any population, how much agency do individuals really have to achieve nutritional health? The answer is anything but simple. Associations between nutrition, health and power relations do not manifest on an immediate basis in terms of current behaviour. Rather, both undernutrition and chronic diseases emerge through cumulative processes stretching across lifespans and generations. The power relations experienced across such lengthy periods may change profoundly. Furthermore, many layers of power are built into the structure of society and are relatively well concealed. In many ways, when it comes to our malnutrition, we have been co-opted to ‘demand our own oppression’. Indeed, I will argue that nutrition is a unique medium that enables this kind of manipulation. To develop this thesis in detail, I will bring together a number of related arguments in a multidisciplinary approach (Figure 1.1). As I will show, we can learn much about the relationship between malnutrition and ill-health by studying human physiology, or developing an evolutionary perspective, or examining the contribution of societal factors. One might assume that each of these contributes part of a broader picture, but Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:39:20, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.002

4

Introduction

Physiology

Multidisciplinary approach Evolutionary biology Figure 1.1.

Society

The multidisciplinary approach adopted in this book.

the logic of a multidisciplinary approach is different: we need to integrate these three approaches, so that together they contribute more than the sum of their parts. On this basis, I can explore how the organization of society shapes our health through nutritional mechanisms. If we can learn how ‘wealth-power dynamics’ generically shape our behaviour and physiology, then we can identify what capitalism does specifically in this context. I hope that this approach will offer a new perspective not only on malnutrition and chronic diseases, but also on capitalism itself. Nutrition and power are always linked. If contemporary capitalist power relations are driving epidemics of obesity, diabetes, stroke and heart disease, we should not forget that the power relations of earlier eras drove chronic undernutrition and associated health penalties. It is as if history is cyclical, and that the fundamental problem of malnutrition is never solved – but this is no accident. I will start this book by showing how the control of food has long been used to coerce people, and that this scenario has persisted through the twentieth century and into the twenty-first. Bizarrely, this historical account will lead us directly to the emergence of public health nutrition. But we will also see that in the era of public health, far from dissolving the link between nutrition and coercion, we have actually magnified and diversified it.

Nutrition as a Tool of Control To highlight a number of issues relevant to the nutrition–power nexus, I begin with a narrative of one particular period, when nineteenth-century European powers were engaging in the ‘scramble for Africa’. The reason why I first focus on the Anglo-Boer War in this period will become clear shortly. On 22 January 1879, British troops in southern Africa suffered a massacre at the Battle of Isandlwana. A force of 7000 men had recently invaded the kingdom of King Cetshwayo, attempting to put into effect a South African federation, like that already established in Canada. Standing in the way of this vision, the Zulu kingdom was the first target. Grossly underestimating the proficiency of their foe, the battle was a disaster for the British, with the death of over 1300 troops. To maintain face, however, a second

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Nutrition as a Tool of Control

5

invasion with greater firepower followed a few months later, resulting in the defeat of Cetshwayo at the battle of Ulundi.8 Defeat at Isandlwana came as a sharp shock, for the scramble for Africa had previously resulted in the acquisition of vast tracts of territory at almost negligible cost in British lives. Only at Khartoum in 1885 had the demise of General Gordon and his garrison shown that incursions into African territory might be repelled with decisive military force. Since the unofficial start of the scramble in 1876, European powers had routinely conquered territories and populations with relative ease, initially through establishing opaque ‘trading treaties’ and then through the enforcement of their strategic aims at gunpoint. Even when Africans had access to firearms, such as matchlock and flintlock rifles, they remained at a major disadvantage against the early Gatling and Maxim guns that could generate the firepower of thirty individual rifles. In German East Africa in 1905, an armed rebellion was easily put down using machine guns, after which the troops celebrated the day’s shooting with champagne. Artillery was regularly used to breach defended settlements, regardless of the indiscriminate loss of life.9 The Zulu kingdom did not recover, but within little more than a decade, British forces encountered a much graver setback when they attempted to invade the fledgling Boer republics of Transvaal and Orange Free State. The Transvaal with its gold mines was a notable jewel in the African crown: its incorporation within a southern African federation under the British flag would have been the climax to a twenty-year campaign to seize the greater slice of what King Leopold of Belgium had termed ‘this magnificent African cake’.10 Britain wanted a ‘Cairo-to-Cape’ railway, opening up the entire continent for ‘trade’ opportunities that would bring riches to the new capitalists, although substantially less to the indigenous populations. This time the war lasted for three years and resulted in substantial loss of life on both sides. The Boers had modern rifles and were excellent marksmen, while the British troops were poorly prepared and suffered from high rates of infectious disease. The Boers initially scored several victories, and though they eventually lost formal control of their territory, resistance continued through guerrilla warfare. In response, the British adopted a scorched earth tactic, stripping the Boer farms of their stock animals and rounding up the families of the rebels for incarceration in concentration camps (Figure 1.2). To restrict guerrilla movements, the farmland was criss-crossed with barbed wire and concrete blockhouses, manned by African troops. In the concentration camps, semi-starvation combined with endemic diseases such as typhoid, dysentery and measles to cause appalling mortality rates. The rations available for ‘genuine refugees’ were reduced in the case of women whose male kin were still fighting the British, so that undernutrition of civilians was deliberately used as a military strategy.11 The total death toll of the war is estimated to have included ~14,000 Africans despite their not being the primary aggressors or defenders, ~20,000 British and ~7000 Boer men, and ~28,000 Boer women and children in the camps. The disproportionate mortality of women and children was noted by the future British prime minister David Lloyd George: ‘The fatality rate of our soldiers on the battlefields, who were exposed to all the risks of war, was 52 per thousand per year, while the fatalities of women and children in the camps were 450 per thousand per year.’12 Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:39:20, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.002

6

Introduction

Figure 1.2.

A child dying of malnutrition in Bloemfontein concentration camp during the Anglo-Boer War. Wikimedia commons.

The Boer War represents a potent example of the fundamental connection between nutrition and power that lies at the heart of this book, but it is anything but unique. Elsewhere in Africa, alongside military force, mass starvation was widely used by European forces in the colonial era to defeat and subjugate indigenous populations. In southern West Africa, now Namibia, the German Imperial army rounded up thousands of rebellious Herero and left them to starve in the desert, and similar approaches were adopted in German East Africa, now Tanzania.13 Through such activities, European nations were merely indulging in the application of modern technology to an age-old component of the empire-building toolkit: control of food represents control of people. In ancient times, direct physical control of large populations was laborious and costly. A rare example is Hadrian’s Wall, built from coast to coast across the north of England during the Roman era (Figure 1.3). For 250 years, the wall not only protected Roman territory from raids by the northern Picts, but also enabled taxation of those crossing the frontier in either direction. Such physical barriers were generally non-viable, however, and armies could typically invade neighbouring territory relatively easily. To resist such physical oppression, early settlements developed fortifications in order to protect their populations. These had one fatal flaw: facing in both directions, walls made it easy for aggressors to impose the ultimate form of coercion, starvation.

Sieges and Starvation Sieges and starvation have been used to exert social control for millennia in all major global regions. Already by 3500 BC, many of the small villages scattered across the Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:39:20, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.002

Sieges and Starvation

Figure 1.3.

7

Hadrian’s Wall, built to separate the north of England from Scotland in the second century AD. Copyright of the author.

Indus Valley floodplain in south Asia had developed fortifications, showing that attacks on the food stores arising from early farming pre-dated the emergence of larger cities. In Scotland, numerous fortified farmsteads from the Iron Age can still be seen in the highlands and islands (Figure 1.4). These ‘brochs’ comprised double-walled stone towers that appear to have supported several internal floors, and may have belonged to elite farming families, combining a defensive role with the ability to signal status and wealth.14 Early urban settlements in the Middle East, Indus Valley and China all incorporated huge defensive walls to prevent plunder. Inside such defences, food reserves could be carefully stockpiled to withstand lengthy assaults. When an Arab army surrounded Constantinople (now Istanbul) from 717 to 718 AD, the Byzantine Emperor had sealed its granaries with sufficient food for up to three years.15 By and large, such early defences were physically successful. Walls of sun-baked bricks or wood generally proved impregnable, though the Spartan King Agesipolis ingeniously captured Mantinea in 385 BC by diverting a river into the city, dissolving the bricks back into mud. Starvation was usually the only feasible strategy of assault, and warfare was restricted to the summer months, so that the besieging army could live off the crops and animals outside the city walls. The balance of power shifted in favour of the attackers only with the invention of multi-storey siege towers in the fourth century BC. From these structures, troops could fire down at the defenders and gain access to the upper walls. By the Roman era, siege warfare had evolved well-established techniques for attack and defence. For example, the end of the Gauls’ resistance to the Romans

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Introduction

8

(a)

Figure 1.4.

(b)

Remains of the fortified Iron Age farmstead or ‘broch’ of Dun Telve from Glenelg, Scotland (dated 500 BC to 100 AD), showing (a) the well-defended entrance and (b) the thick outer wall. Copyright of the author.

came with the siege of Vercingetorix in the fort of Alesia, by Julius Caesar in 52 BC. Caesar walled his army in between inward fortifications facing the fort, and an outward stockade preventing the arrival of a relief force. Inside the fort, 80,000 defenders competed for food with many civilians, and though the soldiers eventually evicted the women and children, Caesar was unmoved and left them to starve in front of his lines. When the Gallic relief force was in due course annihilated, Vercingetorix had no option but to surrender.16 Individual sieges could be combined into a more sophisticated strategy. The Mongols sometimes sacked a number of smaller cities so that the refugees, falling back on a larger city, would deplete its food stores faster and hence accelerate its capitulation. They were also known to catapult plague corpses over the city walls, using disease to hasten the garrison’s demise.17 Sieges were routine in medieval Europe, precipitating a surge in castle-building. Figure 1.5 shows the assault of William of Normandy on the motte-and-bailey castle of Dinan in the eleventh century AD, shortly before he invaded England. The only redeeming feature of this scenario was that since the castle was the primary objective, it was less common for entire cities to be surrounded and starved. Nevertheless, civilian populations were frequently caught up in blockades. In the siege of Rouen by the English in 1418, we get some idea of the consequences of food supplies failing among the

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Starvation in Modern Wars

Figure 1.5.

9

Siege of the castle of Dinan by William of Normandy in the eleventh century AD, from the Bayeaux Tapestry. Wikimedia commons.

French defenders: ‘They ate up dogs, they ate up cats, they ate up mice, horses and rats.’ Cannibalism was not unknown during lengthier blockades. Other historical documents record how defeated defenders emerged with heads bowed, thin and deathly pale.18 Eventually, castles became redundant, too easily circumvented, or destroyed by modern artillery. In 1940, the defensive ‘Maginot line’ of forts in France was simply bypassed by mechanised German forces. But this offered no escape from the use of starvation as a weapon of war. Instead, in the twentieth century large cities once again became key battlegrounds because they were major centres of population and industrial activity, and because it was difficult to dislodge well dug-in troops. The Second World War reminds us that modern nations may still go to war over food, while using food restriction as a weapon of war.

Starvation in Modern Wars In her book The Taste of War, the historian Lizzie Collingham described how the territorial aggression of Germany and Japan in the mid-twentieth century stemmed in large part from the desire of these countries to construct large agrarian empires in neighbouring countries, in order to gain independence within a global economic system that favoured the US and the British Empire.19 As war broke out, nutrition became a key weapon on all sides. After the end of the First World War, Britain had maintained a food blockade on Germany in order to force her to accept the unfavourable terms of the Versailles treaty. In the following decades, Hitler’s National Socialist Party prioritized industrial independence,20 while making plans to acquire huge areas of farmland (lebensraum) Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:39:20, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.002

10

Introduction

to enable agricultural self-sufficiency. Central to these aims was the ‘Hunger Plan’ of the Minister for Food and Agriculture, Herbert Backe, who proposed to eliminate 30 million Soviet peasants, thus freeing up increased volumes of food for the German population. In 1941, Hitler explicitly proposed that ‘what India was for England, the territories of Russia will be for us’.21 Across the other side of the world, Japan had noted Germany’s vulnerability to blockade, and made its own plans for a self-sufficient food economy. After invading Manchuria in 1931, Japan scaled up its acquisition of Asian territory in concert with Hitler’s early conquests in Europe. Food blockades were used throughout the war as a routine military tactic, at huge cost to civilian populations. Hunger was systematically exported by Germany and Japan to their occupied empires, while the Allied powers made extensive use of blockades to weaken their opponents’ military capabilities. The distribution of food eventually influenced the outcome of the conflict in both Europe and the Far East. Japan had grossly miscalculated its vulnerability to naval blockade, and both its soldiers and its civilian population experienced starvation as the war progressed. Britain, in contrast, benefitted from the industrial might of the US, which built new merchant vessels faster than the German U-boats could sink them, and shipped vital supplies across the Atlantic. The height of Japanese children fell drastically during the war, whereas in Britain there was no detectable decline, and infant survival even improved.22 The 20 million civilian deaths attributable to starvation during this conflict exceeded the 19.5 million deaths from combat. While attention has deservedly been directed to the 6 million Jews liquidated in the Holocaust, civilians in general paid a horrific toll in many different countries. By the end of the war, around 11 per cent of the Greek population had starved to death, victims of the combination of an Allied blockade and German retribution for resistance activities. In the Soviet Union, millions died in besieged cities such as Leningrad, Stalingrad and Kharkov (Figure 1.6), prior to more intensive German efforts to eliminate the Jewish population and Soviet prisoners of war. In total, the war killed about 14 per cent of the pre-war Soviet population, equivalent to some 25–30 million individuals, of whom the majority were civilians dying most commonly from malnutrition. Nor were the combatant nations the only ones affected: by the end of the war, approximately one-third of the world’s population was facing severe food shortages.23 From the second half of the twentieth century, the increasingly pivotal role of markets in food supplies has meant that rural and urban populations alike remain vulnerable to blockades. In the Nigerian Biafran war in the late 1960s, humanitarian organizations continued to find that most of those requiring medical aid were undernourished civilians, especially children. In the absence of outright war, famine could still be co-opted to subjugate large populations, as for example by Stalin in the Ukraine (1932–3) when around 7 million peasants starved to death during the imposition of collectivization.24 In 1981, the economist Amartya Sen argued that famines were political rather than natural events, in the sense that they were failures of food distribution, not of food production. In 1996, a UN charter outlawed the control of food distribution for political Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:39:20, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.002

Starvation in Modern Wars

Figure 1.6.

11

Civilians in the siege of Leningrad, 1941–2. Wikimedia commons.

ends,25 yet there are few signs that hunger has been dropped as a weapon of mass control. A report published in 2001 highlighted the continued imposition of food restriction for political and military ends in each continent in the early twenty-first century.26 The effects of wartime hunger propagate not only across geography, but also across time. A classic study from the Second World War showed that maternal famine impacts the unborn fetus, affecting its health into adult life.27 Over half a century later, unborn babies were still experiencing wartime starvation. The siege of Sarajevo from 1992–6 was associated with increased perinatal mortality, while after the imposition of sanctions on Iraq in the 1990s, the prevalence of low birth weight was estimated to have increased sixfold, due primarily to maternal malnutrition.28 Many of the nutritional costs of conflict are paid by future generations.29 Starvation and warfare have thus gone hand in hand as the two traditional means for controlling large populations, widely used in tandem. This strategy has been acknowledged explicitly by states and rulers. In the early 1980s, the Guatemalan dictator Rios Montt adopted a scorched earth strategy against civilians, known as ‘frijoles y fusiles’ (beans and bullets), summed up in his statement: ‘if you are with us, we’ll feed you, if not, we’ll kill you’. The Mexican President Porfiro Diaz had employed a very similar strategy in the late nineteenth century, known as ‘pan o palo’ (bread or stick).30 At the 1974 World

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Introduction

Food Conference in Rome, US Agriculture Secretary Earl Butz openly described food restriction as a weapon, referring to it as ‘one of the principal tools in our negotiating kit’.31 Much of this book will return to the fundamental connection between nutrition and power. For now, this wider context reminds us that the Anglo-Boer War, with which this historical review began, seems just like countless other wars: a power contest that exposed huge numbers of people to physical violence, nutritional stress and infectious disease, killing tens of thousands in the process. But there is something else very important about the Anglo-Boer War, for it was this conflict in particular that drew the British government’s attention to the importance of nutrition for good health.

Nutrition and Healthy Development Even as thousands of Boers suffered malnutrition and disease in the new concentration camps, back in Britain the disastrous military campaign provoked open discussion of the physical quality of the British population. During a recruitment drive for the war between October 1899 and July 1900 in Manchester, 60 per cent of those who had volunteered for enlistment had been rejected for their poor physical condition. Even among those accepted, only a minority were found to achieve the ‘standard of muscular power and chest measurement’ required by the military authorities for active duty, and there was little reason to believe that men from other regions were in better condition.32 ‘Now,’ declared the British Medical Journal in an editorial entitled ‘Physical Degeneration’ in 1903, ‘more than at any other time in the history of the British people, do we require stalwart sons to people the colonies and uphold the prestige of the nation. . .’.33 The British government was rapidly realizing that health was a major political and economic issue, and a potential national ‘resource’ that could be directed to the imperial programme. The evidence of physical deterioration attracted attention from several interest groups, each of them concerned with the implications of poor population health.34 By the late nineteenth century, much attention was already being directed to the miserable condition of the British working class, which Friedrich Engels had described in detail in 1844, and which Karl Marx had subjected to political economic critique in Das Kapital, published in 1867.35 In opposition to the proponents of laissezfaire economics, various individuals and organizations attempted to improve squalid living conditions. The troubles of the Anglo-Boer War merely brought the issue of urban poverty to wider attention by highlighting particular costs, inspiring pioneering efforts in the new arena of ‘public health’. In this respect, Britain was not alone. Following the American Civil and FrancoPrussian Wars, nineteenth century statesmen of many countries were acutely aware that future international conflicts would be resolved by large armies recruited primarily from the working class. In Britain, it was clear that undernourished men would not last long against Germany, with which war seemed increasingly likely as imperial competition intensified.

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Nutrition and Healthy Development

13

As noted by the historian Deborah Dwork, the paradox that public health efforts might be stimulated by a need for soldiers was not specific to the Boer War. In 1914 a physician emphasized the importance of maintaining the birth rate, on the grounds that ‘babies . . . are the true dreadnoughts of the nation’.36 In 1917, a National Baby Week was held to publicize the importance of infant health. During an address to the Fulham Babies Hospital, the Bishop of London echoed Lloyd George’s concerns from two decades earlier, noting that ‘while nine soldiers died every hour in 1915, twelve babies died . . . so that it was more dangerous to be a baby than a soldier’.37 Writing just before the Second World War, the pioneering public health physician Sara Josephine Baker put it even more bluntly: ‘When a nation is fighting a war or preparing for another. . . it must look to its future supplies of cannon fodder.’38 Throughout this period, investment in babies was explicitly analogous to investment in armaments. Nor is this scenario particular to modern times. In the fourth century BC in the military Greek state of Sparta, breast feeding for two years was required by royal decree, in order to ensure a healthy fighting force a generation later. Similarly, adolescent girls were encouraged to undertake physical training, to bear strong sons (Figure 1.7).39 More

Figure 1.7.

Bronze figure of a running girl from Greece, about 520–500 BC, thought to originate from Sparta. © Trustees of the British Museum.

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14

Introduction

generally, early armies also looked after their soldiers and invested in public health. The forts defending the Roman Empire were built to a common plan across Europe, and were systematically equipped with a hospital, granaries to ensure high quality food supplies, and even latrines flushed by rainwater, to minimize the burden of infectious disease. During the Second World War, nutritionists in both Britain and Germany continued to study the nutrient needs of specific groups such as soldiers, industrial workers and pregnant women, even as their governments continued to use food blockades as a military strategy against the enemy.40 At the German Institute for the Physiology of Work, Heinrich Kraut calculated that on top of basal energy requirements of 1800 calories per day, hard labourers required an additional 1800–2400 calories to support their physical activity.41 These calculations fed directly into Backe’s ‘Hunger Plan’, which aimed to supply at least 3000 calories a day to each of Germany’s 9.5 million troops.42 With industrialization and modern nationalism in Europe, therefore, came growing awareness of the importance of nutrition and health for national ‘productivity’, defence and imperial ambition. Critically, however, these public health efforts at home contrasted starkly with the treatment of colonized populations overseas.

Nutrition and Underdevelopment The period during which the British government became aware of the importance of early-life nutrition for long-term health was likewise a defining period in the nutritional experience of a huge proportion of the world’s population. This was the period that saw the emergence of the ‘third world’, though it would not be described in this way for another half century, in the context of Cold War geopolitics. The soldiers so important to the Boer campaign were merely one contingent of broader British efforts to enforce what the historian Mike Davis termed the ‘structural adjustment’ of the Victorian world economy.43 As industrialization consolidated, European countries sought cheap raw materials for their new factories, and food supplies for their growing urban labour forces. Overseas markets for the new industrial goods were likewise key to economic growth. On both grounds, European countries demonstrated a voracious appetite for overseas territories and populations over which they could exert economic influence. By the eve of the First World War, Britain and France had sufficient imperial assets to more than compensate for their trade deficits. Rent, dividends, royalties and interest flowed back from colonial labour forces, enabling reinvestment in further foreign assets.44 It was Germany’s lack of opportunity for such overseas wealth extraction that persuaded her to invade her neighbours. Already the formal ruler of India from 1858, after superseding the East India Company, Britain eventually acquired half the territory of Africa and numerous other territories in the middle East, Pacific and Caribbean, to join her dominions in Canada, Australia and New Zealand (Figure 1.8). Other European imperial powers carved up the rest of Africa in the ‘scramble’, just as they had been doing in Asia in earlier centuries. Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:39:20, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.002

Nutrition and Underdevelopment

15

Table 1.2. Estimates of famine mortality during severe droughts in the Victorian eraa

Brazil China India a

Figure 1.8.

1876–78

1899–1900

0.5–1 million 10–20 million 6–10 million

1 million 10 million 6–19 million

Davis, 2002

Territory of the British Empire, not necessarily held simultaneously. (Wikimedia Commons).

Very few non-European countries escaped formal occupation, and even those were not immune to imperial influence. Latin America, though largely independent of Europe by the early nineteenth century, remained vulnerable to the same global influences. The obligation to pay imperial taxes forced farmers across the globe into the new market system.45 The enforcement of a ‘liberal’ world economy, Davis argues, made tropical populations devastatingly vulnerable to a series of severe climate shocks, now known as El Niño events. Even as the national recruitment drive of 1899–900 was highlighting the poor nutritional status of young British men, extreme droughts were killing millions in India, from the Punjab in the north to Madras (now Chennai) in the south. Similar famines struck many other global regions, including southern Africa and the Sahel, China and Latin America, with the same effect (Table 1.2). Historical research shows that although droughts regularly caused food shortages and famines in many global regions, the death toll was substantially exacerbated by Victorian policies that strengthened food security in the imperial countries at the direct cost of health and lives in the colonies.46 In the last few years of the nineteenth century, for example, even as India experienced several famines in quick succession, vast quantities of wheat were still being exported from India to Britain, accounting for approximately one-fifth of total British wheat consumption.47 Famine relief was Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:39:20, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.002

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Introduction

considered at odds with the prevailing principles of ‘laissez faire’ economics. When American farmers from Kansas sent a shipment of grain to their starving Indian counterparts, the British promptly taxed it.48

Nutrition as Discipline This very brief historical review has highlighted several disparate scenarios – sieges in antiquity and the middle ages, the Victorian scramble for Africa, the Second World War, and the emergence of the so-called ‘third world’ – that nevertheless show a unifying theme: the imposition of hunger as a means to exert social control. Across geography, society and history, nutrition has provided an ever-reliable means to discipline populations on a variety of scales. So far, I have focused on the larger scale, on efforts to subjugate entire communities or countries, but the same issues pertain within communities and families in relation to the daily organization of social life. In the middle ages, for example, European peasants were obliged to have their corn ground at the manorial lord’s mill. Millers were widely considered to exploit this power over their clients, especially women. The following poem seems light-hearted, but it reminds us of the asymmetric relations that characterized access to food on a daily basis. A brisk young lass so brisk and gay She went unto the mill one day. . . There’s a peck of corn all for to grind I can but stay a little time. Come sit you down my sweet pretty dear I cannot grind your corn I fear My stones is high and my water low I cannot grind for the mill won’t go. Then she sat down all on a sack They talked of this and they talked of that They talked of love, of love proved kind She soon found out that the mill would grind. . .49

In the modern era, nutrition remains embedded in multiple dimensions of power relations, at the level of both family and society. Since antiquity, some have inverted the relationship, adopting hunger strikes in the hope of forcing a political response.50 The effects of nutritional discipline may be long-lasting, and indeed transgenerational. Today, childhood undernutrition remains concentrated in the countries that were subordinated to European and American interests in the colonial era (Figure 1.9). This cannot be considered a ‘natural’ geographical pattern, for a recent study by the World Health Organization found that across diverse countries, children from privileged backgrounds grew relatively similarly.51 Global inequity in childhood malnutrition is in part the legacy of past efforts to control colonial populations through nutritional means, complemented by inadequate policy responses subsequently. Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:39:20, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.002

Nutrition as Discipline

1.2 m 1.7 m

High income countries

0.2 m

0.7 m 1.8 m

Latin America/Caribbean

Wasting Underweight Stunting

5.1 m

0.1 m

Oceania

13.4 m

Africa

0.5 m

7.1 m 36.1 m

Asia

17

69.1 m

95.8 m

27.9 m 56.3 m

0 Figure 1.9.

5

10

15 20 25 Prevalence (%)

30

35

40

Prevalence of stunting, underweight and wasting across the main global regions. Numbers of children affected (millions) are given above the columns. ‘Stunting’ refers to inadequate height, while ‘wasting’ refers to severely inadequate weight-for-height. Data from Black et al., 2013.

Despite public health efforts, ~165 million children remained stunted in 2011, while ~52 million were wasted. The aggregate effect of undernutrition, summing together fetal growth retardation, infant growth faltering and inadequate nutritional intakes, was estimated to cause over 3 million deaths annually, equivalent to 45 per cent of the global burden of child mortality.52 Among those who survive to adulthood, chronic energy deficiency and micronutrient deficiencies remain common in these countries.53 But the situation in low- and middle-income countries is far more complex than widespread undernutrition, and nowhere is this more evident than India. On the one hand, India is home to over 40 per cent of the world’s malnourished children, and many adults remain underweight.54 On the other hand, rapid changes in diet and activity patterns in urban populations are associated with abdominal obesity and burgeoning rates of diabetes and heart disease.55 An estimated 65 million people in India were suffering from diabetes in 2013.56 The same scenario is emerging in other populations undergoing rapid urbanization and modernization, such as in China, Brazil and many sub-Saharan African countries.57 With a national adult prevalence of around 10 per cent in 2011, China may have as many as 90 million diabetics.58 Already, the majority of chronic disease cases occur in low- and middle-income populations, those that still bear the greatest burden of undernutrition and infectious disease.59 Why should India, still heavily burdened by undernutrition, have rapidly become a global ‘diabetes capital’ as well? More generally, why are chronic diseases so unevenly distributed within and between populations? At a proximate level, differences in physiology are relevant: for example, in comparison with Europeans, Indians tend to develop diabetes and cardiovascular disease at lower thresholds of overweight, and at

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Introduction

younger ages.60 But while such physiological differences may incorporate broader patterns of evolutionary adaptation to contrasting environments, the imprint of power relations must not be discounted.

The Aims of this Book The organization of society has a dynamic two-way association with the distribution of malnutrition and ill-health. As of now, scientists recognize that the hierarchical structure of society influences the distribution of malnutrition and ill-health, but they have paid far less attention to the instrumental role of nutrition in constructing social hierarchies. For example, the United Nations Children’s Fund (UNICEF) emphasizes various ‘basic causes’ of child malnutrition, such as lack of financial and socio-economic resources available to households, and inadequate political will at the national level, but stops short of discussing the geopolitical interests that powerfully structure the global economy of food.61 Yet it is primarily through control over nutrition that the international hierarchical order is maintained. Failing to recognize this two-way relationship, scientific solutions to each of chronic undernutrition, obesity and chronic diseases tend to be technical rather societal. Policymakers consider that global undernutrition will be resolved by technological advances in the production of food, along with more efficient markets for distributing it. The global epidemic of chronic disease is to be tackled through novel pharmaceutical treatments and the reorganization of lifestyles at the level of the individual. Despite some progress, these efforts are failing to resolve global malnutrition. Only a few scientists have attempted to theorize the complex relationships between society, health and disease. The ‘social determinants of health’ paradigm of Michael Marmot and colleagues is one such effort, while Richard Wilkinson and Kate Pickett have argued that unequal societies impose health penalties on all social groups.62 While path-breaking, these efforts still consider nutrition residual to ‘broader social forces’, and hence do not address the role of nutrition in structuring hierarchical orders. Researchers such as Marion Nestle, David Stuckler and Kelly Brownell have described the powerful grip of food industries over consumer behaviour, while Robert Albritton examined the influence of capitalist economics on both food production and consumption.63 More generally, classic work by Lesley Doyal and Imogen Pennell highlighted numerous ways in which capitalism and health are antagonistic, and specifically explored nutrition in this context.64 I will revisit many of those issues, although the distribution of malnutrition and degenerative diseases has changed profoundly in the intervening 35 years. I aim to explore this dynamic link between nutrition and society in order to deepen our understanding of the fundamental nutritional basis of health. I will focus in particular on chronic diseases, simply because they have become the dominant cause of morbidity and premature mortality worldwide. Through these diseases, the penalties for malnutrition stretch across the adult life-course. Conditions such as diabetes, stroke, angina and chronic lung disease can diminish quality of life for decades, before provoking Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:39:20, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.002

The Aims of this Book

19

premature mortality. For those most incapacitated, ‘. . . living might be the price, not the reward of survival’. However, it is also clear that chronic diseases do not strike people with equal likelihood: they occur with greater frequency in those previously malnourished, or whose parents were malnourished. This reminds us that nutrition embodies disempowerment across generations. My message is stark: if we cannot define the structural link between nutrition and power relations, we will never gain the power to resolve global malnutrition and its numerous health costs. The first part of the book describes the physical manifestation and life-course aetiology of chronic diseases. I introduce the concept of homeostasis, whereby the body maintains itself in working order. I show how chronic diseases develop when homeostasis is impaired, and how this degeneration is shaped by multiple stresses acting both during development and during adult life. I use this approach to appraise the variability in chronic disease risk that is evident across social hierarchy, and across populations and ethnic groups. This allows us to see what chronic diseases are, and how they emerge through the life-course, but it does not explain why humans are so susceptible to their development. In the second part of the book, I develop an evolutionary perspective to elucidate how the body makes ‘physiological decisions’ throughout the life course. I describe the environments in which humans and their ancestors evolved, and how our biology responded to these stresses. I will emphasize a range of components of plasticity in both metabolism and social organization, helping understand the fundamental link between social hierarchy and malnutrition. Using the metaphor of the ‘metabolic ghetto’, I illustrate this link with several historical examples. Nevertheless, this evolutionary approach still leaves crucial questions unanswered. Why is the chronic disease epidemic emerging now, and what can explain its paradoxical affliction of the poor in rich nations, and the rich in poor nations? The third part of the book therefore considers the evolution of human society following the emergence of agriculture. I show that changes in the structure of society were invariably orchestrated through the reorganization of nutrition. In one sense, the political economy of capitalism is just part of the general scenario, but there is also something different: uniquely, capitalism gave rise to a new ‘double burden’ of malnutrition – the co-existence of undernutrition and overweight in populations and individuals. What can we learn from this history, in order to improve future success in the prevention of chronic diseases? The final part of the book integrates the three previous sections by summarizing our physiology, behaviour and political economy as a series of ‘dynamic games’. This then offers the possibility of developing game-theoretical approaches to look for new solutions to the ongoing problem of malnutrition. Readers may wonder why my perspective makes substantial use of economic language, given that I criticize our prevailing political economic order. ‘Leave economics out of biology’, argued an anonymous reviewer of my work on body fat as a form of physiological capital.65 One might as well suggest that we leave mathematics out of biology. Economic terminology and language are invaluable for considering many biological issues: investments, trade-offs, pay-offs, conflicts of interest and the social

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20

Introduction

coordination of behaviour. Ironically, economic ideas may prove more successful at explaining what goes on in the body than what goes on in society. Above all, far from evolutionary biology offering a ‘legitimization’ of capitalism, my conclusion is the opposite: capitalism inherently requires coercion and violence for its persistence in society, and explicitly uses nutrition to achieve its disciplinary effects. This means that the violence increasingly leaves its legacy inside the body: in malnutrition, perturbed metabolism and chronic diseases.

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Part I

The Physiology of Chronic Disease

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2

Models of Chronic Disease

If we want things to stay as they are, things will have to change Guiseppe di Lampedusa – The Leopard

The idea that our nutritional status and lifestyle shape our health is nothing new, for both chronic diseases and potential treatments were recognized in antiquity. The Ebers papyrus from ancient Egypt, named after the archaeologist who unearthed it, dates from around 1500 BC, but much of it appears to have been copied from writings dating from earlier periods. Among the diseases described in a passage from about 3400 BC was a condition of excessive urination. The suggested remedy was as follows: A measuring glass filled with water from the bird pond, elderberry, fibres of the asit plant, fresh milk, beer-swill, flower of the cucumber, and green dates.1

Whether this remedy had any success is not known, but the disease was most probably diabetes, where the body is unable to regulate blood glucose levels, and excess glucose is expelled through increased water turnover. Nor was Egypt unique: ancient Indian texts record that the urine of some individuals was sweet, and would attract ants.2 In the early twentieth century, pioneering analyses of Egyptian mummies revealed that diseased arteries were common in middle-aged or older people of high social status.3 More recent studies of preserved bodies from diverse populations spanning 5000 years are consistent, indicating that arterial disease was widely present in antiquity (Table 2.1).4 In ancient Greece, Hippocrates described the characteristic pain of angina,5 while obesity was sufficiently common to have elicited clinical treatment in Greek, Roman and Byzantine societies.6 These findings, relating to populations that lived several thousand years ago, remind us that chronic diseases are not entirely new. It is their prevalence that is increasing in most populations, though at varying rates. Understanding the emergence of chronic diseases is nonetheless challenging, due to the lack of records. Until the post-medieval period, only literary or archaeological data are available. Excavations at Merton Priory, a medieval monastery in southern England that was active from 1140 to 1540 AD, revealed excessive growth of bony tissue in many skeletons, a trait now associated with late-onset diabetes.7 Gluttony seems to have been recognized at monasteries of this period: in Geoffrey Chaucer’s fictional ‘Canterbury Tales’ of the fourteenth century, the monk stated that he ‘liked fat swan best, and roasted whole’, and members of his profession were frequently described as portly.8 Records from Westminster Abbey in the fifteenth century indicate that its monks dined Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:36:36, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.003

24

Models of Chronic Disease

Table 2.1. Evidence for arterial disease in past populationsa

Population

Date BP

Preservation

Sample

Number affected

Tyrolean Alps Egypt

5300 5100–1600

1 76

1 29

Pueblo Peru Inuit Aleutian

3500–2500 1000–480 1600 100

Frozen Mummification by embalming Natural mummification Natural mummification Frozen Natural mummification

5 51 1 5

2 13 1 3

BP – before present, indexed as 2000 AD a Murphy, 2003; Zimmerman, 1993; Thompson et al., 2013

handsomely on a daily basis.9 Since obesity and physical inactivity are key risk factors for diabetes, a high prevalence of this condition at Merton Priory is certainly plausible. From the mid-seventeenth century, Bills of Mortality were collected in London, reporting the probable cause of death (Figure 2.1). These data were obtained by uneducated women lacking medical training, and the diagnoses are not necessarily reliable or even recognizable to contemporary clinicians. Not all deaths would have been included, preventing the accurate estimation of disease prevalences. Despite these limitations, the bills are the most comprehensive source of data on mortality from the post-medieval era, and are sufficient to demonstrate both the dominance of infectious diseases during this period, and the eventual rise in chronic diseases. In 1775, for example, consumption, convulsions, fever (scarlet and purple spotted) and smallpox accounted for almost three quarters of all deaths from natural causes in London, whereas diabetes was recorded only twice. However, 4 per cent of deaths in 1775 were attributed to dropsy, or pitting oedema, which is strongly associated with heart failure.10 While tuberculosis accounted for the demise of heroines of nineteenth century operas such as Puccini’s La Bohème and Verdi’s La Traviata, the same disease struck contemporary artists and novelists themselves, such as the three Brontë sisters in the Yorkshire village of Haworth.11 In 1880, infectious and parasitic diseases still accounted for a third of deaths in England and Wales, and respiratory diseases another 10 per cent. Many of these deaths occurred in infants and children, while almost two thirds of deaths occurred in those aged below 60 years. Less than one tenth of the population died of cancers or circulatory diseases. By 1990, these patterns had reversed: only 17 per cent died from infectious diseases compared to 70 per cent for cancers or circulatory diseases, and only 12 per cent of deaths occurred prior to 60 years, indicating a massive reduction in premature mortality.12 It is difficult to define these trends accurately, as approaches to diagnosis also changed. In the early nineteenth century, sudden deaths were often diagnosed as ‘apoplexy’: a term that might incorporate several modern diseases, but even at this time the role of diseased arteries was noted.13 Through the early twentieth century,

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Models of Chronic Disease

Figure 2.1.

25

London Mortality Bill for the year 1632, recording the frequency of causes of death. Wellcome Images L0023269.

doctors increasingly used new ‘cardiovascular’ terminology in death certificates, with several implications.14 First, heart failure was increasingly likely to be identified as the cause of death, downplaying the role of other organs. Second, such emphasis on physiology shifted attention away from the social and economic factors that predisposed people to heart failure, so that malnutrition, neglect and poverty were rendered invisible. For these reasons, an epidemic of cardiovascular disease appeared to manifest very suddenly, even though autopsies from the first half of the twentieth century showed that the prevalence of heavily diseased arteries was in fact declining (Figure 2.2).15

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26

Models of Chronic Disease

65–69 60–64

Age (years)

55–59 50–54 45–49 1944–1949

40–44

1903–1913

35–39 30–34 0 Figure 2.2.

10

20

30 %

40

50

60

Declines in the prevalence of advanced arterial disease by age between 1903–13 and 1944–9. Data from Morris, 1951.

We still lack a reliable profile of disease trends, and the picture is further complicated by demographic shifts that are partly the consequence of disease changes. Nevertheless, the relative decline in the burden of infections is undoubtedly real, and one consequence was increased infant survival. Some of the increase in chronic diseases can thus be attributed to longer lifespans, creating a new ‘reservoir’ of older people prone to these conditions, and some to environmental changes in sanitation, hygiene, nutrition and healthcare. In high-income countries such as Britain, the primary influence on health has clearly shifted from pathogens to the constitution of the body. In 1971, the epidemiologist Abdel Omran termed this the ‘epidemiological transition’, where the old ‘age of pestilence and famine’ is steadily replaced by a new ‘age of degenerative and man-made diseases’.16 The pattern that he documented is shown in Figure 2.3. Few of us will need reminding of the proximate causes of chronic diseases, as presented to us by family doctors, public health organizations and government health services. For decades we have been told to take responsibility for our health: eat healthily, take regular exercise, maintain a healthy weight, cut down on alcohol and tobacco and avoid exposure to pollutants and toxins. All of these factors affect our metabolism, and the majority fall within the remit of nutrition. Our lifestyles are fundamentally implicated: the question is, how to incorporate our behaviour in the overall model of disease. Biomedical practitioners can only promote health if they have accurate models of disease aetiology. Such models inevitably evolve over time, and in the present era we still do not understand chronic diseases nearly as well as we would like to. Scientific understanding of what constitutes healthy nutrition seems to change constantly, making the public distrustful of public health recommendations. While the pathophysiology Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:36:36, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.003

Changing Models of Disease

27

100

Per cent

80

Other Violent CNS Heart Cancer Respiratory Infectious

60

40

20

0 1850 Figure 2.3.

1870

1890

1910

1930

1950

Changes in the cause of mortality in England and Wales from 1850 to 1947. CNS – vascular diseases of the central nervous system. Data from Logan, 1950.

itself has become increasingly well understood, its relationship with societal factors is still subject to controversy.

Changing Models of Disease Models of disease require both concepts and empirical data that allow them to be tested. The sacred Hindu text Atharvaveda from the second millennium BC considered diseases to be caused by living agents – malevolent spirits and demons known as the yatudhānya, the kimīdi, the kṛimi and the durṇama.17 This might seem a highly inappropriate approach for chronic diseases, but the aim of this book is to understand the role of power relations in shaping health through nutritional pathways. Chronic diseases are ultimately caused by living agents, and these agents are other humans – manipulating each other through the complexities of social life. The ancient Greeks developed a complex model of disease, subsequently maintained by the Romans and early Islamic physicians, which considered the body to be composed of four different substances or ‘humours’ known as black bile (melan chole), yellow bile (chole), blood (sanguis) and phlegm (phlegma).18 In a healthy body, these humours were assumed to be in a state of equilibrium, but various factors could perturb this. An excess or deficit in any one humour would induce certain characteristics of ill-health. Despite all the advances conferred by modern medical understanding, this model of disease is still present in everyday language. For example, individuals may be termed phlegmatic (accepting), sanguine (full-blooded), melancholic (sad) or choleric (hot-tempered), and personality traits have been associated with cardiovascular disease risk.19 Nor is this Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:36:36, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.003

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Models of Chronic Disease

disease model entirely alien to our modern medical understanding, which sees health as a state of balance. As recently as the eighteenth century, practices such as bloodletting, or applying hot cups to the skin to stimulate blood flow, acknowledged the humour model of disease. Any physician might have been hard pressed to explain exactly how these remedies worked, but the same scenario can be found in contemporary clinical practice, where many elements of terminology (‘essential’ or ‘idiopathic’) are simply a euphemism for ‘we can’t yet explain it’.20 Another theory of illness that persisted for several centuries across Europe and Asia was Hippocrates’ notion of ‘miasma’, which considered disease to arise through exposure to environmental pollutants conveyed by foul air or mist, associated with unhygienic living conditions. Even in mid-nineteenth-century London, outbreaks of cholera and infant diarrhoea were still being attributed to miasma, and the notion of contagion only became widely accepted towards the end of the century, through the emergence of a new ‘germ theory’. The credibility of miasma was undermined in 1854 when the physician John Snow demonstrated that an outbreak of cholera in London could be traced to a specific contaminated water source in Broad Street, thus implicating a discrete biological agent.21 Germ theory, attributing diseases to microorganisms, became orthodox in part because it could link specific pathogens to specific diseases. In quick succession, the organisms responsible for cholera, puerperal fever, typhoid, tuberculosis, plague and anthrax were discovered. The theory also emerged during an era when infectious diseases still dominated morbidity and mortality in all populations. Although it remains unclear how much late nineteenth century health improvements in England were due to vaccinations and treatments, as opposed to ‘social hygiene’ programmes,22 germ theory revolutionized the mindset and practice of medicine. For each disease, the aim was to identify the pathogen and its route of transmission. Then, the weak point in the disease cycle could be identified, to allow effective prevention or treatment. The microbial basis of disease remains the dominant paradigm in medicine, and models of chronic disease aetiology remain cruder in comparison. Medicine thus has a long history of imperfect models of disease that were nevertheless widely applied, and often passed on for generations or even centuries. We should bear this in mind as we consider more recent models, generated using state-of-the-art biostatistics and technology. It would be ridiculous to suggest that current models of chronic disease risk are not useful to clinicians, but they may nevertheless contain errors or gaps, and require further development. A major challenge posed by chronic diseases is their poor fit with the germ theory paradigm. One could argue that rapid technological advances have enabled us to understand in extraordinary detail what chronic diseases are, and yet have failed to provide equivalent understanding of why they develop, what the relevant vectors are, and why individuals and groups vary in their susceptibility. In science, technology alone may not generate accurate knowledge. When Galileo Galilei scanned the solar system in the early seventeenth century, he brought together his new refractor telescope and the courage to discard orthodox theory when interpreting his Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:36:36, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.003

The Healthy Body

29

data. The idea that the earth rotated around the sun, rather than vice versa, had been proposed by Copernicus in 1543, but although it made mathematical sense, empirical evidence was lacking. Galileo’s observations of planetary movements refuted the ancient cosmological models and vindicated Copernicus. New ideas often face a backlash, however: in this case, the Catholic Church accused Galileo of heresy, and placed him under house arrest until his death. Despite plenty of modern equivalents of Galileo’s telescope, providing abundant data on the physiological and molecular basis of chronic diseases, we still have a poor understanding of how to prevent them. To do better, we need to get to grips with the noninfectious agents of ill-health, which means understanding their societal basis. In developing a broader theoretical model we are likely to face the same kind of scepticism as Galileo encountered, simply because we need to go beyond the orthodox. Such an approach is the central aim of this book and will take us into the realms not only of physiology and biochemistry, but also evolutionary biology, anthropology, archaeology, history, philosophy, politics and economics. To build this complex model, we need to start with a simple description of ‘what goes wrong’ at the physiological level in chronic diseases. And to do that, we first have to take a further step back and describe the physiology of the healthy body.

The Healthy Body Our health depends on the ability of a variety of organs and tissues to maintain homeostasis, a term which refers to the myriad physiological processes that maintain optimal cellular conditions despite continuous environmental perturbations. Degenerative diseases are effectively the product of ‘wear and tear’ or larger-scale physiological damage to this system, and emerge in concert with cellular aging or ‘senescence’. It is possible to define various different degenerative diseases, according to which particular organ or tissue has been affected. Such an approach is both useful, as it aids address specific symptoms, yet also problematic, as it artificially isolates a broader process of disease in the specific regions of the body most affected. Both in this and subsequent chapters, some of the unifying features of chronic disease aetiology will be elucidated. Nevertheless, to help link the underlying biology with the kinds of conditions familiar to clinicians and their patients, it is helpful to consider how the various tissues and organs normally function, and how their degeneration leads to ill-health. Despite the complexity of physiology, a valuable conceptual overview may be gained from the analogy of the body as a mechanical system, such as a car. Scientists in the seventeenth century had already discovered that life is a combustion process by demonstrating that a mouse and a candle both expired simultaneously when exposed to a lack of oxygen.23 The car and the body each represent a system in which fuel is converted into work. This analogy is far from new: in 1942, physicians studying the effects of starvation in the Warsaw Ghetto observed that ‘the motor of life stops not because of a dissociation between particular parts but because of a lack of fuel’.24

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Models of Chronic Disease

Within this overall remit, the body contains a number of organs and tissues with specialized functions. The brain, representing the centre of the nervous system, comprises large numbers of neurone cells embedded in connective tissue. These neurones collectively exert centralized control over all other tissues through neuromuscular or hormonal mechanisms. Brain functions include both the regulation of metabolism and the coordination of behaviour. Cerebral blood flow varies markedly according to which regions are active, but the organ maintains a high metabolic rate and requires a continual supply of glucose or backup fuel. A powerful ‘blood–brain barrier’ stabilizes cerebral metabolism, keeping it relatively independent of metabolic variability elsewhere in the body.25 The heart comprises a pair of muscular pumps, together about the size of a clenched fist, that propel the blood through a network of major and minor vessels to the different tissues and organs. The blood supplies the body with nutrients and oxygen for metabolism and growth, and removes waste products including carbon dioxide. Regional control over this supply system is aided by local variability in blood pressure, as the size and elasticity of the blood vessels determine the rate of flow. Blood has many specific functions relevant to chronic disease risk: as well as transporting fuel, it contains diverse clotting agents for staunching blood flow following external injury, and transports immune agents to affected tissues. The liver is the largest internal organ, and contributes to a wide range of vital metabolic processes, including the synthesis, breakdown and storage of diverse molecules. Among its most important roles are the synthesis and storage of glycogen (‘animal starch’, one of the primary cellular energy supplies), the metabolism of dietary fat and protein, the production of clotting factors and the breakdown of toxins. Humans consume very diverse diets, and the liver plays the most important role in converting foods into simpler molecular units that can enter metabolic pathways. The two kidneys remove waste products from the body through a complex filtration system. Each kidney contains hundreds of thousands of small units known as nephrons, which themselves contain tiny blood vessels known as glomeruli. Each glomerulus filters the blood, retaining cells and valuable proteins while allowing waste products and excess fluid to exit into the bladder. On average, an adult’s kidneys process ~200 litres of blood per day while removing ~2 litres of fluid and waste products. The kidneys also produce a hormone, renin, whose function is to maintain sufficient blood pressure to force blood through the filtering mechanism. Through this mechanism, kidney function is closely associated with blood pressure regulation. The lungs are an asymmetrical pair of sponge-like organs sitting high in the thoracic cavity, where they act as the primary site of respiratory gas exchange. The high density of airways inside lung tissue provides a total surface area similar to a tennis court, across which oxygen diffuses into the blood and carbon dioxide diffuses out of it. Muscular pumping of the ribcage ventilates the lungs at variable rates, depending on the demand of the tissues for oxygen.26 The pancreas is a gland located in the abdomen playing vital roles in digestion and fuel metabolism. Exocrine cells produce enzymes that contribute to the breakdown of food in the gut, while endocrine cells secrete hormones that ensure a viable supply of Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:36:36, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.003

Homeostasis

31

energy to the cells. In particular, pancreatic beta-cells produce the hormones insulin and amylin, which each contribute to the control of blood sugar levels as well as regulating other physiological processes. Muscle tissue provides contractile force in the body, either as smooth or cardiac muscle in organs, or as skeletal muscle that allows voluntary control of body movement, posture and expression. Muscular activity is a major site of energy use, and is enabled by the oxidation of glycogen and lipid stored in muscle tissue, and also by the uptake of fuel across the cell membrane. Glucose enters muscle cells through the action of transporter proteins under the influence of insulin, which binds to receptors on the plasma membrane. In contrast, the entry of free fatty acids into cells is regulated passively by a concentration gradient. The demand of muscle tissue for fuel is strongly dependent on physical activity level, such that exercise stimulates both fuel uptake in the short term and muscle physiology over the longer term. Adipose tissue represents a specialized store of energy in the form of fat, with a supporting network of blood vessels. Until recently it was regarded as inert: simply a fuel tank for storing excess energy and releasing it again when demand rises. This view has changed profoundly, and adipose tissue is now considered a complex endocrine organ, the source and recipient of diverse signalling molecules transmitted through the blood circulation or between neighbouring tissues.27 In this way, adipose tissue responds to ongoing metabolic dynamics while contributing to the regulation of physiological processes. The skeleton represents the chassis of the body; its development is a fundamental component of the process of growth. Like adipose tissue, the skeleton was long considered a relatively inert tissue, but it secretes a range of signalling molecules, as well as containing active bone marrow tissue that produces red and white blood cells.28 Even in adult life, bone undergoes remodelling, allowing it to respond to ecological stresses as well as to repair itself following fractures.29 These are the main organs and tissues relevant to chronic diseases, and we can now consider in more detail what they do, and how their functions shape the manner of their deterioration.

Homeostasis It was the physiologist Claude Bernard who first expressed the value of metabolic stability with the statement, ‘la fixité du milieu interieur est la condition de la vie libre’.30 Bernard had understood that all living organisms need to maintain a relatively steady internal state, in the face of environmental or behavioural stresses that fluctuate over time. The vital organs and tissues all contribute to this process of ‘homeostasis’, maintaining optimal cellular conditions through feedback mechanisms.31 The brain clearly plays a key role, but one could also argue that it has ‘outsourced’ most of the important activities to other biological systems, while also fencing itself off from metabolic perturbations through its resistant blood–brain barrier.

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Models of Chronic Disease

(a)

Pancreas sensing increasing blood glucose levels

Insulin secretion

Blood glucose concentration – 4–8 mmol/L

Glucagon secretion

Pancreas sensing decreasing blood glucose levels

Figure 2.4.

(b) Carbohydrate oxidation Muscle metabolism

32

Lipid oxidation

Inflexibility

Flexibility Meal Time

(a) Blood glucose levels are regulated by counterbalancing effects of the hormones insulin and amylin, both secreted by the pancreas. (b) Muscle tissue can metabolize glucose or free fatty acids. Its ability to switch these two fuels improves with physical fitness. Redrawn with permission from Corpeleijn et al., 2009.

The cardiovascular system is responsible for maintaining a stable supply of nutrients and oxygen to tissues while also transporting many other molecules that address unpredictable stresses (such as infectious disease, or physical activity) or coherent processes (such as growth and reproduction). The kidney regulates blood volume by excreting excess fluid despite large perturbations in the intake of water and salt, or the effects of exercise and sweating. The control and distribution of blood volume must be maintained continuously. The tendency of humans to eat discrete meals means that food boluses of inconsistent size and composition enter the body at uneven intervals. This supply chain must be smoothed, to ensure an even delivery of nutrients to the cells. High blood levels of glucose are associated with damage to tissues and organs; blood glucose regulation, known as glycaemic control, is therefore a central component of homeostasis. Following digestion, macronutrient molecules pass from the gut to the liver, placing this organ on the front line of stabilizing blood fuel concentrations. The liver converts glucose into glycogen, and another sugar, fructose, into fat. It also synthesizes lipoprotein molecules that transport free fatty acids to adipose tissue.32 However, the liver cannot achieve complete glycaemic control, so the pancreas contributes an additional level of regulation, secreting insulin. By dispatching glucose to muscle or adipose tissue, insulin prevents excessive blood sugar levels. If the demand of organs and tissues for glucose increases, the pancreas responds by secreting the hormone glucagon, which induces the liver to release glucose from its glycogen stores (Figure 2.4a).33 Muscle tissue can also switch to metabolizing free fatty acids, released into the circulation from adipose tissue, which occurs when glucose supply is insufficient. In a state of physical fitness, muscle switches readily between these two fuels, but such ‘metabolic flexibility’ can be compromised if fitness declines (Figure 2.4b).34 Because fat repels water, its transport in the blood is facilitated by being encased inside lipoprotein molecules. Fatty acids released directly from the digestion of fatty food are processed in different ways, depending on their size. While the smallest remain Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:36:36, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.003

Pathophysiology and Chronic Disease

33

free, larger molecules are converted into triglycerides, which may then be transported by lipoprotein molecules (comprising chylomicrons and cholesterol) to muscle and adipose tissue. Here they are absorbed into cells through the action of enzymes on the cell membrane, leaving the chylomicrons and cholesterol to be dealt with by the liver. This means that variability in the intake and synthesis of fatty acids directly impacts circulating concentrations of triglycerides and cholesterol. Below, we will see that there are three different types of lipoproteins, with contrasting metabolic properties.35 Supplying tissues and organs with energy and oxygen while regulating fluid volumes, in the face of inconstant environmental conditions, is therefore the most important component of homeostasis. In a state of health, the vital organs act in concert with one another, and the individual can tolerate a wide range of environmental conditions and physiological activities.

Pathophysiology and Chronic Disease So, when chronic diseases develop, what goes wrong and why? At the proximate level, chronic diseases may be considered to arise from mechanical, signalling or control defects that emerge through cumulative wear and tear within the organs and tissues. Physiological studies and autopsies after death provide a great deal of information on such pathophysiology, but the picture remains incomplete. One of the primary components of chronic disease comprises cardiovascular malfunction, which may affect the heart itself, blood vessels in various body regions, or kidney function. In turn, inability to regulate metabolism may increase the risk of these outcomes. Normal function of the blood vessels requires elasticity of their walls or endothelium; however, a number of factors can reduce that plasticity – a process termed endothelial dysfunction. Repeated mechanical, hemodynamic or immunological injuries can all promote hardening of the arteries, and these stresses are addressed collectively as the ‘response to injury’ hypothesis.36 The heart muscle is supplied by three major blood vessels, known as the coronary arteries. Over time, these vessels may become restricted through the accumulation of a fat-like substance named plaque in the vessel wall, known as the process of atherosclerosis. This plaque develops when lipoprotein molecules, involved in fatty acid transport, enter the blood vessel wall and generate atherosclerotic lesions.37 If any of the major blood vessels becomes entirely blocked by plaque, part of the heart muscle may die, an event known technically as a myocardial infarction, and to the lay-person as a heart attack. Partially blocked blood vessels can be treated in several ways. A class of drugs known as statins impedes the production of plaque-inducing cholesterol in the liver while also increasing its removal from the bloodstream. Individual blood vessels can be reopened by inserting a stent, a tiny mesh scaffold, while heart valves can be replaced with mechanical prostheses. A more extreme treatment comprises coronary bypass surgery, whereby blood vessels from elsewhere in the body are grafted to the blocked artery to Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:36:36, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.003

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Models of Chronic Disease

circumvent the constriction. For obvious reasons, public health efforts aim to prevent plaque formation in the first place. A similar interruption of blood supply may occur in the brain, either through a ruptured blood vessel or through a clot. In each case, as in the heart, the lack of oxygen and fuel causes local cell death. This process is termed a stroke, either haemorrhagic if due to blood vessel rupture or ischaemic if due to a clot. Depending on where in the brain this occurs, different functions may be adversely affected such as speech, muscular movement or memory, but in many cases strokes are fatal. The brain is substantially less accessible to the surgeon than other organs, making it very difficult to manage cerebral blood vessel malfunction. There is only a very brief time window after a clot has formed during which drugs can be used to dissolve it. Various drugs can reduce the likelihood of damage occurring, as can management of blood pressure. Prevention is therefore crucial for reducing the public health burden of stroke. The likelihood of heart attacks and strokes is greatly increased by excessive blood pressure on the artery walls. High blood pressure (hypertension) is both a consequence of hardened arteries, and also a risk factor for cardiovascular disease because it increases damage to the arteries, while making the heart work harder. Regulation of blood pressure is therefore critical for health, and hypertension is often called the ‘silent killer’ because, despite its serious consequences, it offers no obvious symptoms and hence requires monitoring. If the blood vessels in the kidney become damaged, they lose their capacity to remove waste and fluid from the body. This excess fluid then elevates blood pressure, generating a vicious feedback cycle: hypertension is a major cause of kidney failure, while kidney disease is also a major risk factor for strokes and heart attacks. A second key component of chronic disease aetiology comprises inadequate regulation of fuel metabolism, resulting in excesses of some molecules and deficiencies of others. These perturbations cause damage to many individual tissues and organs, and also increase the risk of cardiovascular problems through perturbations of blood lipid content, known as dyslipidaemia. As we saw above, glycaemic control depends on several hormones, in particular insulin. However, some tissues may become insensitive to its effects, a condition known as insulin resistance. Initially, this can be compensated through the production of extra hormone by the pancreas, so that glycaemic control can be maintained through higher insulin turnover. Over time, however, this compensation may prove insufficient, leading to excess levels of blood glucose, some of which is eventually expelled into the urine. This condition, incurable once it has developed, is known as type 2 diabetes.38 It is often described as a ‘two-hit’ disease, because neither high levels of insulin resistance nor low levels of insulin secretion appear sufficient to cause the disease on their own.39 When pancreatic failure occurs, treatment is required to maintain glucose homeostasis and prevent serious damage to tissues. Since this damage extends to blood vessels, type 2 diabetes is a major risk factor for cardiovascular disease, but it also causes other types of tissue degeneration that can lead to blindness, kidney failure and a reduced capacity for wound healing. Through its provocation of ulcers, diabetes is the primary cause for foot amputations worldwide, although less invasive management strategies are now available. Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:36:36, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.003

Pathophysiology and Chronic Disease

35

Initially, treatment for type 2 diabetes involves modifications to diet and physical activity level, which can improve glycaemic control, but in more severe cases medication is necessary, including injections of insulin. Obesity is a key risk factor for diabetes, as discussed in the next chapter. This model of type 2 diabetes is the basis for diagnosis and treatment worldwide, and yet there are increasing indications that it is incomplete, fails to recognize pathophysiological variability, and ignores other components of homeostasis and the effects of insulin on diverse functions.40 These limitations suggest that we have only a partial understanding of how diabetes develops, and hence of how we might prevent and treat it. While diabetes is primarily associated with deterioration of the cardiovascular system and skeletal muscle tissue, the brain also appears vulnerable to disorders of fuel metabolism. Dementia refers to progressive brain damage affecting higher-order cognitive functions such as memory, judgement and calculation.41 Diabetics have an increased risk of Alzheimer’s disease, the most common form of dementia, and recent work has linked Alzheimer’s with perturbed insulin signalling in the brain, leading to the accumulation of protein clumps known as ‘brain plaque’.42 The common role of insulin perturbations in this disease and type 2 diabetes has prompted the suggestion that Alzheimer’s disease be considered ‘type 3’ diabetes.43 Blood lipid levels also shape chronic disease risk. The three main classes of lipoprotein molecules (high-density, low-density and very-low-density, labelled HDL, LDL and VLDL) differ in their relative proportions of protein, cholesterol and triglycerides, and their relative levels in the blood influence the overall profile of cholesterol metabolism.44 HDL is considered healthy as it removes cholesterol from plaque in the artery walls, whereas LDL and VLDL are considered harmful and are associated with plaque formation. In terms of chronic disease, the main significance of the liver is that its functional decline reduces the capacity for processing lipids and cholesterol, as well as mild toxins such as alcohol. The liver can accumulate excess fat, which does not cause disease in the organ itself but nevertheless elevates the risk of diabetes, stroke and cardiovascular disease. For example, fatty liver disease is associated with thickening of the blood vessel walls and with decreased arterial elasticity.45 There are several other degenerative diseases whose aetiology has much in common with the general model explored here. These include sarcopenia, a progressive decline of muscle mass and function which reduces the capacity for physical activity; osteoporosis, an age-related decline in bone mineral density, increasing the risk of fracture; and chronic obstructive lung disease, which arises through progressive restriction of the airways. This causes shortness of breath, restricting physical activity. Even more broadly, we can consider certain cancers, whose development is associated with the levels of hormones that are sensitive to nutrition and metabolism. While these diseases are all common and important, and fit many of my general arguments, they will not be addressed in detail in this book. My focus is on the cluster of metabolic diseases that are making such rapid impact on global morbidity and premature mortality: obesity, cardiovascular disease, stroke, hypertension and type 2 diabetes. Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:36:36, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.003

36

Models of Chronic Disease

As we have seen, degenerating organs or tissues represent the proximate cause of chronic diseases. Most individuals do not develop these diseases suddenly; rather, they have a slow rate of onset arising from cumulative exposure to risk factors. Furthermore, homeostasis fails at widely varying rates across individuals, so that some develop illhealth in early adulthood, whereas others enjoy several additional healthy decades.

Aging, Disease and Wear and Tear To help understand how damage accumulates in the body, let us return to the analogy of the body as a mechanical system, such as a car. In this analogy, basic skeletal anatomy is equivalent to the chassis and the cardiovascular system to the engine, with its fuel pump and ‘combustion’ metabolism. The mix of fatty acids and glucose fuelling the cells is equivalent to petrol feeding the engine, and the blood vessels and gut represent various pipes in and around the engine. Cars have ‘start-up’ and mainstream energy supplies from the battery and fuel tank respectively, not unlike the contrasts between glucose and fatty acids. Waste products and heat must be expelled by exhaust systems, while a constant supply of oxygen is required to support fuel combustion. In the car, any of these functions may fail, bringing the vehicle to a halt, in which case a mechanic must diagnose the problem and repair the faulty part. The process of physiological aging resembles the wear and tear that accumulates on every part of the car. The way in which the car is driven and maintained – its ‘lifestyle’ – can be highly influential on the process of deterioration. Some types of car are also manufactured to a higher quality, and on average last much longer than those assembled with poorer materials. Physiological robustness may likewise be considered a function of development in early life. However, important contrasts between mammalian physiology and mechanical vehicles are immediately apparent: for example, no car directly uses petrol as the fuel for the signalling systems and controls, whereas the human brain remains dependent on a supply of fuel by cerebral blood vessels. If the engine in the car breaks down, the control systems are generally still intact, and vice versa. Cars are therefore less vulnerable than people to systemic failures, making it much easier to repair almost every individual part. But that of course is life: living bodies cannot be conveniently disassembled into discrete inactivated parts for maintenance, although surgeons do their best to achieve exactly that. Nor do engineers need to start with a tiny car the size of a needlepoint, and steadily expand it while keeping the engine running. Although it is obvious when a car has broken down, there is not always much warning that such failure is imminent. In the same way, our understanding of the overt manifestation of diseases such as heart disease, hypertension and diabetes is more advanced than that of their slow physiological development. Clinicians may recognize strong signs of metabolic or cardiovascular ill-health in patients, but the patients themselves may not necessarily understand or accept the importance of those symptoms. Other symptoms, yet to have attracted the interest of scientific researchers, may pass under the radar of both clinicians and patients. Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:36:36, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.003

The Metabolic Syndrome and the Evolution of Risk

37

Table 2.2. Definition of the metabolic syndrome by Alberti and colleagues, adapted for worldwide use Essential: Central obesity, defined using ethnic-specific criteria Plus any two: Raised triglycerides, or treatment for this abnormality Reduced HDL-cholesterol, or treatment for this abnormality Raised blood pressure, or treatment of hypertension Raised fasting plasma glucose, or diagnosed diabetes

The Metabolic Syndrome and the Evolution of Risk To understand the aetiology of chronic diseases, a new paradigm of ‘risk factors’ replaced germs and pathogens as the primary causative agents of ill-health. Heart attacks, strokes and diabetes have conventionally been considered diseases of middleage onwards, so the first risk factors to attract attention were adult lifestyle and genotype. Because overt diseases develop slowly, clinicians conceptualize the accumulation of risk through the lens of the ‘metabolic syndrome’, which refers to a cluster of physiological traits associated with ill-health. The more risk factors present, the higher the risk of suffering a heart attack or stroke, or developing type 2 diabetes.46 Established risk factors include elevated values for blood pressure, fasting blood glucose, triglycerides and waist girth, along with low levels of HDL cholesterol; hence these traits are widely used to monitor disease risk. One widely used categorization of the syndrome is given in Table 2.2.47 The importance of these traits is very clear: worldwide, the five leading risk factors for mortality all refer to metabolism rather than pathogens, and comprise high blood pressure, tobacco use, high blood glucose, physical inactivity and overweight/obesity.48 Though widely applied, however, the metabolic syndrome is considered by many to be problematic. It is a rather nebulous concept: diagnosis is based on different criteria according to different health organizations, and in many cases requires simply at least three risk factors to be present. This means that two individuals, apparently diagnosed with the same syndrome, may have quite different clinical symptoms, and may require contrasting treatments. One particular source of dissatisfaction relates to insulin resistance.49 Although some consider it so important that they refer to the ‘insulin resistance syndrome’, the potential role of insulin was originally identified solely on the basis of its correlations with other risk factors.50 As yet, only the World Health Organization’s definition incorporates insulin resistance in its classification.51 The substantial emphasis placed on cholesterol is partly due to its being the first blood metabolite to be routinely measured by clinicians.52 Inflammatory markers, triglycerides or specific lipoproteins are now considered better markers of disease risk, and we must remember that the criteria for evaluating chronic disease risk represent a work in progress. A second problem is that although epidemiological studies have identified various risk factors at the population level, these often perform poorly in accounting for variability in disease predisposition at the level of the individual.53 Similarly, associations between

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38

Models of Chronic Disease

simple risk markers and more overt disease symptoms can vary between populations, so that ethnic groups tend to differ in their susceptibility to chronic diseases.54 Recently, increasing attention has been paid to the role of inflammation, comprising the physiological response to injury or pathogens. Markers of inflammation such as C-reactive protein have been linked with atherosclerosis and pancreatic beta-cell dysfunction.55 In turn, inflammation is prospectively associated with the risk of developing overt heart disease, hypertension, stroke and type 2 diabetes.56 In addition, chronic diseases themselves manifest as chronic inflammatory states and hence accumulate damage by positive feedback processes. By provoking all components of the metabolic syndrome, inflammation may be a key factor contributing to the tendency of chronic diseases to cluster in individuals. For example, the inflammatory state of chronic obstructive pulmonary disease is associated with an increased risk of developing cardiovascular disease and type 2 diabetes.57 Even taking inflammation into account, however, the ability of clinical factors to predict chronic diseases in individuals remains limited. One way to attempt to resolve these problems is to ‘dig deeper’ into metabolism. Recent work has focused on cellular metabolism and signalling systems. Particular interest has been directed to two cellular structures, mitochondria and telomeres, each of which appears fundamentally implicated in the process of aging.

The Role of the Mitochondria Mitochondria are often considered to act as ‘batteries’ in our cells, providing the machinery for energy metabolism. Mitochondria are the site of respiratory metabolism, where fuel is oxidized to release energy. Glucose is first split into simple molecules, which are then steadily stripped of electrons by a chain of proteins on the mitochondrial membrane, releasing energy to fuel chemical reactions. In this process, the mitochondria also release free-radical oxygen species that can cause cellular damage.58 To contain this damage, cells produce a number of enzymes to scavenge the free-radicals and dispose of them, but the less perfect the scavenging system, the more damage accumulates. The level of oxidative stress in a tissue therefore represents a balance between free radical production and antioxidant capacity.59 Although mitochondria manifest as cell organelles, they are considered originally to have been free-living bacteria, which became engulfed by larger cells in a process that succeeded because of mutual benefits to each party. The resulting eukaryotic cells, packed with mitochondria, could generate several orders of magnitude more energy than bacterial cells, at a fraction of the running costs.60 One consequence of this merger is that the vast majority of the mitochondrial genome moved to the cell nucleus, leaving just 37 genes within the mitochondrion itself. Whereas nuclear DNA is wrapped in a protective coat of histone proteins, mitochondrial DNA has no such protection. Both because of this, and because it is immediately next to the site of free-radical production, it is highly susceptible to damage if free-radical scavenging is not adequate.61 Mutations in these mitochondrial genes are now strongly implicated in metabolic dysfunction, and Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:36:36, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.003

The Role of Telomeres

39

the mutation rate of these genes is 10–20 times the rate of that of nuclear genes.62 In this way, the accumulation of mitochondrial mutations is a key component of ageing. Lifestyle factors such as diet and exercise impact directly on the rate of free radical production. Both dietary energy restriction and moderate exercise are protective, reducing the rate of free radical leakage and hence slowing the rate of aging. At the other extreme, dietary excess can overload the ability of the mitochondria to process lipid or glucose, resulting in the development of insulin resistance.63 This protects the mitochondrial DNA in the short term, but may eventually lead to diabetes because oxidative stress can damage pancreatic beta-cells and hence decrease the capacity for insulin secretion.64 Mitochondrial dysfunction is a highly plausible candidate for explaining more of the variability in chronic disease risk that manifests across and within populations. It also links with a second cellular marker of aging, the state of the chromosomes inside the cell nucleus.

The Role of Telomeres Just as damage to mitochondrial DNA accelerates aging, so does damage to nuclear DNA. In general, chromosomes in the nucleus are much better protected than mitochondrial DNA due to their protective protein wrapping. They do, however, have one specific weak-spot, namely the protective ‘caps’ at the ends of the chromosomes, known as telomeres. Telomeres preserve the stability of the genome by preventing damage to the chromosomes during mitosis (the process of cell division). With each successive division, DNA base-pairs are lost due to the inability of the participating enzymes to replicate the very ends of each chromosome.65 In order to avoid losing functional DNA in this way, telomeres are made of non-coding DNA, which can be slowly shed without loss of function. The decline in base-pairs with each cell division represents a ‘mitotic clock’, marking the number of divisions that have occurred.66 Such telomere attrition is not inevitable. The enzyme telomerase can restore telomere length by rebuilding the protective caps after each cell division, but it does so primarily in stem cells or germ cells, which have much higher levels of replication.67 In the majority of cells, telomere attrition provides a benefit, preventing unrestricted cell proliferation and tumour formation. The price for this protection against cancer is that repeated cycles of cell division eventually induce cellular senescence, and hence contribute to the ageing process.68 The importance of telomeres for protecting against aging has been demonstrated in studies of mice, where telomere degradation provokes progressive tissue atrophy and organ failure.69 Switching off the telomerase gene accelerated aging and led to premature death, whereas reactivating the gene reversed these aging effects.70 Tissuespecific work also shows exactly how telomere attrition damages homeostatic capacity. In diabetes, for example, a deficiency in the telomerase enzyme reduces replication of the insulin-producing beta-cells, thereby impeding glycaemic control.71 Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:36:36, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.003

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Models of Chronic Disease

Table 2.3. Association between shortened telomeres and chronic diseasesa Disease parameter

Outcome

Cardiovascular disease

Endothelial dysfunction Myocardial infarction Coronary artery disease Stroke Hypertension Type 2 diabetes Glucose intolerance Insulin resistance Chronic obstructive pulmonary disease

Blood pressure Insulin metabolism

Lung function a

Minamino et al., 2002, Brouilete et al., 2007; Zee et al., 2009; 2010a; Ogami et al., 2004; Willeit et al., 2010; Adaikalakoteswari et al., 2005, 2007; Sampson et al., 2006; Demissie et al., 2006; Amsellem et al., 2011

An increasing number of human studies have shown that the metabolic syndrome and chronic diseases are associated with shorter telomeres in blood cells (Table 2.3), although as yet the evidence for vascular dementia and stroke is inconsistent.72 This discrepancy may arise because telomeres may not shorten with age in brain tissue.73 Shorter telomeres are also found in many of the tissues whose deteriorating function provokes chronic disease, such as atherosclerotic plaque, or myocardial tissue in patients with heart disease.74 Overall, telomere length predicts longevity in humans, while shorter telomeres in men compared to women may even help explain the longer life expectancy of women in many populations.75 Most importantly, recent work has elucidated a clear link between telomere deterioration and mitochondrial function, demonstrating their combined role in the biology of aging.76 It is now clear that oxidative stress, independently of cell division, can damage telomeres, and that antioxidants can decelerate this attrition.77 Thus, at a cellular level, chronic diseases can collectively be considered both cause and consequence of ‘accelerated aging’.

The Other Genes The biology of wear and tear is clarified by probing deeper into metabolism, but increasingly, researchers have needed to think laterally and ask whose metabolism is actually involved. The human gut contains a community of micro organisms known as the ‘gut biota’, dominated by ~1014 bacteria of 500–1000 different species. In totality, the biota contain millions of genes: around 100 times the number in the human genome.78 These bacteria colonize the gut from fetal life onwards, under the influence of diverse factors such as the maternal biota, diet and genetic factors.79 Collectively, they constitute a ‘microbial factory’ that contributes to a wide range of metabolic functions that cannot be performed by human metabolism on its own.80 Among these functions are dietary energy harvest

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The Global Chronic Disease Epidemic

41

Tuberculosis Diarrhoeal diseases Malaria Protein-energy malnutrition Cancers Ischaemic heart disease Ischaemic stroke Cirrhosis (alcohol abuse) Diabetes mellitus –50 Figure 2.5.

–25

0 25 50 % Change from 1990 to 2010

75

100

Percentage changes in the number of global deaths attributed to selected causes between 1990 and 2010. Data from Lozano et al., 2012.

and nutrient acquisition, stimulation of the innate and adaptive immune systems, and resistance against pathogens.81 It is rapidly becoming clear that the composition of the gut biota, and its response to ecological stresses, has major impacts on the metabolic traits that drive chronic disease risk. For example, accelerations in the rate of dietary energy harvest elevate the risks of obesity and diabetes, through increasing adiposity or promoting inflammation.82 Research on the biota may be considered a mechanistic revolution in biological understanding, whose full ramifications are hard to predict at this stage. Already, it is clear that many of the signals underlying the metabolic syndrome are transmitted to and from these other organisms. Once we know that transplanting biota from male to female mice changes testosterone levels in the females, it is clear that mammalian physiology is a collective entity.83 I will make little explicit reference to the gut biota, telomeres or mitochondria in the rest of this book, but the important point is that the arguments that I make about health, metabolism and society are consistent with current understanding of physiology, even though it is clear that new insights will materialize in the future. In the meantime, the diseases themselves are all too evident.

The Global Chronic Disease Epidemic The global chronic disease epidemic represents a profound signal of the ‘state of contemporary metabolism’. The speed with which these diseases have come to dominate global mortality patterns is revealed by trends between 1990 and 2010 (Figure 2.5).84 Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:36:36, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.003

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Models of Chronic Disease

Broadly, overall deaths from infectious diseases declined over this period, although those from malaria, dengue fever and HIV/AIDS increased. Deaths from overt undernutrition decreased, but those from chronic diseases surged, with increases of ~35 per cent for ischaemic heart disease, ~25 per cent for ischaemic and haemorrhagic stroke and ~90 per cent for diabetes. In 2010, ischaemic heart disease and stroke collectively killed one in four people worldwide, compared to one in five in 1990. Ischaemic heart disease is among the top four causes of death in every global region except Oceania and sub-Saharan Africa, and stroke is also one of the commonest causes of death in many regions. Already, 80 per cent of the deaths from chronic diseases occur in low- and middle-income countries, and a quarter in those below 60 years.85 These trends reflect both epidemiological transitions in living conditions and demographic trends, so that the rise in chronic diseases cannot be disconnected from the increasing life expectancy that is occurring in most populations. Roughly one in five deaths still occur in infants and children,86 attributable largely to infectious disease and under nutrition. Being diseases of ‘wear and tear’, chronic diseases inherently increase in prevalence as childhood mortality declines and the proportion of older people in the population rises.87 By analogy, a car will only start to rust and decay if it escaped being written off in a crash earlier. Beyond premature mortality, chronic diseases are also a key source of illness. Ischaemic heart disease and stroke rank sixth and seventh respectively in terms of the total global burden of morbidity. Even where effective treatment is available, many people live for decades with degenerative illnesses. Before the heart attack comes tiredness, shortness of breath and severe chest pain. Survivors of stroke suffer debilitating loss of memory, speech or motor movement in various combinations. Diabetics are at substantially elevated risk of amputated limbs and blindness. Such ill-health severely depletes quality of life. Put simply, chronic diseases steadily or suddenly disempower individuals before they kill them. When large portions of populations develop chronic diseases, it is not just a problem for individuals and families, it is also a major burden on society. In turn, we must ask why our societies are bearing this burden. Whatever their final physical manifestation, chronic diseases are fundamentally metabolic – generated by the internal biochemistry and physiology of the body. At the same time, given the importance of lifestyle and living conditions, chronic diseases are orchestrated by human behaviour. The central factor affecting metabolism is nutrition, in its broader sense. But how exactly does nutrition shape the cumulative wear and tear that comprises degeneration and ageing? It has taken over a century of research to understand this, as described in the next chapter.

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3

Links Between Nutrition and Ill-Health

A blur of soot and smoke . . . Coketown in the distance was suggestive of itself, though not a brick of it could be seen. Charles Dickens – Hard Times

In small-scale societies, illness is commonly attributed to magic and sorcery as well as biological agents. In early complex societies, gods and deities were likewise considered to have an important role in health, so that the activities of physicians were complementary to religious activities at sanctuaries and temples. Yet it was already clear to the philosophers of ancient Greece that disease and pathology arise as the consequence of two basic factors: external pathogens and stresses; or the inherent susceptibilities and predispositions of the individual. Modern medicine has simply aimed to elucidate these extrinsic and intrinsic pathways to ill-health with greater accuracy. The success of germ theory in the nineteenth century raised expectations that most diseases could be traced to specific microbial organisms. Important public health questions would then include: what was the organism; how was the disease transmitted; how could this be prevented; and how could the disease be treated – which would usually require disposing of the pathogen. Whereas the incubation period of some diseases such as cholera is only a day or two, others have a longer period, such as two to three weeks for rubella, or up to twelve weeks for tuberculosis. Nevertheless, most infectious diseases tend to have a sufficiently short gap between exposure and illness to aid in identifying the agents responsible. This approach is much harder to utilize in the context of nutrition and chronic diseases. One link between nutrition and ill-health is the increased susceptibility to infections among the undernourished, but the overall relationship is far more complex. Diseases of wear and tear have a lengthy aetiology, much of it nested within our living conditions and behaviour: in other words, our lifestyle. The notion that normal human behaviour, in the sense of what is habitual or conventional, can be a primary agent of ill-health represents a fundamental challenge to medicine that has yet to be adequately addressed. Unlike infections, chronic diseases have no specific origin or onset. This makes it difficult to specify exactly what causes disease, or to identify how we could reduce our risk. The challenge only increases when we try to move beyond individual-level factors to those that operate at the level of society. In 1993, the epidemiologists Dianne Kuh and George Davey Smith described how scientists of the twentieth century explored several different models of disease, to

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Links Between Nutrition and Ill-Health

understand which period of the life-course exerted the strongest influence on lifespan.1 This chapter extends their approach, focusing on the experience of Britain, and examining the importance of nutrition in different stages of the life cycle. We will see that early efforts to improve infant nutrition aimed to reduce mortality from infectious diseases; it took several decades before early-life nutrition became recognized as an independent risk factor for degenerative diseases in adults. We will also find that public health nutrition was invariably embedded in efforts to guarantee the national supply of soldiers and workers. Finally, we will see that health in contemporary populations incorporates a metabolic legacy of nineteenth century industrial poverty.

The Paradox of Persistent Infant Mortality In the late nineteenth century, infectious diseases still dominated mortality in industrializing European countries. While people were generally living longer, some age groups were faring worse. In Britain, for example, whereas general mortality had dropped from 21 to 17.4 per 1000 population between 1876 and 1897, infant mortality had increased from 146 to 156 per 1000 live births, with the greatest burden occurring in the first three months of life. Meanwhile, the crude birth rate had dropped from 35.5 to 30.5 per 1000 over the same period.2 The combination of rising mortality and declining fertility exacerbated concern over Britain’s ability to maintain its imperial activities.3 George Newman, a Medical Officer of Health in London, published a detailed examination of infant mortality in 1906, and highlighted the key contribution of ‘epidemic diarrhoea’ along with respiratory diseases.4 The epidemiology of diarrhoea clearly indicated an environmental causation. It was eight times more common in urban than in rural populations, and peaked in summer months. In 1845–54, rates of mortality were almost twice as high in industrial northern regions such as Lancashire and the East Riding of Yorkshire than in southern or rural regions such as Devon, north Wales and Surrey (Figure 3.1). By 1901–5, infant mortality had fallen moderately in all regions, but the regional disparities persisted (Figure 3.2). Newman observed that mortality rates were typically highest in populations living over the major British coalfields, suggesting that urban industrial poverty was an important factor. Despite widespread recognition among physicians and laypeople of the detrimental effects of squalid living conditions, the importance of the environment for public health was challenged from the 1870s by eugenicists, who invoked Darwin’s theory of natural selection to claim that infant mortality was needed to maintain the ‘genetic quality’ of the population. In 1912, for example, Karl Pearson argued that inverse correlations between infant mortality and early childhood mortality represented a ‘winnowing effect’ whereby weaker infants were selected out of the population, thus improving the average quality of surviving children.5 For Pearson, high infant mortality was not a public health problem; rather, it represented a long-term beneficial process, just like the selective breeding of farm animals. Unsurprisingly, those working in the new field of public health disagreed, and the mainstream view was that improving the living conditions of slum dwellers would lead Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:35:49, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.004

The Paradox of Persistent Infant Mortality

Figure 3.1.

45

Map of infant mortality rate per 1000 births in counties across England and Wales. From Newman (1906) (Reproduced with permission of Methuen).

to better health. Much effort was devoted to sanitation and hygiene, reducing the transmission of infectious agents, but nutrition was also attracting attention. In the 1890s, the Dutch physician Christiaan Eijkman had identified the first vitamin deficiency disease,6 and the twentieth century saw new efforts to understand the association between nutrition and health. Already by 1899, breastfeeding was thought to prevent infant epidemic diarrhoea. In Croydon, for example, mortality of breastfed infants was barely one seventh that of infants fed on cow’s milk, and larger studies confirmed these findings in Birmingham and Brighton.7 What remained unclear was the underlying mechanism. Indeed, epidemic diarrhoea was one of the last diseases to be attributed to archaic theories of

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Links Between Nutrition and Ill-Health

170 160

Infant mortality rate

150 140 130 120 Industrial Non-industrial

110 100 1840 Figure 3.2.

1850

1860

1870

1880

1890

1900

1910

Infant mortality rates (mean and standard error) over ~60 years, comparing 15 industrial against 30 non-industrial counties. Data from Newman, 1906.

miasma.8 Even as scientists were isolating the microorganisms responsible for various infectious diseases,9 meteorological conditions were still assumed important for diarrhoea. Several studies were conducted, but failed to link the rate of infection with soil temperature, rainfall patterns or ventilation.10 Instead, cow’s milk appeared a likely vehicle of infection, although not necessarily the ultimate cause. In the US, research had already linked bacterial contamination of milk supplies with infant mortality.11 Subsequent studies showed that milk could transmit not only diarrhoea, but also tuberculosis, scarlet fever, diphtheria and typhoid.12 This led to efforts to clean up the entire supply chain, from cow to consumer. In Britain, research further linked infant diarrhoea with the seasonal appearance of the housefly.13 Collectively, this research highlighted the health benefits of improving infant nutrition, if possible through breastfeeding. In fact, France had already understood the political implications of declining fertility and increasing infant mortality a generation earlier, following defeat in the Franco-Prussian War of 1870–1. Epidemic diarrhoea accounted for around 40 per cent of French infant deaths and, as in Britain, artificial feeding drastically increased mortality risk. While French scientists struggled to identify the pathogen responsible, physicians in Paris and the provinces developed outpatient clinics to promote breastfeeding and provide advice on infant health.14 The first such clinic, initiated by Pierre Budin in 1892, achieved spectacular reductions in mortality and stimulated efforts elsewhere.15 A decade later, similar clinics began to open in Britain. In general, they were less successful than their French counterparts, due partly to their reduced emphasis on promoting breastfeeding and medical care. Instead, attention focused on the issue of ‘poor motherhood’, considered to stem from ignorance, even though research on the working poor indicated that insufficient income rather than education was the primary Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:35:49, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.004

Child Health

47

hindrance to adequate nutrition.16 The main legacy of early twentieth century milk clinics in Britain was not the promotion of breastfeeding, but rather the introduction of health visitors with their function of improving maternal education and hygiene. In 1907, an Act of Parliament made the registration of every birth mandatory, so that the local medical officer could arrange for a trained health visitor to advise the mother on her child’s health in her own home. In 1914, local authorities employed 600 health visitors, and by the end of the First World War this number had increased to 2577.17 The number of voluntary maternity and child welfare centres also grew, while other Acts of Parliament mandated training for midwives (1902) and the provision of meals and medical services in schools (1906, 1907).

Child Health Chapter 4 will describe what these health visitors went on to achieve, but let us first return to the high proportion of men failing the Boer war recruitment examination, described in Chapter 1. Beginning in 1903, the British Medical Journal ran a series of editorial articles on physical degeneration. Discarding the notion that the health of the entire population was deteriorating, it recognized that industrialization involved a large proportion of the rural population moving to cities, where they were exposed to overcrowding, poor sanitation, inadequate diet and social deprivation. In 1890, the typical city-dweller was described as ‘neurotic, dyspeptic, pale and undersized in its adult state, if it ever reaches it’.18 Since the army recruited mainly from urban populations, the impact of early industrialization on health was very apparent. Air and water pollution were defining features of nineteenth-century urban life, and provoked regular epidemics of cholera and typhoid while also promoting respiratory and intestinal diseases.19 Work for the new proletarian labourers comprised monotonous exertion in harsh factory conditions. It was the overcrowded slums hosting these economic transformations, immortalized as ‘Coketown’ by Charles Dickens in his novel Hard Times, that fostered the physical decline encountered by the recruitment campaign. The editorials probed several possible causes for physical degeneration, focusing on living conditions.20 Over 3 million people were identified as living in overcrowded accommodation, sharing bedrooms and occupying back-to-back houses with no possibility of through-ventilation. Can anything be more gloomy and wretched looking than our English system of laying out towns with rows of small badly-built houses, separated only by narrow streets, devoid of trees, and perhaps miles from any open space or park?21

These squalid conditions offered numerous pathways to poor health, demonstrated by the small size of town children and adults compared to their rural counterparts.22 In contrast with contemporary patterns, heights were greatest in Scotland in the nineteenth century and lowest in London.23 Manual employment of teenage children was Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:35:49, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.004

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Links Between Nutrition and Ill-Health

associated with adverse effects on growth, muscular development, posture and dental health.24 Among the specific reasons for military recruitment failure were stunting and underweight, flat feet and decaying teeth, each of which could be attributed to poor physical development in early life.25 It was also recognized that working couples were most likely to experience poverty precisely when rearing children, due to the increased expenses.26 Thus, both maternal and child nutrition were identified as crucial determinants of variability in adult health. The editorial continued: It is useless to undertake to solve a question without going to the root of it, and the root of the national deterioration is in the health of the mother during pregnancy and the feeding of infants during their earliest years. Until women lead healthier lives during pregnancy, and until there is a plentiful supply of pure clean milk available for infants that cannot be suckled and also for small children after weaning, they will grow into puny, sickly, rickety human beings who will never recover their false start in life.27

Nor was nutrition healthier after infancy. Studies of the diet of working-class families indicated an overreliance on cheap foodstuffs that provided inadequate nutrition, especially protein. ‘Wheaten bread, tea, jam, and tinned goods may be said to be the chief diet of the wives and children of the labouring classes.’28 These foods were ‘empty’ – offering calories, but increasing the risk of various dietary deficiencies that are especially deleterious to pregnant mothers and young children. It was concluded, simplistically, that it was not income that prevented healthy nutrition but a lack of understanding as to which foodstuffs would provide valuable nutrients. Commenting on the blandness of the diet, the editorial suggested helpfully that cookery teachers might visit peasant families in France to ‘learn the secret of economy combined with excellent results’.29 Exercise was understood to promote good physique: a wide range of movements would ‘gradually bring into play every muscle and articulation in the body’.30 In an era when gender differences were actively promoted, the editorial observed that ‘boys and girls dressed in ordinary clothes can perform the movements with equal readiness, though we cannot help thinking it a pity that there should not be a distinctive dress for the girls, and in particular special shoes’.31 Diet and physical activity, two mainstays of contemporary preventive medicine, were thus recognized early in the twentieth century to be fundamental for health, especially in early life. Unsurprisingly, during the unstable period preceding the First World War, interest resurfaced in the need for healthy development. Whereas the Boer War had highlighted the consequences of poor infant health, deteriorating relations with Germany drew attention to the physical condition of schoolchildren, who would be the soldiers of the immediate future. In this age group, nutrition was still considered the most valuable target for intervention.32 Following once again the lead from France, the British state increasingly took responsibility for providing meals to poorly nourished schoolchildren. In 1908, a school medical officer in Bradford had shown that offering deprived children meals rich in protein and fat led to greater weight gain than in control children.33 By the start of the First World War, the provision of such meals for undernourished children had been Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:35:49, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.004

Poverty, Nutrition and Growth

150 145

49

Boys Girls

Height (cm)

140 135 130 125 120 Figure 3.3.

Lower

Middle

Upper

Height by income group in British boys and girls aged 13 years in 1880. Data from Oddy, 1982.

mandated by Parliament. In August 1918, just before the war ended, further legislation was passed to ensure the provision of welfare services for pregnant and nursing mothers, and children of school age.34 This reflected growing interest in how social and material deprivation impacted on development.

Poverty, Nutrition and Growth To overturn the arguments of eugenicists, who considered ‘disproportionate breeding of poorer-quality stock’ to underlie physical degeneration, several studies investigated potential causes of poor growth. In 1901, Seebohm Rowntree had published a seminal book, Poverty: A Study of Town Life, that explored the living and working conditions in working-class York.35 He offered the first objective assessment of those living in poverty, unable to meet basic nutritional needs, and demonstrated direct relationships between poverty, short stature and poor health. Data from Victorian Britain showed a powerful social gradient in growth, with a height gap of over 10 cm between rich and poor at around 13 years (Figure 3.3).36 In 1903, the physician Noel Paton published observations on the relationship between maternal body condition and offspring birth weight in guinea pigs.37 Although this experiment suffered a minor setback when two of the animals were devoured by a dog, the data showed that well-nourished guinea pigs produced 0.35 gram of offspring weight for each gram of maternal weight, whereas malnourished guinea pigs produced only 0.25 gram of offspring weight: a reduction of 28 per cent. The study highlighted the importance of maternal size and nutrition during pregnancy for offspring growth, albeit in a different species. Paton concluded that his study ‘probably helps to explain the very high infant mortality among the very poor. The infant starts life at a low-level and readily succumbs to the hardships to which it is too often subjected.’ Downloaded from http:/www.cambridge.org/core. University of Warwick, on 11 Dec 2016 at 08:35:49, subject to the Cambridge Core terms of use, available at http:/www.cambridge.org/core/terms. http://dx.doi.org/10.1017/CBO9780511972959.004

50

Links Between Nutrition and Ill-Health

80 Meals

70

Milk

60

%

50 40 30 20 10 0 1938/9 Figure 3.4.

1941

1942

1943

1944

1945

Percentage of school children in England and Wales receiving school meals or milk during the Second World War. Data from Oddy, 1982.

Despite increasing evidence of the benefits of school meals and milk in the 1930s, nutritional policy was confounded by economic and political interests, and initial proposals for a ‘welfare milk’ programme came not from the Ministry of Health but the Milk Marketing Board.38 Nevertheless, nutritional surveys confirmed high levels of dietary inadequacy among lower socio-economic groups. While the affluent consumed most of the national supply of meat, fish, dairy products, fruit and vegetables, the diet of the working class remained built around white bread, jam, margarine and tea, with bacon the main source of meat.39 Just before the Second World War, driven once again by the need for healthy troops, the government made a concerted effort to improve diets.40 The proportion of children receiving school meals and milk increased rapidly between 1940 and 1945 (Figure 3.4). These efforts contributed to the lack of any decline in British children’s stature during the challenging wartime period. In fact, the opposite occurred, with height increasing in the majority of regions surveyed. While nutrition programmes played a key role, the evacuation of children from cities to rural areas and full employment of the labour force also helped.41 Even as public health efforts targeting children’s nutrition consolidated, however, attention began to shift to older age groups.

Nutrition and Adult Health While improvements in health might be very welcome to families and governments, they were proving a challenge to the life insurance companies, obliged to address the

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Adult Nutrition and Chronic Disease Risk

51

financial implications of lengthening adult lifespans. Analysing data on age at death from the eighteenth to twentieth centuries, the actuary Victor Derrick concluded in 1927 that each generation had a lower mortality risk than the previous generation, and carried this risk through its own life. Biomedical scientists analysing the same data agreed.42 None of these analyses suggested that higher rates of infant mortality were contributing, because, as discussed above, infants were the one age group in whom mortality was failing to fall consistently over time. Thus, adult health was not improved by infant ‘winnowing’; rather it seemed that environmental conditions were impacting differently on successive generations.43 As the twentieth century progressed, however, mortality stopped declining. By the 1930s, declining infectious disease mortality in industrialized countries was counterbalanced by increasing mortality from cardiovascular disease and cancers, occurring from middle-age onwards. To identify the risk factors, prospective cohort studies were initiated, such as the first national birth cohort in Britain (1946), and the Framingham cohort of middle-aged adults in the US (1948).44 Such studies consistently identified components of adult lifestyle, including diet, smoking and physical inactivity, along with physiological traits such as blood pressure and serum cholesterol levels, as predictors of degenerative diseases.45 This research therefore shifted attention away from health as a generic lifelong component of individuals, with early development of particular importance, back to a disease-specific approach, searching for risk factors present in middle-aged adults. Following elucidation of the structure of DNA in the early 1950s, the importance of individual genotype was also increasingly acknowledged. Family and twin studies highlighted the tendency for chronic diseases to cluster among relatives,46 indicating a genetic contribution, and by the 1970s, the aetiology of chronic diseases was considered primarily to involve the interaction of genetic and lifestyle risk factors. From the end of the Second World War, public health efforts addressing these diseases therefore converged on adult diet and behaviour.

Adult Nutrition and Chronic Disease Risk The ‘lifestyle’ approach identified a number of nutritional factors relevant to adult health, and these remain very influential in our current understanding of chronic disease aetiology. By the 1980s, a link between industrialized society and ill-health was being emphasized through the concept of the ‘Palaeolithic’ diet. This approach argued that Western lifestyles subjected the body to environmental stresses for which the human genome, assumed to have undergone natural selection over thousands of generations prior to agriculture, was unprepared.47 The idea of ‘Stone Agers in the fast lane’ became popular, inspiring efforts to rediscover ancestral diets and behaviour patterns. This was part of a broader effort to understand what was ‘natural’ about humans, and drew on studies of the few remaining foraging populations, which hunt and gather wild foods.

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52

Links Between Nutrition and Ill-Health

No contemporary diet is ‘Palaeolithic’, but the metabolic impact of industrialized diets certainly differs from that of foragers’ diets. Glycaemic load refers to the amount of glucose and other sugars that a given food releases during digestion, which in turn dictates how much insulin is required to regulate blood glucose levels. Most wild foods are high in fibre and bulk, and release energy relatively slowly.48 The predominance of starch-rich grains in early agricultural diets must have elevated glycaemic load, and this trend has been exacerbated by recent developments in food technology that have promoted the consumption of refined carbohydrate. Both agriculture and industrialization have therefore involved ‘carbohydrate transitions’, with major implications for insulin metabolism.49 Historically, however, nutritionists have emphasized fat rather than carbohydrate as the primary dietary cause of chronic diseases, following the research of Ancel Keys. Trying to understand the burgeoning increase in cardiovascular disease during the first half of the twentieth century, Keys suggested that the American diet had changed profoundly, with a high-grain diet giving way to one rich in fat.50 Other studies seemingly supported the idea that high dietary fat was the key to heart disease.51 Since atherosclerotic plaque contains cholesterol, a component of animal fat, the hypothesis was considered compelling. Recently, this simple model has been reconsidered. First, greater attention has been directed to the different types of fat in the diet. Most fat manifests as triglycerides, comprising a glycerol molecule attached to three fatty acids that can be differentiated by their structural composition (saturated, monounsaturated or polyunsaturated) and their carbon chain length (n-3 or n-6). Unsaturated fatty acids can also, through the industrial process of hydrogenation, be converted into ‘trans-fats’. Studies have shown that n-6 fats increase clotting risk, artery occlusion and inflammation, whereas n-3 fats reduce these risks.52 Similarly, trans-fats have been associated with atherosclerosis,53 whereas the scenario for saturated fats is less clear. The main implication of this research is that it is less the total fat content of the diet, and more the lipid composition, that matters for cardio-metabolic health (Figure 3.5).54 Diets rich in oily fish or n-3 vegetable oils are considered healthy, whereas diets rich in hydrogenated oils increase disease risk.55 Saturated animal fats are considered proatherogenic by some, but the evidence is increasingly considered unconvincing. Moreover, research has also clarified that levels of triglycerides and LDL and VLDL cholesterol, which are most strongly associated with chronic disease risk, reflect dietary carbohydrate intake as well as fat intake. A separate issue is that high-fat diets are energy dense and may promote obesity. Refined carbohydrates, with high glycaemic load and low fibre level, have been repeatedly associated with chronic diseases.56 Figure 3.6 illustrates the risk of being newly diagnosed with diabetes according to dietary carbohydrate profile in urban India.57 Attention has recently focused on diets rich in sucrose, a composite sugar molecule comprising 50 per cent glucose and 50 per cent fructose. Whereas glucose is regulated by insulin, fructose is not, and is metabolized instead in the liver, where it promotes the synthesis of both fat and glucose, which then perturbs insulin

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Adult Nutrition and Chronic Disease Risk

Saturated fat

Monounsaturated fat

Polyunsaturated fat

53

ns

p = 0.05

p = 0.003

p 30 kg/m2, with the normal range 18.5–25 kg/m2, and chronic energy deficiency