In order to place western diseases in an evolutionary context it is necessary to consider the experience of human disease throughout human evolutionary history. To achieve this I adopt a framework drawn from the work of Boyden (1987) and Cohen (1989), illustrated in Table 2.1. This approach emphasises the need to understand the way of life, ecology and health experience of hunter–gatherer people, because such an understanding informs us about the context in which members of our species lived for so much of its evolutionary history. An examination of the enormous impact of agriculture and then of urban living on human health illustrates how changes in ways of life have had profound effects on disease experience in the past. As will become clear in later chapters, it is also increasingly apparent that an understanding of the evolutionary history of human exposure to infectious disease and nutritional pressures, which was profoundly affected by these innovations, is relevant to our understanding of western diseases. Finally, I consider the decline of infectious diseases and rise of non-communicable disease in the west, the so-called epidemiologic transition, and trends in the prevalence of western diseases over the nineteenth and twentieth centuries.

Human ecology and health in the Palaeolithic

Anthropologists have used various kinds of evidence to try to find out more about the ways of life of humans during this period, and to characterise their experiences of health and disease.

In this chapter I focus on three aspects of female reproductive life that have been adversely affected by affluent western life: the relatively unrecognised problem of a high rate of impaired reproductive function and infertility in women; the consequences of a lack of breastfeeding for mothers and children; and the menopause. The focus on women is not exclusive and I also discuss briefly how men's reproductive function has been affected by life in the affluent west and consider the debate about whether an analogy can be drawn between menopause in women and the less extreme age-related decline in reproductive function experienced by men.

Impaired reproductive function

My main purpose here is to examine the effects of the high levels of obesity, insulin resistance and insulin seen in western populations (see Chapter 3) on reproductive function. I also consider some other features of the western lifestyle that may affect reproductive function.

Obesity, hyperinsulinaemia and impaired reproductive function

Women living in western societies generally experience higher levels of the ovarian steroid hormones progesterone and oestradiol over a lifetime than do those living in less affluent countries and in the affluent east (see Chapter 5). In fact, ovarian hormone levels in western women are considered to represent the extreme of global variation in ovarian function. As we have seen, this is likely to be a result of mechanisms that evolved to link the availability of energy with fecundity in hunter–gatherer populations.

Breast cancer is one of the biggest causes of mortality in western societies. Other reproductive cancers are less well known but also common, including endometrial and ovarian cancers in women and prostate cancer in men. They are often cited as examples of ‘western’ cancers, since levels are much higher in affluent western populations than elsewhere. As with most other cancers, and non-communicable diseases in general (see Chapter 2), increased lifespan is one obvious explanation of high rates of these diseases in affluent western populations, but increased lifespan cannot explain all of the association between westernisation and reproductive cancers. So, why does an affluent western lifestyle bring an increased risk of reproductive cancers?

In this chapter I draw on the work of biological anthropologists and epidemiologists to answer this question. After summarising geographical and temporal trends in the incidence of reproductive cancers, I describe the main known risk factors for these diseases. I then go on to show that the affluent western lifestyle has increased exposure to all of these risk factors, focusing in particular on the evidence linking western life to increased exposure to endogenous gonadal hormones: oestrogen and progesterone secreted by the ovaries in women, and androgens secreted by the testes in men. Here I draw particularly on the pioneering work of Ellison (Ellison 1999).

What are reproductive cancers?

Cancerous tumours, including those of the reproductive system, result from the unregulated division of undifferentiated cells.

In 1974 a seminal paper drew attention to the very high rates of type 2 diabetes in many native populations of the Americas, Greenland, Polynesia, Micronesia and Melanesia (West 1974). West suggested that diabetes was probably uncommon in these groups prior to 1940, and noted that rates were still very low in those least touched by market economies. The high rates of diabetes in these populations were initially most often ascribed to a genetically based susceptibility to the development of obesity and associated diseases on the adoption of a western way of life. This explanation is commonly known as the ‘thrifty genotype’ hypothesis. An alternative explanation is that the susceptibility of these populations lies solely in the rapid changes of lifestyle they have experienced. Thus, it has been suggested that those born into a relatively poor environment may, if they later encounter a more western environment, be vulnerable to the development of obesity-related diseases. This latter explanation is sometimes referred to as the ‘thrifty phenotype’ hypothesis, to highlight its contrast with the thrifty genotype hypothesis. In this chapter I describe the populations best known for their very high rates of type 2 diabetes and cardiovascular disease, and then go on to consider in detail the competing explanations offered for these high rates of disease. I focus particularly on the debate about the causation of type 2 diabetes.

The inspiration for this book originates with Professor Geoffrey Ainsworth Harrison of the University of Oxford, who taught me and many others the value of the evolutionary approach to human biology. The third edition of the textbook he wrote with Paul Baker and others (Harrison et al. 1988) was a defining part of the curriculum at Oxford and I draw strongly on the approach of that volume in this book. He also introduced us to literature on western diseases published in the 1970s and 1980s by Boyden, and by Trowell and Burkitt, described at the beginning of Chapter 1. His supervision of my postgraduate work provided invaluable further opportunity to learn from his methods and ideas. In my subsequent career I have benefited greatly from this solid and stimulating foundation.

In my own teaching of advanced undergraduates and graduate students at Durham University I have felt the lack of an up-to-date equivalent of these texts, a feeling that was the main motivation for me to write this book. In the intervening years I have also benefited from exposure to epidemiological research on cardiovascular disease and other western diseases, and I hope that the end result profits from my learning beyond anthropology. My aim has been to draw these two approaches together to create a new synthesis. I am aware, of course, that in aiming for such a synthesis I have failed to provide the level of evolutionary theory that some evolutionary biologists and biological anthropologists would wish to see, while offering less detail of biomedical and epidemiological research than might be expected from the other side.

This book sets out to examine why certain non-communicable diseases have become common, first in affluent western populations and now, increasingly, worldwide. I use an evolutionary perspective because of its value in showing us why and how human bodies are vulnerable to these diseases. In this chapter I introduce the concept of western diseases and outline the evolutionary perspective applied throughout the book.

Western diseases

In the 1960s and 1970s concerns developed about the rise of diseases such as coronary heart disease, type 2 diabetes and colon and breast cancer as important causes of mortality and morbidity in the western world (Cleave et al. 1969; Boyden 1970; Burkitt 1973). The origins of the term western diseases, and of the approach I adopt in this book, lie in this work. The diseases identified were linked to ‘modern western civilisation’ and were considered to be ‘man-made’ (Trowell and Burkitt 1981a). Specifically, the rise of western diseases was blamed on increased availability of food (accompanied by a decline in the consumption of dietary fibre) and a reduction in physical activity. These authors also acknowledged the impact of an increase in life expectancy, which led to a higher proportion of susceptible older people in the population. The emergence of western diseases in non-western societies, for example in the Far East and in Africa, was linked to the process of westernisation, that is, the adoption of elements of the modern western lifestyle in other areas of the world (Trowell and Burkitt 1981b), a simplistic but nevertheless helpful concept.

Many researchers and lay members of society have expressed, or can identify with, the view that the modern western lifestyle does not nurture good mental health. The biggest foci of concern are depression and stress, both identified as increasingly important causes of ill health around the world, particularly in western societies.

According to biomedicine, depression can be an emotion, a symptom, or a disease. Lesser feelings of depression form part of the normal range of emotional experience, while clinical depression is classified as a psychiatric illness. Rates of diagnosed clinical depression have increased in the United States, Sweden, Germany, Canada and New Zealand since the Second World War and there appears to have been a decrease in the average age of onset of depression (Klerman and Weissman 1989). Projections suggest that depression is likely to be only second in importance to coronary heart disease as a cause of ill health worldwide by 2020 (Murray and Lopez 1997) and to maintain that position in 2030 (Mathers and Loncar 2006).

When people talk about being stressed, they usually mean that they are struggling to cope with the demands being made of them, and this is also the sense in which the term stress is now most often used by academics. There is a shared notion that people living in affluent industrialised societies live increasingly stressful lives, working long hours, undertaking long commutes, juggling the demands of work and family, struggling to find time for exercise, and suffering from ill health as a consequence, and that this kind of life generates more stress and stress-related disease than humans have ever felt before.

The rise of asthma and allergic diseases in most affluent countries of the world over the last 40 years has been striking, and many theories have been proposed to explain the phenomenon. These theories help us to understand what has gone wrong in our bodies when we have an allergic response to apparently harmless substances, such as cat dander, pollen or peanuts. Some of these ideas incorporate evolutionary insights, in particular, the suggestion that the human immune system is now lacking contact with organisms that would previously have had an important role in directing its development.

The scale of the problem

What is asthma?

The term asthma has usually been used to describe attacks of shortness of breath and wheezing caused by swollen and inflamed airways that are prone to constrict suddenly and violently. It is more commonly seen in children than in adults. However, there is increasing concern that the term is used to describe a range of conditions that do not necessarily share common underlying pathologies (Lancet Editorial 2006). There is no single biological marker or clinical test for asthma, and symptoms, triggers and responses to treatment are variable. The most common distinction is between allergic and non-allergic asthma, with allergic asthma being more common, particularly in children. But categorising a given case of asthma, even according to this broad dichotomy, can be difficult (Wenzel 2006).

Living in an affluent western society brings many advantages for health, notably security from hunger and from the serious infectious diseases of infancy and childhood that plagued western countries prior to the twentieth century and continue to inflict a heavy burden on populations in poorer countries today. However, as we have seen, westerners suffer from a characteristic set of relatively new non-communicable diseases, and these diseases are seen in non-western populations at increasingly high rates. In this concluding chapter I first summarise what an evolutionary perspective offers to the study of human vulnerability to western diseases. Next, I consider prospects for the future, focusing on what ‘westernisation’ means for the health of the millions of people subject to its influence, and on the insights that an evolutionary perspective provides in relation to possible preventive strategies.

Human vulnerability to western diseases

This book has shown that humans are vulnerable to western diseases because, as a species, we evolved in very different environments from those experienced today. We can summarise these effects in relation to obesity, in many respects the core pathology underlying western diseases. When the genus Homo emerged, selective pressures related especially to having a large brain led to these early hominins becoming proportionately fatter than other species of the tropical savannah. Humans also evolved under selective pressures imposed by the necessity of eating wild animals and plants and being physically active. The human genotype was ‘thrifty’, making effective use of scarce resources.

Obesity is common and increasing in prevalence in Europe, North America, Australia and Latin America, particularly among the young (Seidell 1995; Martorell et al. 1998; Midthjell et al. 1999; Catanese et al. 2001; Tremblay et al. 2002; Thorburn 2005). While obesity emerged first in western populations, it is rapidly spreading to poorer countries (Yoon et al. 2006). Considerable concern has been expressed in the medical literature, as well as more widely, about the obesity ‘epidemic’ and its associated health consequences. In this chapter I outline the evolutionary context for the emergence of obesity as a major health problem, comparing what we know about diet and energy expenditure, the main determinants of obesity levels, in hunter–gatherer societies and in industrialised countries today. I also examine the closely related diseases type 2 diabetes and cardiovascular disease. Some populations seem to be particularly vulnerable to the development of obesity and related diseases, an issue explored in Chapter 4.

Diet, physical activity and body composition in humans before agriculture

The first members of the taxonomic group to which apes and humans belong (hominoids) lived 30 million years ago and subsisted largely on fruit, with some vegetable foods and meat. Meat began to assume more importance in the hominin line from around 7 million years ago, particularly with the advent of stone tools about 2 million years ago (Richards 2002).