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# 2.3 Obesity – an evolutionary perspective

If you were now to take a broader biological approach to the data discussed in the previous section you might still be puzzled. Excess body weight leads to a variety of diseases, including diabetes, osteoarthritis and so on – surely this must reduce overall biological fitness.

## Activity 21

> What is biological fitness?

### Answer

The formal definition is ‘lifetime reproductive success’. It can be estimated by measuring the number of offspring (or perhaps even grandchildren!) left by an individual relative to other members of that population.

So why are we, as a species, apparently so unresponsive to the potential reduction in fitness that may result from obesity? Why has natural selection not equipped us with satiety mechanisms that are tuned to the types of nutrients found in our diet? A speculative answer to this question is provided by Prentice and Jebb (2003). They suggest that the critical point to consider is the environment in which our evolutionary ancestors lived. Genetic and fossil evidence suggests that our species, Homo sapiens, evolved in Africa, around 200 000–120 000 years ago, from an ancient Homo species, which had a hunter–gatherer lifestyle. Since then, for most of the time, humans have also been hunter–gatherers, until about 12 000 years ago, when subsistence farming became established. Both the hunter–gatherer and the subsistence farming diets have a much lower energy density than those available in many societies in the developed world. Even today some groups of subsistence farmers exist on diets with an average energy density of about 500 kJ per 100 g, which is only a quarter of the value for a typical fast food meal. Although the diets of other primates species, e.g. chimpanzees, are highly variable, their energy density and fat content are also very much lower than that characteristic of present industrialized societies. Thus our apparent failure to adapt may be because our distant ancestors were not exposed to diets of high energy density and we therefore don't have the appropriate physiological and behavioural responses to such foods.

The idea that humans are best adapted to an environment that is quite different from that in which we now live was first discussed by the child psychologist John Bowlby in 1969 when he referred to our ‘Environment of Evolutionary Adaptedness’ (EAA). This concept has become very influential in both human behavioural ecology and evolutionary psychology. However, the concept also has its critics because it is very difficult to get unambiguous evidence about exactly what kind of environment our EAA might have been. Prentice and Jebb (2003) suggest that modern day subsistence farmers in Gambia may provide a good model for the kind of diet available during much of our evolutionary past. However, it is likely that early humans lived in a wide variety of environments and that different populations consumed very different types of diet. Even in recent times, hunter-gatherer and subsistence farming populations show tremendous variety in their food sources.

## Activity 22

> From your general knowledge, suggest some examples of this type of variety.

### Answer

The traditional diet of Inuit Indians living in Northern Canada consists almost entirely of protein and fat derived from the seals and salmon that are abundant there. The traditional diet of Masai warriors is also very high in animal fat and yet is not associated with high levels of either obesity or heart disease.

Several alternative, though not mutually exclusive, mechanisms to account for some cases of obesity involve the possibility that some of our ancestors might have had adaptive responses to nutritional shortages. One of the most interesting of these explanations is known as the 'thrifty phenotype’ hypothesis (Ozanne and Hales, 2002); it suggests that poor fetal nutrition leads to adaptive changes in physiology that prepare an adult for a life of poor nutrition (Figure 7). However, if poor fetal nutrition is followed by good nutrition in later life then the consequences may include obesity and type 2 diabetes. Evidence to support this idea comes from studies of individuals who were born at the end of a severe famine that occurred in the Netherlands towards the end of World War II – the Dutch Hunger Winter. Pregnant women who were affected by the famine tended to have children of lower birth weight than women who were unaffected by the famine. However, the affected children, as adults, were more likely to be obese and suffer from type 2 diabetes. By contrast, studies of the children of pregnant women in sub-Saharan Africa who also suffered from famine both in utero and as adults showed no increase in diabetes. Instead, not surprisingly, they continued to be thin and well adapted to a life of relatively low calorie intake.

Figure 7 The ‘thrifty phenotype’ hypothesis.

Recent studies of monozygotic (identical) twins in Denmark suggest that these effects are a direct result of fetal nutrition and do not depend on genetic differences between individuals. Where identical twins do differ in birth weight, it is the twin with the lighter birth weight who is at greater risk of obesity and diabetes as an adult.

## Activity 23

> Why should it be the lighter twin that is most at risk of obesity and diabetes?

### Answer

Monozygotic twins have identical genotypes so it must be differences in their environment that have led to differences in birth weight. Although they have the same mother and lie in the same womb, one must have been less well nourished. The thrifty phenotype hypothesis would predict that physiological changes had occurred in the lighter twin who would now be better adapted for a life of poor nutrition. As with the children born after the Dutch Hunger Winter, these Danish twins are likely to be well nourished, a situation for which they are not best adapted.

This ability to vary or ‘programme’ adult physiology as a consequence of early life experiences may be a general feature in mammals since exactly the same responses to fetal malnutrition can be obtained in laboratory rats.

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