GENETIC VERSUS ENVIRONMENTAL EFFECTS
Clearly both the environment and genetics are responsible for obesity, but how do they interrelate? There are large differences in the amount of obesity between populations. Some of this variation can be explained by differences in body frame which makes it difficult to compare, for example, Samoans with Cambodians. However, even within Caucasian populations there is a wide range in the percentage of people who are obese. In many Eastern European countries, about 30-45 per cent of females would be classified as obese compared with about 10-13 per cent in Australia and New Zealand. These differences in the prevalence of obesity are largely dependent on differences in the environment (fat content of the typical diet, food variety and availability, and availability of labour-saving devices). This is also shown by the increases in obesity within a population over time and in ethnic groups who migrate from ‘low obesity’ to ‘high obesity’ countries.
Within any particular environment, however, the response of individuals to that environment will vary. Some may respond to a high fat diet with only a small gain in weight, whereas others will gain a lot. How much an individual responds to the environment is largely dependent on his or her genetic makeup. The most convincing evidence for this has come from a series of studies performed by Dr Claude Bouchard and others from Laval University in Quebec, on identical twins. They increased the calorie intake of twins by 1000kcal/day for 3 months under strictly controlled conditions. Naturally, everyone gained weight, but some gained much more than others. If one twin only gained a few kilograms, the other twin tended to have a small weight gain as well. If one twin gained a lot of weight, so did the other twin. In other words, under identical environmental conditions, people gain weight at different rates and the amount they gain seems to be genetically determined.
This can be viewed in another way using the population distribution of body size . Consider a population that lives in an environment which does not promote obesity—such as a remote Pacific island with little contact with the outside world, where the food has to be gathered, and where deep-fried chicken is still unknown (environment A). There will be a variety of body sizes, but very few will be classified as obese. Then an airport is built, the tourists arrive, motorised transport takes over from legs and paddles and the fried chicken takeaways set up business. Ten years later, the population distribution of body size has shifted to the right and more people are now classified as obese (environment B). However, the distribution is skewed, so not everyone gained weight at the same rate. A person X who is ‘genetically lean’ and is at the left hand side of the curve gained only a small amount of weight as the environment changed from A to B. Person Y happens to be genetically more predisposed to weight gain and is on the right hand side of the curve. He or she gained considerable weight and in environment B is now obese (Y).
This shift in population levels of obesity also provides evidence for approaches to deal with the problem. Individual, one-on-one approaches (the ‘high risk’ approach) are obviously necessary. But these do little to affect the total population. A small shift in the total curve shown in Figure 1.3 to the left on the other hand, will have a major effect on public health. In other words, small fat losses in a large number of people will have a greater impact on the health of the population as a whole than larger losses in a small number.
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