Disorders of eating and weight control
Whether or not we describe somebody as obese depends on the reason for providing a label. In general, the term obesity may be used simply to refer to having more than average body fat. Despite recent doubts about the quality and consistency of some of the research on which the conclusion is based, it is generally accepted that a high level of obesity, medically significant obesity, is injurious to health, contributing to a wide range of morbid conditions, especially cardiovascular disease (Rand, 1994). Aside from this, obesity may be culturally defined, that is, a person may be described as obese if he or she has more body fat than is considered aesthetically acceptable by the person’s society. In this section, I will not be concerned with such distinctions, but will look at the factors that cause variations in body fat between individuals, and will use the general definition given above, of having more than average body fat.
Obesity results only from taking in more calories than we expend. However, beyond this simple relation is a large number of potential reasons for the existence of such an imbalance. One obvious factor, as we have seen, is the easy availability of processed foods of high palatability in western societies. This clearly can increase calorie consumption and may change the set point so that body weight stabilises at a higher level. But this cannot be the sole explanation. Not everybody exposed to such a potential diet becomes obese, and obesity has a higher incidence in some developed countries (USA and UK, for example) than in others, even if the others actually have a higher average calorie consumption (e.g. Denmark).
One undoubted factor is learning. Children in many families are encouraged or even forced to eat all the food placed in front of them. This can lead to eating more calories than required and can become an habitual pattern. This is exacerbated by the division of meals into more than one course, with the opportunity this provides for sensory-specific satiety to increase total calorie intake, particularly if the meal pattern reserves energy-dense foods until the end of the meal. Energy-dense foods, that is foods with a high concentration of calories per unit weight, usually fat- based foods, are highly rewarding, particularly if they are sweet. The association of sweetness with high-fat content of many processed foods is, as we saw earlier, the basis for a learned preference for these foods. Many obese people, and others who indulge in binge eating, show a preference, and often a craving, for such high- density foods, but not, the most recent research suggests, for low-fat sweet foods (see Drewnowski, 1996). Drewnowski et dl. (1995) have shown by the use of opiate receptor blockers that this preference is based on endogenous opioid circuits (presumably beta-endorphins).This can account for phenomena related to ‘comfort- eating’ when food is used to elevate mood, and may permit us to talk about food addictions (see Chapter 8).
There is certainly a genetic factor involved in weight control as well. Stunkard et at. (1986) showed that the weight of people who had been adopted in infancy is more highly correlated with the weight of their natural parents than with that of their adoptive parents. Strains of mice and rats have been bred with a genetic predisposition to obesity. Although these particular strains of rodent develop obesity even on standard laboratory diets, other strains show individual differences in their predisposition to obesity which are only manifest if they are given high calorie and/or varied diets. The genetic basis of human obesity is likely to be of this latter type, depending on the individual being exposed to particular family, social and cultural environments. People clearly differ in metabolic efficiency, and most people respond to excessive calorie intake in a different way from very obese persons. In one study, Sims and Horton (1968) gave normal weight prisoners varied, highly palatable, high calorie meals several times each day. All subjects increased their calorie intake enormously, with some eating more than twice the average amount for sedentary people. Despite this, they only gained a small amount of weight, and at the end of the experiment they returned to their usual diets and their previous weights.
It is partly because of the hereditary contribution that obesity, with its implications for health, is difficult to treat. Whatever method is used, ranging from calorie- reduced diets to surgical removal of fat and reduction of the size of the stomach, weight loss is rarely maintained in the long term. Another factor maintaining obesity has been called the ‘yo-yo’ effect.This is the increased metabolic efficiency that occurs after severe calorie restriction, and has been demonstrated in laboratory animals and in humans. In one such study Brownell et al. (1986) fed rats a high calorie, palatable diet until they became obese. On average it took 46 days for the rats to reach the criterion of obesity. The animals were then starved until their weights returned to normal and were then again fed the high calorie diet.This time it took only 14 days for the rats to become obese. The implication is that their metabolic efficiency had increased so that more energy was stored as fat. This same process may take place in people who lose weight by calorie restriction, making it harder for them to avoid putting weight on again.