SECTION IV. OTHER DISORDERS
CHAPTER 19. OBESITY
Doctors consider a person to be obese if their body weight exceeds by 20 percent the standard weight listed in height-weight tables.
It may seem strange to included obesity in a book on deviancy, but many persons see fatness as deviance. In a laissez-faire capitalist society with an equality of opportunity ethic like the United States, there is a tremendous pressure on each individual to be materially successful. Americans see the opportunity structure to be a fair one, which explains the importance placed on individual effort. Accompanying this stress on individual effort is a belief in the importance of free will and voluntarism. The end result of the equality of opportunity thesis is a moralism that stresses that those people who are successful are good and those who are not successful are bad. In a culture that also stresses the equality of middle class people, there is pressure to appear humble even when successful. This places great stress on individuals to use symbols of conspicuous consumption to indirectly indicate that they are wealthy and, therefore, good and successful. Weight is perceived as a symbol of conspicuous consumption -- as an extension of material well-being. Therefore, overweight people tend to be seen as being unsuccessful and bad, while normal weight and thin people tend to be seen as successful and good.
There is definitely a heredity factor working in obesity. Correlational investigations have demonstrated that obesity tends to occur in families (Mayer, 1957, Withers, 1964). Hartz, Giefer, and Rimm (1977, reported in Jeffrey, Dawson, & Wilson, 1988:239) collected data from approximately 10,000 individuals and reported that hereditary factors accounted for 11% of the variance of obesity, whereas the family environment accounted for 35%.
The physiology of weight is somewhat involved. Fat cells, once acquired, do not decrease in number, although the size of the cells may vary (Agras, 1987:8-9). Early in life, children who will become obese have a greater number of fat cells than nonobese children, and also experience a more rapid increase in the number and size of such cells during childhood and early adolescence.
The amount of fat in the body appears to be precisely regulated and maintained. This means that it is relatively difficult to change one's amount of body fat; if a change does occur, physiological reflexes will act to restore fat levels to normal. Studies have also shown that when the overweight person is put on a low-calorie diet, the body reduces its oxygen consumption, a measure of energy utilization, to compensate for the caloric deficit. This adjustment may occur quite rapidly, so that the benefits of lowered caloric intake may be largely offset in a period of a few weeks. Exercise can only offset this compensatory mechanism to a limited extent.
The experience of dieters also demonstrates the body's weight regulation system. As weight is lost, there is a tendency for appetite to increase, and underweight people become more and more uncomfortable over time. The all too frequent result is that, after the period of enthusiasm for dieting wanes, slight overeating occurs and weight is restored. Most obese people regain the weight lost during treatment (Stunkard, 1983:12). Repeated episodes of dieting may create the "yo-yo" effect of losing and regaining weight. This yo-yo effect may actually make it more difficult to lose weight in the long run, as the body may become more resistant (Woods and Brief, 1988:299).
These dieting-related phenomena have led to the concept of a "set point" for body weight, suggesting that the brain and other systems try to maintain a fixed or constant amount of fat. And one means of control over the amount of fat in the body is the amount of food eaten (Woods and Brief 1988:299, cited in Jeffrey et al. 1988:241). Research suggests that the hypothalamus is directly linked to weight regulation (Kennedy, 1957; Powley & Keesey, 1970) with some areas acting to increase it (a feeding center) and others to decrease it (a satiety center).
Many people believed that metabolic and endocrinological problems were the base cause of obesity. Some studies have shown that, rather than causing obesity, these anomalies actually result from increases in fat tissue (Jeffrey, et al. 1988:241).
Obesity is not an example of a failure to regulate weight. Obese individuals regulate their weight perfectly well; hence their difficulty with losing weight. Rather, obese people seem to have an elevated set point that their systems try to maintain (Kessey and Corbett, 1984). Nisbett (1972) has a theory that obese people regulate body weight, but that they are biologically programmed to be fat. Their set point, however, is higher than that which social pressures tolerate.
It is unclear what factors determine the set point that one has. Genetic factors, and perhaps nutritional factors early in one's life, may be most important (Woods and Brief, 1988:300). Fat tissue itself may be important in setting the set point (Stunkard 1983:7-8). It may be adipose tissue. Particularly for those obese people where obesity began early in life, their adipose tissue may contain more fat cells than does the adipose tissue of either nonobese persons or of persons whose obesity began during adult life. Indeed, the adipose tissue of morbidly obese persons may contain five times as many fat cells as that of persons in the other two categories. When they reduce, the fat content of their individual fat cells must be reduced to one-fifth the size of a "normal" fat cell for them to reach statistically normal levels of body weight.
Fat-cell size, perhaps particularly events at the cell membrane, may thereby set a biological limit to weight reduction. This is because at precisely the point when further weight loss can only be achieved by reducing fat cells to subnormal size, most people stop their weight loss routine treatment at widely varying levels of body fat.
The best candidate for the regulator of the set point -- the elusive fat signal -- is the hormone insulin (Woods and Brief, 1988:300): insulin levels in the blood are directly correlated with the amount of fat tissue in the body; blood insulin accesses areas of the brain important for fat and appetite regulation; and the experimental administration of small amounts of insulin directly into animal brains reduces food intake and body weight.
There is a high incidence of emotional disturbance in both inpatients and outpatients treated for obesity. Morbidly obese people who diet suffer even more severely from emotional disturbances than do less obese persons. There may be, however, physiological reasons for some of these disturbances. In its desire to maintain a set point of weight, the body may use depression and other neurotransmitter induced signs of distress as a means of forcing the dieter to eat. Manipulations of insulin may also be used as a technique of coercion to force a dieter to eat.
Blundell (1980) has developed a working conceptualization of brain chemistry and feeding; the model shows how norepinephrine, dopamine, and serotonin systems could interact to control the moment to moment consumption of food and the selection of certain dietary components. Dopamine plays an indirect role in feeding, possibly by acting as a "gate" to permit the expression of eating or by influencing the rate of the feeding process. Any eating episode may be divided into three stages: the initiation of eating; the actual articulation of eating; and the termination of the episode. There is a different constellation of neurochemical events associated with each stage.
Consistent with this observation, food and eating often become subject to misperceptions (Polivy, Herman, and Garner 1988:275- 276). The dieter becomes preoccupied with thoughts of food and eating. Weight regulation may be maintained by making it very difficult for a dieter to distinguish emotion from hunger, or differentiate between being hungry or sated. This state of misperception then makes it more likely that the dieter will eat in response to inappropriate (e.g., emotional) internal sensations.
More evidence that the body uses emotional confusion to insure the weight set-point comes from studies of restrained eaters (Stunkard 1983:16). Studies have shown that if obese people consumed a preload of sandwiches and soft drinks, they subsequently ate more test food than they would have without the preload. The tendency of restrained eaters to eat more following a preload is related to both guilt and depression. Once a food rule is broken (a high preload), binge eating tends to occur (Agras, 1987:12). When depressed some people eat less and some people more. Herman and Polivy (1975) say that it is the unrestrained eater who shows the classical pattern of anorexia and weight loss during depression. By contrast, restrained eaters eat more and gain weight when they are depressed. Depression disinhibits restraint, and, therefore, the restrained eater violating a food norm loses cognitive controls over eating. Subsequently, biological pressures to eat force body weight back up to the set point (Stunkard, 1983:16-17).
Obese people have certain common characteristics: preoccupation with food; increased taste responsiveness; emotionality; physical inactivity; and elevated levels of free fatty acids in the blood (Stunkard, 1983:6-7). But these are not characteristics of obesity per se, but rather of restrained eaters. Because of the great frequency of dieting, many persons have body weights below their physiological set point. According to this view, much of their distinctive behavior is not a result of their being obese, but of their not being obese enough. Indeed, the characteristics of obese people listed above are also characteristics of starving people.
In some cases, there may be psychiatric disturbances involved in obesity. Many eating disorders are expressions of psychiatric obsessions. Research has suggested an association between obsessive-compulsive disorder and organic problems such as abnormalities in the bifrontal and temporal areas of the brain (Behar et al., 1984; Flor-Henry, et al. 1979). Tricyclic antidepressants have been reported to relieve the symptoms of the disorder (Quay and Werry, 1986:475).
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