|
Page 3 of 11
Preprogrammed Obesity
In his influential internal-external model of obesity, Schachter (1968) proposed that fat people had a different style of eating, one that depended on external cues to tell them when to eat or not. Unlike those of normal weight, Schachter's overweight subjects apparently could not rely on internal physiological signs to decide whether they were hungry. As a social psychologist, Schachter originally emphasized cognitive and environmental stimuli that encouraged the obese to eat. However, his model left open the question of the source of this insensitivity to somatic cues, suggesting the probability that this was an inherited trait. Schachter's (1971) view of the sources of overeating became increasingly physiological in nature when he began comparing the behavior of ventromedial-lesioned rats with obese humans. Several of Schachter's prominent students followed his lead in this direction. For example, Rodin (1981) eventually rejected the internal-external model (as most researchers have by now) with an eye toward locating a neurological basis for overeating. Meanwhile Nisbett (1972), another Schachter student, proposed an extremely popular model of body weight based on an internal regulatory mechanism, called set-point, which is inherited or determined by prenatal or early childhood eating habits.
Peele (1983b) analyzed Schachter's evolution into a purely biological theoretician in terms of biases Schachter and his students had shown all along against personality dynamics; against group, social, and cultural mechanisms; and against the role of values and complex cognitions in the choice of behavior. As a result, the Schachter group consistently failed to pick up discrepant indicators in their obesity research, some of which led eventually to the jettisoning of the internal-external model. For example Schachter (1968) noted that normal-weight subjects did not eat more when they were hungry (as predicted) because they found the type of food and the time of day inappropriate for eating. In another study that had important implications, Nisbett (1968) discovered that formerly overweight subjects who were no longer obese behaved similarly to obese subjects in an eating experiment. That is, they ate more after having been forced to eat earlier than when they had not eaten before. Nisbett interpreted these results as showing that these subjects were unable to control their impulses to overeat and could therefore not be expected to keep excess weight off.
This line of thinking was solidified in Nisbett's set-point hypothesis, which held that the hypothalamus was set to defend a specific body weight and that going below this weight stimulated a greater desire to eat. The idea that obese people could not lose weight, based on laboratory studies and the performance of clients in weight-loss programs, had been the central tenet in all of the Schachter group's work on obesity (cf. Schachter and Rodin 1974; Rodin 1981). Yet such pessimism seems an unlikely deduction from a study like Nisbett's (1968), in which subjects who had been obese and who continued to display an external eating style had indeed lost weight. When Schachter (1982) actually questioned people in the field about their weight-loss histories, he found remission was quite common in obesity: of all those interviewed who had ever been obese and who had tried to lose weight, 62.5 percent were currently at normal weight.
Schachter's serendipitous finding disputed the entire thrust of over a decade's research—namely, that people were locked into obesity by biological forces. The idea would not die easily, however. Another Schachter student and his colleague recorded Schachter's (1982) finding but dismissed its significance by indicating it was probably only those obese subjects who were above their set-points who had been able to lose weight in this study (Polivy and Herman 1983: 195-96). Polivy and Herman based this calculation on the estimate that from 60 to 70 percent of obese people were not obese in childhood. Their assertion requires that we believe that nearly all of the people in the Schachter study who have been overweight for reasons other than biological inheritance (and only these) had lost weight. Yet undoubtedly many in this category would remain fat for whatever presumably nonset-point reasons had caused them to become obese in the first place. Rather than being the underlying source of obesity its adherents had painted it to be, set-point now seemed not to be a major factor in most cases of overweight.
Polivy and Herman's (1983) description of their outlook did not reflect this understanding about set-point and obesity. Instead, they argued that "for the foreseeable future, we must resign ourselves to the fact that we have no reliable way to change the natural weight that an individual is blessed or cursed with" although "perhaps, as research progresses, we will be able to imagine such biological interventions—including even genetic manipulations" that will enable people to lose weight (p. 52). Polivy and Herman furthermore attributed binge overeating—the extreme of which is bulimia—to people's attempts to restrain their eating in the effort to go below their natural weight (see chapter 5). These researchers' work agrees with that of popular writers (Bennett and Gurin 1982) and the dominant research approaches in the field (Stunkard 1980) in maintaining a view of human eating and overeating that is essentially the same as that held by biological theorists of alcoholism and drug addiction toward drinking and drug consumption. In all cases, people are seen to be under the sway of invariant forces that, in the long run, they cannot hope to contravene.
Meanwhile, Garn and his coworkers (1979) have shown that similarities in weight levels among people who live together are a result of similar eating habits and energy expenditure. This "cohabitational effect" holds for husbands and wives and is the largest factor in weight similarities between parents and adopted offspring. People who live together who become fat do so together (Garn et al. 1979). The longer parents and their children live together (even when the children are age 40) the more they resemble each other in fatness. The longer parents and children live separately, the less pronounced such similarities become until they approach 0 at the extremes of separation (Garn, LaVelle, and Pilkington 1984). Garn, Pilkington, and LaVelle (l984), observing 2,500 people over two decades, found "those . . . who were lean to begin with generally increased in fatness level. Those who were obese to begin with generally decreased in fatness level" (pp. 90-91). "Natural weight" may be a very variable thing, influenced by the same social values and personal coping strategies that affect all behavior (Peele 1984).
Interpersonal Addiction
The enormity of the implications of the genetic transmission of addictive impulses is driven home by several theories claiming that people are compelled by chemical imbalances to form unhealthy, compulsive, and self-destructive interpersonal relationships. Tennov (1979) maintained that such "limerent" people, who are in every other way indistinguishable from other people, have a biological propensity to fall head-over-heels in love and create disastrous romantic attachments. Liebowitz (1983) proposed that a failure in neurochemical regulation—similar to that hypothesized to cause manic-depressive reactions leads people (almost exclusively women) to fall heatedly in love, often with inappropriate partners, and to become inordinately depressed when the relationships fail. These theories illustrate mainly the temptation to believe that compelling motivations must have a biological source and the desire to mechanize human differences, imperfections, and mysteries.
|
