But the trap that Stunkard and Mayer had identified is built into the logic of the positive-caloric-balance hypothesis; there is no escaping it. Mayer, as we’ve discussed, proceeded to insist in his book Overweight, as in all his writing, that obesity was the result of sedentary behavior, which simply implicated sloth rather than gluttony and still left the issue defined as a behavioral one. Although Mayer gets credit for convincing his peers that obesity has a genetic component, he implied that the only role of these genes was to make us want to be more or less sedentary. By the end of Overweight, Mayer was insisting not only that the obese must exercise more, but that they must also try harder to eat less. “Obesity is not a sin,” he wrote. “At most, it is the consequence of errors of omission, the result of not having kept up the life-long battle against an inherited predisposition and against an environment which combines constant exposure to food with the removal of any need to work for it physically. In the pilgrim’s progress of the constitutionally plump, salvation demands more than the shunning of temptation. It requires…the adoption of an attitude almost stoic in its asceticism and in the deliberate daily setting aside of time for what will be often lonely walking and exercising.”
Stunkard became a leading authority in the study of behavioral therapy for obesity, which can be defined as a system of behavioral techniques by which obese patients might come to endure semi-starvation, while avoiding the explicit judgment that they achieved their obesity because they lacked willpower or had a defect of character. For instance, they eat too fast, or they are overly responsive to the external cues of their environment that tell them to eat, while being unresponsive to the internal cues of satiation, as one popular theory of the early 1970s had it. “Fat Americans: They Don’t Know When They’re Hungry, They Don’t Know When They’re Full,” as a New York Times headline suggested in 1974. By that time, obesity, like anorexia, was categorized as an eating disorder, and the field of obesity therapy had become a subdiscipline of psychiatry and psychology. All these behavioral therapies, call them what you may, were in fact aimed at correcting failures of will. Every attempt to treat obesity by inducing the obese to eat less or exercise more is a behavioral treatment of obesity, and implies a behavioral-psychological cause of the condition.
Even if we accept that obese individuals are possessed of a defective character, then we’re still left in the dark. Why doesn’t the same defect—“the combination of weak will and a pleasure seeking outlook upon life,” said Louis Newburgh—cause obesity in everyone? “It exists in many non-obese individuals as well,” observed Hugo Rony; “in some of these it leads to chronic alcoholism, or drug addiction, others may become gamblers, playboys, prostitutes, petty criminals, etc. Evidently, such mental makeup, in itself, is not conducive to obesity. Those who do become obese apparently have something additional to and independent from this mental makeup: an intrinsic tendency to obesity.”
If we can believe that people become obese because they simply ignored the fact that they were getting increasingly fatter, year in and year out, with the passive accumulation of excess calories, and that by the time they noticed it was either too late to do anything about it or they really didn’t care (despite claims they might make to the contrary); if we can believe that obese individuals fail to survive indefinitely on semi-starvation diets because they are gluttonously unwilling to forgo temptation and so prefer, consciously or unconsciously, obesity to a life of moderation, then, as Stunkard observed in 1959, the matter is settled. Our job is done. But, of course, it isn’t.
The more thoughtful analyses of obesity over the years have inevitably taken a more empathic view of those who suffer from it. They posit that there is no scientifically justifiable reason—or evidence—to assume that the obese are any more defective in character or behavior than you or I. Eric Ravussin, a diabetologist and metabolism researcher who began studying obesity among the Pima in 1984, has reported that Pima men who gained excessive weight—more than twenty pounds—over the course of a three-year study had a significantly lower basal-metabolic rate before their weight gain than men who remained relatively lean. (This same observation, as Ravussin points out, was made in infants: those who are heavier at one year of life have abnormally low daily energy expenditures when they are three months old.)*85 This suggests a constitutional difference in these individuals; it would be difficult to explain it in terms of sloth and a weak character. As a result, Ravussin questioned the logic and implications of the positive-caloric-balance hypothesis. “If obesity was only caused by an excessive appeal for food,” Ravussin asked in a 1993 article in the journal Diabetes Care, “how can we explain the complete failure of treating it with behavioral therapies? Can we really believe that so many obese patients are liars and are cheating their doctors? How many more times do we need to demonstrate the high rate of recidivism among obese patients after weight loss to persuade others that unwanted metabolic forces contribute significantly to the causes of obesity in man?”
When Ravussin was interviewed more recently, he insisted that overeating and sedentary behavior could not explain the prevalence of obesity and diabetes in modern societies, and particularly not in the Pima. “I was shocked when I went to work with the Pima and I saw the amount of suffering in this population,” he said. “It’s not fun to see your mother [having a limb] amputated when she’s thirty-two or thirty-five because she’s had poorly controlled diabetes for twenty years. There’s not a population in the world as aware as the Pima of the damages of diabetes and obesity. They know that. They are told from the age of two to avoid it, and still they cannot make it.”
Hilde Bruch is now given credit for initiating a “revolution in thinking about childhood obesity”—doing “the first systematic investigation of the inner compulsions of the fat person,” as the New York Times reported in 1950—and so purportedly demonstrating that its roots are not physiological but behavioral. Indeed, Bruch may be the person most responsible for initiating the belief that obesity is an “eating disorder,” and thus sending several generations of psychiatrists and psychologists off to work with obese patients. Yet, ironically, Bruch never embraced this conclusion herself and always considered the primary underlying cause of obesity to be metabolic and/or hormonal.
Despite Bruch’s research linking childhood obesity to overeating and pathologies in the mother-child relationship, she was all too aware that her own research had failed to establish what was cause and what was effect. Her research had been uncontrolled, she noted, because she had studied only obese children and their families. “The literature on behavior disorders in childhood abounds with references to maternal rejection and overprotection,” she explained. There was no way to know whether what she had discovered about her obese subjects actually played a major role in the development of obesity. It was also possible that the children had a predisposition to fatten and that this affected the children’s desire to eat to excess, which in turn affected the family dynamics and how the families treated the children. What appeared to be a cause could in fact be an effect. “Life situations and emotional experiences of this kind,” Bruch wrote, “provoke increased desire for food only in a certain type of person and result in obesity only when such a person has a special tendency to store fat in larger amounts than others and does not increase the energy expenditure correspondingly.”
After publishing her observations on childhood obesity, Bruch put aside her clinical practice temporarily to study psychiatry, in the hope of helping these children. Through the early 1960s, she practiced psychiatry in New York, and then took a position as professor of psychiatry at Baylor College of Medicine in Houston. Throughout this period, she continued to specialize in anorexia and obesity. In 1957, with the publication of The Importance of Overweight, she was still questioning the role of psychological factors in obesity. (She described the book as a “critical re-evaluation and reintegration” of the obesity literature, including her own research.) Bruch couldn’t escape the fact that restricting calories failed to bring obesity under control for any extended period of time, and she was simply unwilling to blame such consistent failure on her patients or their upbringing. “The efficacy of any treatment of obesity can be appraised only by the permanence of the result,” Bruch stated. “When I began to work with obese children,” she wrote, “I was impressed by the seeming ease with which some were able to lose weight once I had gained their co-operation. Having followed such cases over twenty years, I am today even more impressed by the speed with which they will regain the lost weight and by the tenacity with which they maintain their weight at an individually characteristic high level. It is possible to force the weight below this individual level, but such efforts are usually short-lived.”
