obesity. He scoffed at the notion that “retarded metabolism” could play a role in obesity, because the obese expend as much energy as the lean, or more. And Bruch’s research, Newburgh went on, constituted the definitive proof that even the most obese children earned their condition by eating too much. If obese children could no longer hide behind the excuse of a constitutional predisposition, then neither could obese adults, Newburgh said. Thus, the only obstacle standing between obesity and leanness was insufficient willpower. As proof, Newburgh offered up a case study of a patient who lost 286 pounds in a year on a diet of three hundred calories a day, and then another eighty pounds the following year while eating six hundred calories a day. By then this patient had returned to his normal weight; “his gluttonous habits had been abolished,” Newburgh wrote, and he had subsequently maintained his weight “without any effort to restrict his food intake.” This may have been true, but if so, Newburgh’s patient was virtually unique in the annals of obesity research.
By the end of Newburgh’s review, he had dismissed any possibility of a constitutional predisposition as a factor in the etiology of obesity. If genes had anything to do with obesity, which Newburgh did not believe, “it might be true that a good or poor appetite is an inherited feature.” If obesity ran in families, “a more realistic explanation is the continuation of the familial tradition of the groaning board and the savory dish.” If women became matronly after menopause, it had nothing to do with hormones—that “the secretions of the sex glands, now in abeyance, formerly had the power to restrain the growth of the adipose tissue,”—but, rather, that the postmenopausal woman now had the time and the inclination to indulge herself. “She does not resist gain in weight, since the friends in whom she has the greatest confidence have assured her that nature intends her to lay on weight at this time of life,” Newburgh wrote.
To the generation of physicians who took up the treatment of obesity in the decade following World War II, Newburgh’s 1942 review was the seminal article on human obesity. “The work of Newburgh showed clearly…,” these physicians would say, or “Newburgh answered that…,” they would respond to any evidence suggesting that obesity was caused by anything other than what Newburgh had called a “perverted appetite”—overeating, or the consumption of more calories than are expended.
But this simple concept had a fundamental flaw, which dated back to von Noorden’s original conception of exogenous obesity. The statement that obesity is accompanied by an imbalance between energy intake and energy output—calories in over calories out—is a tautology. As Marian Burros said, it has to be true, because it is implied by the law of energy conservation. So, then, what causes this imbalance? Von Noorden’s proposition that the imbalance is caused by “overeating and deficient physical exercise” (or “excess calorie consumption and/or inadequate physical activity,” as the Surgeon General’s Office put it) is both an assumption (unproved) and a tautology. The assumption is that something that accompanies the process of becoming obese—overeating and deficient physical activity—causes it. The tautology is that these terms are defined in such a way that they have to be true.
The terms “overeating” and “deficient physical exercise” are applied only to the overweight and obese. “If eating behavior did not produce deposits of body fat we could not call it overeating,” is how this phenomenon was phrased in 1986 by William Bennett, then editor of the
Von Noorden’s proposition, which still obtains today, is the equivalent of saying that “alcoholism is caused by chronic overdrinking” or “chronic fatigue syndrome is caused by excessive lethargy and/or deficient energy.” These propositions are true, but meaningless. And they confuse an association with cause and effect. They tell us nothing about why one person becomes obese (or alcoholic or chronically fatigued) and another person doesn’t. Moreover, as Bennett noted, even if fat people did eat more and/or expend less energy than most or all lean people— something that has never been shown to be true—it would still beg what should be the salient question in all obesity research: why wasn’t intake adjusted downward to match expenditure, or vice versa? Nor does it explain why reversing this caloric imbalance fails to reverse the weight gain reliably.*83
Those who are overweight or obese, with exceedingly rare exceptions, do not continue to gain weight year in and year out. Rather, they gain weight over long periods of time and then stabilize at a weight that is higher than ideal, remaining there for a long period of time, if not indefinitely. Why, as Bennett asked, “is energy balance achieved at a particular level of fat storage and not some other?” This is another question that any reasonable hypothesis of obesity must address. In 1940, the Northwestern University endocrinologist Hugo Rony described the problem in a way that brings to mind Hirsch’s comment of fifty years later: “An obese person who maintains his weight at 300 pounds indefinitely, is in caloric equilibrium the same as any person of normal weight. The conception that his obesity is due to positive caloric balance might be useful in explaining how he reached this excessive weight, but cannot inform us why he maintains it, why he resists attempts to reduce it to normal, why he tends to regain it after successful reduction.”
It’s tempting to suggest that one reason why the obesity-research community has paid little attention to the logical and scientific deficiencies of the overeating/sedentary-behavior hypothesis is that it becomes difficult even to discuss the subject without constantly tripping over the solecisms it engenders. To say someone “overeats” or “eats a lot” immediately raises the question, Compared with whom? One of the most reproducible findings in obesity research, as I’ve said, is that fat people, on average, eat no more than lean people. They may not eat as little as they say or think they do, but they don’t necessarily eat any more than anyone else. “On the few occasions when the food intake of a group of obese persons has been measured with an approved technique,” wrote the British physiologists J.V.G.A. Durnin and Reginald Passmore in 1967, “it has been found to be no greater than that of a control group of persons of normal weight. Fat people are not necessarily gluttons: some indeed are truly abstemious.” Passmore and Durnin neglected to ask then how such an abstemious individual becomes fat. Rather, they insisted that there was “not a shred of evidence” to support the belief of the obese and “also their friends and sometimes regretfully their medical attendants that they are ‘mysterious engines’ and can conserve energy in an unknown manner.” A mysterious conservation of energy does, however, seem to be the only explanation. Why do they remain fat when others would remain effortlessly lean on the same diet? What does it mean to overeat, if that’s the case?
James Boswell and Samuel Johnson struggled with the same paradox in the late eighteenth century, as Boswell reported in
Talking of a man who was growing very fat, so as to be incommoded with corpulency; [Johnson] said, “He eats too much, Sir.” Boswell. “I don’t know, Sir; you will see one man fat who eats moderately, and another lean who eats a great deal.” Johnson. “Nay, Sir, whatever may be the quantity that a man eats, it is plain that if he is too fat, he has eaten more than he should have done.”
But to clarify, as Johnson did, that obesity is caused by eating more than one should have, is not a satisfying answer. We’re still left asking why.
This question is built into the logic of the overeating/sedentary-behavior hypothesis. Why do people overeat, or why are they so sedentary, if the inevitable result is obesity? And because both overeating and deficient physical activity are, after all, behavioral conditions, not physiological ones, the only answer allowed by the hypothesis is a judgment on the behavior of the obese. To say that the obese eat more than they should, as Johnson phrased it, or are less active than they should be—thus, inducing their positive caloric balance—implies only two possibilities. Either it’s beyond their control, in which case there is another, more profound cause of their condition—perhaps a metabolic or hormonal disorder for which we should still be searching—or it is within their control, and so we are led to the judgment that the obese are weaker of will than the lean. It may be true, as von Noorden noted, that their appetite is unable to regulate their energy consumption, but why, then, do they not consciously adjust? The
