Good Calories, Bad Calories (52 page)

Though men expended more energy than women on average, and large men more than smal , there were huge variations. For men who weighed roughly 175 pounds, the minimal energy expenditure daily ranged from sixteen to twenty-one hundred calories. This implies that one 175-pounder could eat five hundred calories a day more than another 175-pounder each day—a quarter-pounder with cheese from McDonald’s—and yet would gain no more weight by doing so, even if the amount of physical activity in their lives was identical. Heavier women also tended to expend more energy, but the variations were striking. One of Benedict’s female subjects weighed 106 pounds, whereas another weighed 176, and yet both had a basal metabolism of 1,475 calories.

The idea that obesity can be preordained by a constitutional predisposition to grow fat, what von Noorden had cal ed endogenous obesity, would ultimately be rejected by the medical community, based largely on the efforts of Hilde Bruch, who did the actual research, and Louis Newburgh, who shaped the way it would come to be interpreted. Bruch was a German pediatrician who in 1934 had immigrated to New York, where she established a clinic to treat childhood obesity at Columbia University’s Col ege of Physicians and Surgeons. She began her career testing what she cal ed the “fashion”

of the day: that obese children must suffer from a hormonal or endocrine disorder. How else to reconcile their claims to eat like birds, as obese adults often claim? Bruch failed to find evidence for this hypothesis and so set out to study in exhaustive detail the lives and diet of her young obese patients.

In 1939, Bruch published the first of a series of lengthy articles reporting what she had learned from treating nearly two hundred obese pediatric patients at her clinic. Al of these children, upon close investigation, reported Bruch, ate significant quantities of food. “Overeating was often vigorously denied and it took some detective work, with visits to the home to obtain an accurate picture,” Bruch wrote. For whatever reason, the mothers tended to be more candid about their children’s eating habits at home than at the clinic. “The terms used for depicting the amounts eaten varied a good deal,” Bruch reported; “they ranged from ‘good appetite’ and ‘he eats very wel ’ to ‘most tremendous appetite,’ ‘he eats voraciously’ and ‘food is the only interest she has.’”

Bruch’s conclusion was that “excessive eating and avoidance of muscular exercise represent the most obvious factors in the mechanisms of a disturbed energy balance.” And this was either caused or exacerbated by psychological factors of the mother-child relationship. A mother wil substitute food for affection, Bruch said, and by doing so overfeed the child. She may compound the damage by being overprotective, which leads her to “keep the child from activities with peers lest the child be hurt.”*82 For the fat children themselves, she wrote, giving up food means “giving up [their] only source of pleasure and enjoyment. The very size itself, although resented because it is being constantly ridiculed, nevertheless gives the fat child, who has no basic security in his interpersonal relations, a certain sense of strength and security.”

It was Newburgh, a professor of medicine at the University of Michigan, who then kil ed off von Noorden’s hypothesis of endogenous obesity once and for al , and with it any explanation for obesity that didn’t blame it on simple gluttony and sloth. Unlike Bruch, Newburgh had easily been convinced that obesity was the result of what he cal ed a “perverted appetite.” “Al obese persons are alike in one fundamental respect—they literal y overeat,” he was insisting as early as 1930. The obese were responsible for their condition, Newburgh argued, regardless of whether or not their metabolism was somehow retarded. If it was, then the obese were culpable because they were unwil ing to rein in their appetites to match their “lessened outflow of energy.” If their metabolisms ran at normal speed, they were even more culpable, guilty of “various human weaknesses such as overindulgence and ignorance.”

In 1942, Newburgh published a sixty-three-page article in the Archives of Internal Medicine meticulously documenting the evidence against von Noorden’s endogenous-obesity hypothesis. He rejected the role of any “endocrine disorder” in fattening—a pituitary tumor, for instance, or the particularly slow secretion of thyroid hormones, which were the two leading candidates—on the basis that these could explain, at best, only a tiny percentage of cases. The great majority of the obese had perfectly normal thyroid glands, Newburgh wrote, and there were considerable cases of pituitary tumors that were not accompanied by 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 wil power. 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 fol owing 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 virtual y 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 fol owing World War I , 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 cal ed 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 cal it overeating,” is how this phenomenon was phrased in 1986 by Wil iam Bennett, then editor of the Harvard Medical School Health Letter and one of the rare investigators interested in obesity ever to make this point publicly. If someone is fat, then he has overeaten by definition.

If he’s lean, the amount of food he consumes is not considered relevant to his weight, nor is the amount of physical activity in his life. This is why lean individuals who consume comparatively large quantities of food are said to have a healthy appetite or are big eaters. No one suggests that they are suffering from excess calorie consumption.

Von Noorden’s proposition, which stil 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 tel us nothing about why one person becomes obese (or alcoholic or chronical y 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 al lean people—something that has never been shown to be true—it would stil beg what should be the salient question in al 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 regretful y 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 Boswel and Samuel Johnson struggled with the same paradox in the late eighteenth century, as Boswel reported in The Life of Samuel Johnson:

Talking of a man who was growing very fat, so as to be incommoded with corpulency; [Johnson] said, “He eats too much, Sir.” Boswel . “I don’t know, Sir; you wil 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 stil 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 al , behavioral conditions, not physiological ones, the only answer al owed 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 stil be searching

—or it is within their control, and so we are led to the judgment that the obese are weaker of wil 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 logic keeps taking us in circles.

We arrive at the same conclusion if we ask why semi-starvation diets fail to cure obesity reliably, inducing only short-term weight loss by creating a negative caloric balance. Again, there are two possibilities. The first is that the obese stay on the diet but the weight loss eventual y stops or even reverses itself. If this is the case, then whatever physiological mechanism is at work may be the cause of the obesity as wel . If so, obesity may be caused not by overeating, whatever that means, and sedentary behavior—i.e., by positive caloric balance—but by some more profound underlying disorder.