stay fat, regardless of how much they ate or exercised (endogenous obesity, driven by internal forces, not external).
In the cases where immoderate lifestyle was to blame—by “far the most common” of the two, von Noorden believed—the metabolism and physiology of the obese individual are normal, but “the mode of living” is defective, marked by that now familiar combination of “overeating or deficient physical exercise.” In endogenous obesity, the lifestyle is normal, and the weight gain is caused by an abnormally slow metabolism. These unfortunate individuals might eat no more than anyone else, but their metabolisms use a smaller proportion of the calories they consume, and so a greater proportion is stored as fat.
Just as heart-disease researchers came to blame cholesterol because it seemed to be an obvious culprit and they could measure it easily, von Noorden and the clinical investigators who came after him implicated metabolism and the energy balance because that’s what they could measure and that, too, seemed obvious. In 1892, a German chemist named Nathan Zuntz had developed a portable device to measure an individual’s oxygen consumption and carbon-dioxide respiration. This, in turn, allowed for the calculation, albeit indirectly, of energy expenditure and the metabolism of anyone who had the patience to remain immobile for an hour while breathing into a face mask. Within a year, Adolf Magnus-Levy, a colleague of von Noorden, had taken this calorimeter to the hospital bedside and begun a series of measurements of what later became known as basal metabolism, the energy we expend when we’re at “complete muscular repose,” twelve to eighteen hours after our last meal. By the end of World War I, calorimetric technology had been refined to the point where measuring metabolism had become “an extremely popular, almost fashionable field.”
Von Noorden’s focus on metabolic expenditure set the science of obesity on the path we still find it. The evolution of this research, however, proceeded like a magician’s sleight-of-hand. By the 1940s, common sense, logic, and science had parted ways.
The most obvious difficulty with the notion that a retarded metabolism explains the idiosyncratic nature of fattening is that it never had any evidence to support it. Before von Noorden proposed his hypothesis, Magnus-Levy had reported that the metabolism of fat patients seemed to run as fast if not faster than anyone else’s.*81 This observation would be confirmed repeatedly: The obese tend to expend more energy than lean people of comparable height, sex, and bone structure, which means their metabolism is typically burning off more calories rather than less. When people grow fat, their lean body mass also increases. They put on muscle and connective tissue and fat, and these will increase total metabolism (although not by the same amount).
The tendency of the obese to expend more energy than do the lean (of comparable height, age, and sex) led to the natural assumption that they
One of the most telling observations that emerged from these studies of metabolic rate was how greatly it might differ between any two individuals of equal weight, or how similar it might be among individuals of vastly different weights. In 1915, Francis Benedict published his studies of the basal metabolism translated into the minimal amount of energy expended over the course of a day, as measured in eighty-nine men and sixty-eight women. Though men expended more energy than women on average, and large men more than small, 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 called 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 College of Physicians and Surgeons. She began her career testing what she called 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. All 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 well’ 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 will 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 killed off von Noorden’s hypothesis of endogenous obesity once and for all, 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 called a “perverted appetite.” “All obese persons are alike in one fundamental respect—they literally 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 unwilling 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
