Good Calories, Bad Calories (66 page)

means “love of fat.” The term was invoked in 1908 by the German internist Gustav von Bergmann to explain why areas of the body differ in their affinity for accumulating fat—a vital y important phenomenon, one would think, since obesity is a malady of fat accumulation. Bergmann considered the energy-balance hypothesis of obesity to be nonsensical: “It seems just as il ogical,” he wrote, “to say: Child, you shoot up in height because you eat too much or you exercise too little—or you have remained smal because you play sports too much. What the body needs to grow, it always finds, and what it needs to become fat, even if it’s ten times as much, the body wil save for itself from the annual balance.”

Just as we grow hair in some places and not typical y in others, Bergmann noted, there are places more or less prone to fatten, and some biological factor must regulate that. Some regions of the body are more or less lipophilic than others. This is the kind of observation that can obsess us individual y: Why do we have love handles or a double chin? Why fat ankles, thighs, or buttocks? Why is it that some men accumulate excessive fat in the abdomen (a beer bel y) and yet are lean elsewhere? Why do some women have significant fat deposits in their breasts and so are considered voluptuous, whereas other women have little or none? These are al variations on the question of which biological factors determine the regional and local distribution of fat.

The example commonly cited in discussions of the nature of this localized lipophilia was that of a twelve-year-old girl in the early 1900s who burned the

back of her hand. Her doctors used skin from her abdomen as a graft over the burn. By the time this girl turned thirty, she had grown fat, and the skin that had been transplanted to the back of her hand had grown fat as wel . “A second operation was necessary for the removal of the big fat pads which had developed in the grafted skin,” explained the University of Vienna endocrinologist and geneticist Julius Bauer, “exactly as fatty tissue had developed in the skin of the lower part of the abdomen.” Some biological factor must regulate this, Bauer believed.

Several clinical conditions also demonstrate this phenomenon of local lipophilia. Benign fat masses a few inches in diameter characterize a condition known as lipomatosis, and there are fatty tumors known as lipomas. In both cases, these masses of fat appear unaffected by any weight loss by the patients themselves; whatever it is that causes fat to accumulate in localized masses seems to be independent of the fat content of the body itself.

There’s also a rare condition known as lipodystrophy, characterized by the inability to store fat in subcutaneous tissue. Those who suffer from it appear abnormal y emaciated; lipodystrophy, too, can be localized, and even progressive. In one case reported in 1913, a ten-year-old girl first lost fat from her face; then, over the next three years, this emaciation gradual y extended down her trunk and arms. “Adiposity of the lower body,” as the report described it, began at age fifteen and eventual y became “lower body obesity.” By the time she was twenty-four, the patient, who was five foot four and weighed 185

pounds, had effectively al of her body fat localized below her waist.

A case of progressive lipodystrophy with lower-body obesity. If emaciation above the waist is followed by obesity below it, can the quantity of calories consumed have anything to do with it?

Bergmann and Julius Bauer, the “noted Vienna authority on internal diseases,” as the New York Times cal ed him, were the two most prominent proponents of the lipophilia hypothesis, but only Bauer wrote about the hypothesis in English, attempting to influence how obesity would be perceived by physicians in the United States. Bauer’s expertise was in the application of genetics and endocrinology to clinical medicine, a field he arguably pioneered in a 1917 monograph entitled Constitution and Disease. Bauer had taken case histories from 275 obese patients and reported that nearly 75

percent had one or both parents who were also obese. He considered this compel ing evidence that the condition had a genetic component, which in turn implied the existence of genetical y determined hormonal and metabolic factors that would bestow a constitutional disposition to put on excessive fat.

“The genes responsible for obesity,” Bauer wrote, “act upon the local tendency of the adipose tissue to accumulate fat (lipophilia) as wel as upon the endocrine glands and those nervous centers which regulate lipophilia and dominate metabolic functions and the general feelings ruling the intake of food and the expenditure of energy. Only a broader conception such as this can satisfactorily explain the facts.”

Lipophilia, as Bauer observed, has nothing to do with energy balance. Where we accumulate fat is regulated by something other than how much we eat or how little we exercise. Someone who has a double chin, fat ankles, or large breasts but is lean elsewhere, or the women of African tribes who have the characteristic fat deposits of the buttocks known as steatopygia, did not develop these fat deposits by eating too much. Rather, as Bauer wrote, “A local factor must exist which influences the fat deposition in particular regions independently of the general energy balance or imbalance.” If a person becomes emaciated above the waist and then, a few years later, obese below it, as in these cases of progressive lipodystrophy, how can the obese half be blamed on overeating? And, if not, why does overeating become the cause when the obesity exists above the waist as wel ? The difference between local lipophilia and generalized obesity, Bauer observed, is one of distribution and not quantity.

Whatever mechanisms lead some parts of the human body to be more or less lipophilic, Bauer argued, exist to different extents in individuals as wel .

Those of us who seem constitutional y predisposed to fatten simply have adipose tissue that is general y more lipophilic than that of lean individuals; our adipose tissue may be more apt to store fat or less wil ing to give it up when the body needs it. And if our adipose tissue is so predisposed to accumulate excessive calories as fat, this wil deprive other organs and cel s of nutrients, and wil lead to excessive hunger or lethargy. “Like a malignant tumor or like the fetus, the uterus or the breasts of a pregnant woman, the abnormal lipophilic tissue seizes on foodstuffs, even in the case of undernutrition,” wrote Bauer in 1929. “It maintains its stock, and may increase it independent of the requirements of the organism. A sort of anarchy exists; the adipose tissue lives for itself and does not fit into the precisely regulated management of the whole organism.”

In 1941, when Bauer turned to the question of which biological factors might determine or regulate this lipophilia, the understanding of the function of hormones and enzymes in regulating metabolism was stil in its infancy. Bauer based his understanding, as Astwood would twenty years later, largely on clinical observations. Local factors in the adipose tissue itself have to be involved, he thought. How else to explain the lipophilic skin graft? Surely something attached to the skin and the adipose tissue determines how much fat it wil hold. Hormonal factors have to be involved. Male sex hormones seem to inhibit the kind of fat formation typical y seen in women—men who are castrated or whose testicles are destroyed by disease often develop a fat distribution that is more typical y feminine. This type of fat distribution, Bauer wrote, is also present in “obese boys in whom the physiologic production of the testicular hormone is not yet sufficient to prevent the accumulation of adipose tissue of the female type. The larger the quantity of fat deposited, the more striking is the resemblance to the female type….” Female sex hormones do not appear to play a major role in determining where fat appears on the body—women who have their ovaries removed put on fat very much like other women. These hormones do, however, seem to affect the quantity of fat, which would explain the tendency of women to gain weight after menopause. Bauer also suggested that insulin plays a role, by enhancing the deposition of glucose in the adipose tissue, a phenomenon first demonstrated in the 1920s, and by increasing the general affinity of the adipose tissue for accumulating fat. The nervous system plays a role as wel , Bauer said: researchers had demonstrated that they could increase the amount of fat in fat deposits by severing the nerve fibers that run to the relevant tissue.

Through the 1920s, discussions of the lipophilia hypothesis were confined to the German and Austrian research communities. The relevant research appeared almost exclusively in the German medical literature. Clinicians in the United States began to take notice only in 1933, after Eugene Du Bois convinced Erich Grafe, director of the Clinic of Medicine and Neurology at the University of Würzburg in Germany, that the American medical community could benefit from an English translation of Grafe’s textbook, Metabolic Diseases and Their Treatment. By that time, as Hugo Rony noted, the hypothesis was “more or less ful y accepted” in Europe. “It seems to me this conception deserves attentive consideration,” Russel Wilder of the Mayo Clinic wrote in 1938. “The effect after meals of withdrawing from the circulation even a little more fat than usual might wel account both for the delayed sense of satiety and for the frequently abnormal taste for carbohydrate encountered in obese persons…. A slight tendency in this direction would have a profound effect in the course of time.”

Knowledge and research on the hypothesis, though, remained largely confined to the German and Austrian research community. When this school of research evaporated with the rise of Hitler and World War I , the notion of lipophilia evaporated with it. Anti-German sentiments in the postwar era may have contributed as wel to the disappearance.*106 In 1955, the year Bergmann died, the primary German textbook on endocrinology and internal medicine included a lengthy discussion of the lipophilia hypothesis in its chapter on obesity, but it was never translated into English. By that time, English had become the international language of science, and the belief that researchers had at least to read German to keep up with the latest advances no longer held sway. (This disappearance of the German and Austrian influence on obesity research is conspicuous in the literature itself. In Rony’s Obesity and Leanness, published in 1940, 191 of 587 references are from German publications; in the 1949 manual Obesity…, written by the Mayo Clinic physicians Edward Rynearson and Clifford Gastineau, only thirteen of 422 references are from the German literature, compared with a dozen from Louis Newburgh alone. By the 1970s, when George Bray, John Garrow, and Albert Stunkard wrote and edited the next generation of obesity textbooks and clinical manuals, this German research was treated as ancient history and entirely absent.)

Bauer published three articles on lipophilia in English: in 1931 (with Solomon Silver, an endocrinologist at New York’s Mount Sinai Hospital), 1940, and 1941, the latter two after he fled to the United States fol owing the German annexation of Austria. By then, however, Bauer was a scholar without an institution. He eventual y took a position with the Col ege of Medical Evangelists in Los Angeles, which was affiliated with the Seventh-day Adventist Church, and he became a senior attending physician at Los Angeles County General Hospital. But these were not institutions that bestowed credibility.

Meanwhile, Newburgh’s seminal paper establishing a perverted appetite as the definitive cause of obesity was published in 1942, and Newburgh rejected the lipophilia hypothesis with the alacrity with which he rejected any explanation that didn’t implicate gluttony as the primary cause.

What made the disappearance of the lipophilia hypothesis so remarkable is that it could easily be tested in the laboratory, in animal models. These experiments should have settled the issue. Instead, they generated two distinct interpretations of the same evidence. The scientists who study weight regulation in animals came to conclude that obesity is caused by a defect in the regulation of fat metabolism, just as Bauer would have predicted. Their interpretation influenced Pennington and informed his metabolic-defect hypothesis of obesity. The clinicians, nutritionists, and psychologists concerned with human obesity, however, concluded from this same work that the cause of obesity is overeating, as Newburgh would have predicted, or sedentary behavior, as Mayer would, although they had to ignore considerable contrary evidence to do so. When these latter researchers were confronted by results inconsistent with their beliefs, the matter was reconciled by rejecting the relevance of obesity in animals to obesity in humans. As George Cahil explained in 1978, it was “indubitable” that animals had evolved a regulatory system of fat metabolism and energy balance that had to be crippled or dysregulated before these animals could gain an unhealthy amount of weight. Such a system “is also probably present in man,” Cahil acknowledged, “but markedly suppressed by his intel ectual processes.”

The value of these animal models of obesity, ideal y, is to see if they can refute or exclude one of the two competing hypotheses. For instance, these models can be used to test the hypothesis that obesity is caused by eating too many calories. We have only to ask a simple question: when laboratory animals grow obese, do they require more food to do so than lean animals would normal y eat? If they grow excessively fat even when their calorie intake is restricted, then that refutes the notion that obesity (at least in these animals) is caused by consuming too many calories. The restriction controls for overeating. The explanation we’d be left with is that they’re redistributing the calories they do eat. The fundamental defect would seem to be in the body, not in the brain. Overeating would be a side effect of the fattening process. And this might wel apply to humans.