Good Calories, Bad Calories

to become fat, even if it’s ten times as much, the body will save for itself from the annual balance.”

Just as we grow hair in some places and not typically 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 individually: 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 belly) 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 all 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 well. “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 abnormally 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 gradually extended down her trunk and arms. “Adiposity of the lower body,” as the report described it, began at age fifteen and eventually became “lower body obesity.” By the time she was twenty-four, the patient, who was five foot four and weighed 185 pounds, had effectively all 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 called 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 compelling evidence that the condition had a genetic component, which in turn implied the existence of genetically 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 well 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 well? 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 well. Those of us who seem constitutionally predisposed to fatten simply have adipose tissue that is generally more lipophilic than that of lean individuals; our adipose tissue may be more apt to store fat or less willing to give it up when the body needs it. And if our adipose tissue is so predisposed to accumulate excessive calories as fat, this will deprive other organs and cells of nutrients, and will 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 still 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 will hold. Hormonal factors have to be involved. Male sex hormones seem to inhibit the kind of fat formation typically seen in women— men who are castrated or whose testicles are destroyed by disease often develop a fat distribution that is more typically 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 well, 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 Wurzburg 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 fully accepted” in Europe. “It seems to me this conception deserves attentive consideration,” Russell 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 well 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.”