Good Calories, Bad Calories

This alternative hypothesis of obesity constitutes three distinct propositions. First, as I’ve said, is the basic proposition that obesity is caused by a regulatory defect in fat metabolism, and so a defect in the distribution of energy rather than an imbalance of intake and expenditure. The second is that insulin plays the primary role in this fattening process, and the compensatory behaviors of hunger and lethargy. The third is that carbohydrates, and particularly refined carbohydrates—and perhaps the fructose content as well, and thus the amount of sugars consumed—are the prime suspects in the chronic elevation of insulin; hence, they are the ultimate cause of common obesity. These latter two propositions—that insulin regulates fat deposition and carbohydrates regulate insulin—have never been controversial, but they’ve been dismissed as irrelevant to obesity, given the ubiquitous belief that obesity is caused by overeating. That, I will argue, was a mistake.

Through the beginning of World War II, the notion that a defect in fat metabolism causes obesity was known as the lipophilia hypothesis. “Lipophilia” 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 vitally 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 illogical,” he wrote, “to say: Child, you shoot up in height because you eat too much or you exercise too little—or you have remained small 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 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?