Good Calories, Bad Calories

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 following the German annexation of Austria. By then, however, Bauer was a scholar without an institution. He eventually took a position with the College 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 Cahill 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,” Cahill acknowledged, “but markedly suppressed by his intellectual processes.”

The value of these animal models of obesity, ideally, 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 normally 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 well apply to humans.

In 1934, the Harvard physiologist Milton Lee reported that when rats had their pituitary glands removed and were injected with growth hormone (a product of the pituitary gland), they gained “significantly more weight” than their untreated littermates, even when eating identical quantities of food. The implication was that the weight gain was caused by the effect of growth hormone, independent of calorie consumption. The treated rats grew heavier, larger, and more muscular, Lee reported; the rats found the calories to do so by consuming what fat they had and by expending less energy in physical activity.

As for genetically obese mice, it is invariably the case, as Jean Mayer discovered in the early 1950s, that these animals will fatten excessively regardless of how much they eat. Their obesity is not dependent on the number of calories they consume, although allowing them to consume excessive calories may speed up the fattening process. “These mice will make fat out of their food under the most unlikely circumstances, even when half starved,” Mayer had reported. And if starved sufficiently, these animals can be reduced to the same weight as lean mice, but they’ll still be fatter. They will consume the protein in their muscles and organs rather than surrender the fat in their adipose tissue. Indeed, when these fat mice are starved, they do not become lean mice; rather, as William Sheldon might have put it, they become emaciated versions of fat mice. Francis Benedict reported this in 1936, when he fasted a strain of obese mice. They lost 60 percent of their body fat before they died of starvation, but still had five times as much body fat as lean mice that were allowed to eat as much as they desired.