Good Calories, Bad Calories

Once human-obesity research became the domain of psychologists and psychiatrists in the 1960s, studies of hypothalamic obesity left behind once and for all the greater context of homeostasis and the use and storage of metabolic fuels, and focused instead on how Brobeck’s dual centers of the hypothalamus allegedly regulate eating behavior. This served to further the conviction that defects in this region of the brain cause overeating, and overeating causes obesity. Hunger, and the overeating that accompanies it, would be considered exclusively a psychological phenomenon, not a physiological one. (Because these psychologists would consider eating behavior to be the subject of their research, they would often screen their animals after surgery and those that didn’t eat voraciously would be “discarded.” They would then omit these animals from their subsequent analyses, even if the discarded animals became obese as well.) Hunger was something that occurred only in the head, and so it could be decoupled from the needs of the body, at least with sufficient willpower.

Animal research continued to confirm Ranson’s hypothesis, even though its author had died, no matter whether the fattening was induced by hypothalamic lesions, genetic defects, or as the naturally occurring seasonal weight gain of hibernators. In 1946, for example, the Johns Hopkins physiologist Chandler Brooks reported that his albino mice become “definitely obese” after VMH lesions, and that they gained six times as much weight per calorie of food consumed as normal mice. In other words, it wasn’t how much these mice ate that determined their ultimate weight, or the number of calories, but how these calories were utilized. They were turned into fat, not used for fuel.

Though Brooks reported that he could prevent his albino mice from growing obese, he could do so only by imposing “severe and permanent” food restriction. If he subjected them to “long continued limitation of food,” the animals would lose some weight, but they would never lose the drive to fatten or the hunger that went with it. Periods of fasting, Brooks noted, were “followed by an augmentation of appetite and development of a greater degree of obesity than had been attained before fasting.” And so Brooks’s lesioned mice, as Hilde Bruch might have noted, were acting exactly like normal healthy humans and obese humans after a semi-starvation diet. These VMH lesions also resulted in changes in the reproductive cycles of the animals, and in their normal nocturnal eating patterns, which Ranson and Hetherington had also reported; once the animals became obese, they slept more than normal animals, all of which suggested that the VMH lesions had profound effects on the entire homeostatic system and could not be written off as simply affecting hunger and thus food intake.

When physiologists began studying animal hibernation in the 1960s, they again demonstrated this decoupling of food intake from weight gain. Hibernating ground squirrels will double their body weight in late summer, in preparation for the winter-long hibernation. But these squirrels will get just as fat even when kept in the laboratory and not allowed to eat any more in August and September than they did in April. The seasonal fat deposition is genetically programmed—the animals will accomplish their task whether food is abundant or not. If they didn’t, a single bad summer could wipe out the species.

This same decoupling of food intake and weight would also be demonstrated when researchers studied what are now known as dietary models of obesity. Certain strains of rats will grow obese on very high-fat diets, and others on high-sugar diets. In both cases, the animals will get fatter even if they don’t consume any more calories than do lean controls eating their usual lab chow. This same decoupling occurs in animals that are regaining weight after lengthy periods of fasting. “It doesn’t matter how long you food-deprive the animal,” said Irving Faust, who did this work in the 1970s; “the recovery of body weight is not connected to the amount of food eaten during the recovery phase.” And this same decoupling of calories and weight has also been made consistently, if not universally, in the recent research on transgenic animals, in which specific genes are manipulated.