The same cause and effect are evident in Type 1 diabetes mellitus. The inability of diabetics to utilize the food they eat, and particularly the carbohydrates, results in a state of starvation and extreme hunger. Diabetics also urinate more, because the body gets rid of the sugar that accumulates in the bloodstream by allowing it to overflow into the urine, and this is why diabetics will be abnormally thirsty as well.

Lesions to the ventromedial hypothalamus can induce tremendous hunger and cause obesity, but now Ranson considered it naïve to assume that the hunger caused the obesity. Rather, the hunger was another consequence of a breakdown in homeostasis—the loss of calories into the fat tissue. This is why the animals get fat even when they aren’t allowed to satisfy their appetite. And this is why these lesioned animals are always hungry, at least until they put on enough fat so that the excess counteracts the damage caused by the hypothalamic lesion. Sedentary behavior is another way their bodies compensate for the loss of calories to the fat tissue. As Ranson perceived it, both hunger and physical inactivity are manifestations of the internal starvation of the tissues. These are the ways that the homeostatic regulation of energy balance compensate for the loss of nutrients into the fat tissue.

It’s hard to avoid the suggestion that one major factor in how this research played out was the preconceptions of the investigators and their urge to make a unique contribution to the science. Ranson had suggested that all the more obvious manifestations of hypothalamic lesions were the consequences of a primary defect in the homeostatic control of energy balance that made the animals accumulate excessive fat in the adipose tissue. Brobeck and the other investigators who took to studying hypothalamic obesity would conclude that whatever phenomenon they happened to find most remarkable in their own postoperative rodents was the critical factor, or at least a critical factor, requiring intensive investigation. By doing so, as Ranson had cautioned in the early 1940s, they oversimplified the physiology and only directed attention away from the fundamental problem. Jean Mayer, for instance, would discuss hypothalamic obesity in the plural—as the “classic type of experimental obesities”—and he would say that one such obesity was caused by lack of physical activity, as in his mice. Philip Teitelbaum, who did his research as a doctoral student at Johns Hopkins in the early 1950s, observed that VMH-lesioned rodents, at the peak of their obesity, became finicky eaters, and he concluded that this was an obvious manifestation of the behavior of taste aversion. This observation established his reputation in the field and also the common belief that the ventromedial hypothalamus controls food preference, too, and the motivation to eat. “Of course they overate,” he said of his obese rodents; “that’s why they became obese.” But he simultaneously acknowledged that they were also so inactive that they would fatten even without overeating.