Good Calories, Bad Calories

In 1925, Wilhelm Falta, a student of von Noorden and a pioneer of the science of endocrinology in Europe, began using insulin therapy to treat underweight and anorexia in adults as well. Falta had argued, even in the pre-insulin era, that whatever pancreatic hormone was absent or defective in diabetes governed not only the use of carbohydrates for fuel, but also the assimilation of fat in adipose tissue. “A functionally intact pancreas is necessary for fattening,” Falta wrote. He also noted that the only way to fatten anyone efficiently was to include “abundant carbohydrates in the diet.” Otherwise, the body would adjust to eating “very much more than the appetite really craves,” by either lessening appetite still further or creating “an increased demand for movement.” The only way to get around this natural balance of intake and expenditure is by increasing the secretion from the pancreas. “We can conceive,” Falta speculated, “that the origin of obesity may receive an impetus through a primarily strengthened function of the insular apparatus, in that the assimilation of larger amounts of food goes on abnormally easily, and hence there does not occur the setting free of the reactions that in normal individuals work against an ingestion of food which for a long time supersedes the need.” After the discovery of insulin, Falta reported that giving it to patients would increase their appetite for carbohydrates specifically, and the carbohydrates in turn would stimulate the patient’s own insulin production. It would create a vicious cycle—although, in the case of anorexic and underweight patients, one that might return them to a normal appetite and normal weight.

By the 1930s, clinicians throughout Europe and the United States had taken to using insulin therapy to fatten their pathologically underweight patients. These patients could gain as much as six pounds a week eating meals “rich in carbohydrates” after receiving injections of small doses of insulin, reported Rony, who used insulin therapy on seven anorexic patients in his own clinic; it worked on five of them. None of these patients had been able to gain weight, but now they added an average of twenty pounds each in three months. “All reported a more or less pronounced increase of appetite,” Rony wrote, “and occasional strong feelings of hunger.” Until the 1960s, insulin was also used to treat severe depression and schizophrenia. Among the more renowned patients subjected to what was then called insulin-shock therapy was the Princeton mathematician John Nash, made famous by Sylvia Nasar’s 1998 biography, A Beautiful Mind. Its efficacy for treating mental illness was debatable, but as Nasar observed, “all the patients gained weight.” Another memorable recipient was the poet Sylvia Plath, who experienced a “drastic increase in weight” on the treatment. (In her autobiographical novel, The Bell Jar, Plath’s protagonist, Esther Greenwood, gains twenty pounds on insulin therapy—“I just grew fatter and fatter,” she says.)

Insulin’s fattening properties have long been particularly obvious to diabetics and the physicians who treat them. Because diabetics will gain weight with insulin therapy, even those who are obese to begin with, clinicians have always had difficulty convincing their patients to continue taking their insulin. When they start to fatten, they naturally want to slack off on the therapy, so the need to control blood sugar competes with the desire to remain lean, or at least relatively so. This is also a clinical dilemma, because the weight gain will also increase the risk of heart disease. In the chapter on insulin therapy in the 1994 edition of Joslin’s Diabetes Mellitus, the Harvard diabetologist James Rosenzweig portrayed this insulin-induced weight gain as uncontroversial: “In a number of studies of patients treated with insulin for up to 12 months, weight gains of 2.0 to 4.5 kg [roughly four to ten pounds] were reported….” This weight gain, he wrote, then leads to “the often-cited vicious cycle of increased insulin resistance, leading to the need for more exogenous insulin, to further weight gain, which increases the insulin resistance even more.”^*109