Good Calories, Bad Calories

IN 1975, THE DUKE UNIVERSITY PEDIATRICIAN James Sidbury, Jr., described a “rational basis” for the dietary treatment of childhood obesity, one that would neither torment his young patients with hunger nor rely on pharmaceutical means to prevent it. Such a diet, he wrote, would induce weight loss with a “minimum of anguish and struggle.” Sidbury had an advantage over other investigators treating obese patients in that he had spent his career studying disorders of carbohydrate metabolism and, indeed, had already earned international renown for his development of a diet, still used today, to treat what are called glycogen storage diseases. The same year Sidbury published his description of a “Program for Weight Reduction in Children,” however, he left his clinic at Duke to become director of the National Institute of Child Health and Human Development at NIH. By then, he had written only one short textbook chapter discussing his dietary treatment and one three-page article for an obscure journal called Connecticut Medicine. In them, he described an approach to obesity therapy that differed from Robert Atkins’s only in the details of the application: Sidbury’s diet was very low in both carbohydrates and calories, and Sidbury was writing for medical professionals, not the general public.

He based the design of his diet on several key observations. Fasted children “rarely, if ever, complained of hunger,” Sidbury noted, and the “enzymes of lipogenesis”—insulin—rapidly decrease during fasting. Insulin is chronically elevated in obese patients, and the obese children referred to him in his practice typically consumed a diet dominated by carbohydrates—“crackers, potato chips, French fries, cookies, soft drinks, and the like.” These foods are digested and absorbed as simple sugars, Sidbury explained, “chiefly glucose, which is the most potent stimulator of insulin release and synthesis.” Since insulin will “facilitate lipogenesis” and inhibit the release of fat in the adipose tissue, this in turn created what Sidbury called the “milieu for positive fat balance” in the cells of the adipose tissue. “Thus it was reasoned,” Sidbury wrote, “that a low carbohydrate diet would create the conditions vis-à-vis insulin metabolism which would decrease the constant stimulation of the [insulin-secreting] cells of the pancreas. The decreased insulin levels would then permit normal fatty acid mobilization.”

The diet that Sidbury eventually used in his clinic and claimed to be uniquely effective contained only 15 percent carbohydrates—“the remaining being apportioned approximately equally between protein and fat”—and from three to seven hundred total calories a day, depending on the child’s age. The older the child, the more calories allowed. “Many parents do not believe their child can be satisfied with so little food,” Sidbury wrote. “Their attitude changes completely,” however, when they see the “obvious change in the amount of food which satisfies the children.”^*131

The phenomena of hunger and satiety have been the running subtext of all our discussions of obesity: the “persistent clamor of hunger” that attends semi-starvation diets; the absence of hunger during fasting and carbohydrate restriction; the question of whether insulin works as a fattening hormone or a hunger hormone when used to treat anorexia. And then, of course, there is the association of hunger, or at least positive caloric balance, with weight gain. If there’s one thing the law of energy conservation does indeed tell us, it’s that anything that works to increase or decrease our body mass must have compensatory effects on the balance of calories consumed and calories expended. Thus, any viable hypothesis of obesity must also be a hypothesis of hunger and satiety, and perhaps, as Alfred Pennington noted, of energy expenditure as well.