Among the few investigators whose careers spanned the war years, Louis Newburgh was the most influential and conspicuous. As late as 1948, Newburgh was still promoting his perverted-appetite hypothesis of obesity. The first obesity textbook published after the war,
An entire generation of young researchers and clinicians effectively started the study of obesity from scratch after the war. They did so with little concern for whatever understanding had been achieved before they arrived, and so they embraced a hypothesis of causation that flew in the face of much of the evidence. The institutionalized skepticism and meticulous attention to experimental detail that are necessary to do good science—“being ruthless in self-criticism and…taking pains in verifying facts,” as the Nobel laureate chemist Hans Krebs said—had also been left behind.
THE CARBOHYDRATE HYPOTHESIS, II: INSULIN
Every woman knows that carbohydrate is fattening.
REGINALD PASSMORE AND YOLA SWINDELLS,
The fact that insulin increases the formation of fat has been obvious ever since the first emaciated dog or diabetic patient demonstrated a fine pad of adipose tissue, made as a result of treatment with the hormone.
REGINALD HAIST AND CHARLES BEST,
I
N 1929, WHEN LOUIS NEWBURGH FIRST rejected the possibility of an “endocrine abnormality” as the cause of obesity, and insisted instead that all fat people had a perverted appetite, hormones were still widely known as “internal secretions” and endocrine glands as “ductless glands.” The first purification of growth hormone had been only nine years earlier, the purification of insulin only eight years before. In 1955, whenIn other words, the editors at
In 1968, Jean Mayer pointed out that obesity researchers may have “eliminated” hormones “from legitimate consideration” as a cause of obesity, or so they believed, but the evidence continued to accumulate just the same. Researchers had demonstrated that insulin seemed to have a dramatic effect on hunger, that insulin was the primary regulator of fat deposition in the adipose tissue, and that obese patients had chronically high levels of insulin. Other hormones, such as adrenaline, had been shown to increase the mobilization of fat from the fat cells. “It is probable that different concentrations of these hormones in blood are characteristic of different body types and fat contents,” Mayer wrote.