This brings us back to the questions we asked earlier: If people eat less on carbohydrate-restricted diets, why aren’t they hungry. And if they don’t eat less, why do they lose weight? If the restriction of carbohydrates works to ameliorate this defect in fat metabolism, as Pennington speculated, then weight will be lost, hunger will be absent, and calorie consumption may decrease, while energy expenditure will increase. This is no more than the consequences of the law of energy conservation applied to a biological system that works to conserve body composition and maintain a healthy flow of fuel to the cells and tissues.

In an ideal world, Pennington’s metabolic-defect hypothesis of obesity would have been tested directly. Instead, it was ignored. Pennington made this easier by speculating that the root cause of obesity was an inability to metabolize properly a compound called pyruvic acid. This made physiological sense, but further research quickly refuted it. Pennington’s error allowed his contemporaries in nutrition and obesity research to dismiss him as just another renegade who refused to accept the reality of energy conservation. He deserved far better, as it wouldn’t be long before researchers pinned down the precise nature of the metabolic-hormonal defect that appears to be the driving force in the accumulation of excess fat.

Chapter 21

Chapter Twenty-one

THE CARBOHYDRATE HYPOTHESIS, I: FAT METABOLISM

Looking at obesity without preconceived ideas, one would assume that the main trend of research should be directed toward an examination of abnormalities of the fat metabolism, since by definition excessive accumulation of fat is the underlying abnormality. It so happens that this is the area in which the least work has been done.

HILDE BRUCH, The Importance of Overweight, 1957

IN JUNE 1962, EDWIN ASTWOOD OF Tufts University gave the presidential address to the annual meeting of the Endocrinology Society in Chicago. Although Astwood was not known as an obesity researcher, he nonetheless took the opportunity to present what he considered the obvious explanation for its cause. A physician who had spent thirty years studying and treating hormone-related disorders, Astwood had discovered the reproductive hormone luteotropin (now known as luteinizing hormone), and he had created the standard technique for purifying pituitary hormones. He had performed what The New England Journal of Medicine would call a “brilliant series of experiments” to demonstrate that hyperthyroidism could be controlled with anti-thyroid drugs. By 1976, when Astwood died, three dozen of his former students had become full professors; eight were department chairmen—“a record perhaps unequaled in medicine,” according to his obituary in the journal Endocrinology. He was a man who knew what he was talking about, even when he was speculating, as he was in his 1962 address, entitled “The Heritage of Corpulence.”