Good Calories, Bad Calories- Fats, Carbs, and the Controversial Science of Diet and Health

Implicit in this hypothesis is the assumption that energy expenditure and energy intake are independent variables.

The hypothesis presupposes that calories are effectively “pulled” into the fat cells, rather than pushed, with our fat tissue playing a very active role in this process. It assumes that energy intake and expenditure are dependent variables: a change in one induces a compensatory change in the other, because the body constantly works to maintain a healthy body composition and a dependable flow of energy to the cells.

Since insulin, as Astwood noted, is the hormone responsible for promoting the incorporation of fat into our adipose tissue and the conversion of carbohydrates into fat, the obvious suspects are refined carbohydrates and easily digestible starches, which have welldocumented effects on insulin. This is what Peter Cleave argued, albeit without understanding the underlying hormonal mechanisms at work, and what the geneticist James Neel, father of the thrifty-gene hypothesis, came to believe as well. And it’s the effect of these carbohydrates on insulin that would explain the dietary observations—the futility of calorie restriction, the relative ease of weight loss when carbohydrates are restricted, and perhaps two centuries of anecdotal observations that sweets, starches, bread, and beer are uniquely fattening.

This alternative hypothesis of obesity ultimately vanished in the 1980s, a casualty of the official consensus that fat was the dietary evil and carbohydrates were the cure. Ironically, it disappeared just as all the relevant physiological mechanisms had been worked out and a causal path established from the carbohydrates in the diet through insulin to the regulatory enzymes and molecular receptors in the adipose tissue itself.

This alternative hypothesis of obesity constitutes three distinct propositions. First, as I’ve said, is the basic proposition that obesity is caused by a regulatory defect in fat metabolism, and so a defect in the distribution of energy rather than an imbalance of intake and expenditure. The second is that insulin plays the primary role in this fattening process, and the compensatory behaviors of hunger and lethargy. The third is that carbohydrates, and particularly refined carbohydrates—and perhaps the fructose content as well, and thus the amount of sugars consumed—are the prime suspects in the chronic elevation of insulin; hence, they are the ultimate cause of common obesity.

men who are castrated or whose testicles are destroyed by disease often develop a fat distribution that is more typically feminine.

Female sex hormones do not appear to play a major role in determining where fat appears on the body—women

As for genetically obese mice, it is invariably the case, as Jean Mayer discovered in the early 1950s, that these animals will fatten excessively regardless of how much they eat. Their obesity is not dependent on the number of calories they consume, although allowing them to consume excessive calories may speed up the fattening process.

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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.

George Wade, the University of Massachusetts biologist who did much of this research, described it as a “revelation” that obesity could be brought on without overeating, just as Pennington had described it as revelatory that weight could be lost without undereating. “If you keep the animals’ food intake constant and manipulate the sex hormones, you still get substantial changes in body weight and fat content,” Wade said.

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.

He also noted that the only way to fatten anyone efficiently was to include “abundant carbohydrates in the diet.”

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.

Whether a carbohydrate-restricted diet is deficient in essential vitamins and minerals is another issue. As we also discussed (see Chapter 19), animal products contain all the amino acids, minerals, and vitamins essential for health, with the only point of controversy being vitamin C.