Good Calories, Bad Calories

By contrast, the alternative hypothesis proposes that the primary defect is hormonal and metabolic—in fat storage and/or the burning of fat for fuel (oxidation)—and is in the body, not the brain. This defect causes the excessive accumulation of calories as fat and compensatory urges to eat more and expend less energy. In this hypothesis, overeating and inactivity (hunger and lethargy) are side effects of this underlying metabolic defect; they are not causes. 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. Immoderate eating and physical inactivity do not induce obesity, because the body adjusts intake to expenditure and expenditure to intake. Neither eating less nor exercising more addresses the cause of the problem, and that’s why these approaches fail. The only effective treatments, according to this hypothesis, would be those that remedy the fundamental regulatory defect.

The only thing missing from this hypothesis as it was originally conceived a century ago, or as reconceived by Pennington and then Bruch and Astwood, was an explanation for the epidemiological observations. In other words, obesity may be caused by a hormonal or metabolic defect determined primarily by genetic inheritance, but the epidemiology tells us that this defect is triggered by environmental factors. Genetics determines our propensity to put on weight, but those genes (nature) have to be triggered by an agent of diet or lifestyle (nurture) to explain the association of obesity with poverty, the present obesity epidemic, and the emergence of obesity in recently Westernized populations. A change in the environment is also necessary to explain why man alone seems to grow chronically obese, not other species of animals. “Something has happened in the past twenty, thirty, forty years in the incidence of obesity, and that has to be environmental,” as George Cahill has said about the present obesity epidemic.

The likely explanation is the effect of diet on this regulation of fat metabolism and energy balance. 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 well-documented 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.

In this hypothesis, obesity is another variation on the theme of insulin dysfunction and diabetes. In Type 1 diabetes, the cause is a lack of insulin. The result is an inability to use glucose for fuel and to retain fat in the fat tissue, leading to internal starvation, as Astwood put it, excessive hunger, and weight loss. In obesity, the cause is an excess of insulin or an inordinate sensitivity to insulin by the fat cells; the result is an overstock of fuel in the adipose tissue and so, once again, internal starvation. But now the symptoms are weight gain and hunger. In obesity, the weight gain occurs with or without satisfying the hunger; in Type 1 diabetes, the weight loss occurs irrespective of the food consumed.

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.