Good Calories, Bad Calories

Consider the kind of young, active men Ancel Keys had employed in his starvation experiments. These men might normally expend thirty-five hundred calories a day, and this was what they would eat from day to day to maintain their weight. In a healthy state, the supply of fuel to their cells would be unimpeded by any metabolic defects, and so the cells would have plenty of energy to burn, and their metabolism would run unimpeded. Every day, the calories temporarily stored in their fat deposits would be mobilized and burned for fuel. But imagine that one of these men develops a metabolic defect that retards the release of fat from the adipose tissue. Now more energy enters his fat tissue than exits. If this amounts to a hundred calories a day, he’ll gain roughly one pound every month. After a while, he’s likely to go on a diet to rid himself of this excess fat. He might try to reduce his consumption to three thousand calories. In a healthy state, this would have worked, but now he is dogged by a defect in fat metabolism. Fat still accumulates in his fat tissue. Rather than remedy the imbalance between the calories coming to and going from the adipose tissue, this self-imposed calorie restriction further decreases the fuel available to the cells, because now fewer calories have been consumed. He’s even hungrier, and if he doesn’t give in to the hunger, his body has to get by on even less fuel than before. His metabolic rate slows in response, and he finds himself lacking the desire to expend energy in physical activity. If he wants to inhibit this accumulation of fat in his adipose tissue, he might further restrict his diet. If he does, however, this will further diminish the amount of calories his cells can expend.

To Pennington, this explained the observation that some obese patients can maintain their weight consuming as little as seventeen hundred calories a day, as Keys had reported. It would also explain why malnutrition and obesity could coexist in the same populations and even the same families, as we discussed earlier (see Chapter 14). The chronic, long-term effect of such a defect in fat metabolism, combined with a diet that continues to exacerbate the problem, would so constrain the energy expenditure of adults that they could conceivably gain weight and grow obese on a caloric intake that would still be inadequate for their children.

“What happens when low calorie diets are applied is that the starved tissues of the obese are starved further,” Pennington wrote. Since the consequences of this food deprivation are likely to be the same in the obese as in the lean, they had already been adequately described by the semi-starvation experiments of Benedict and Keys. “The first noticeable effect of such a calorie shortage is limitation of the voluntary activities of leisure hours,” Pennington wrote. “The various avenues of caloric expenditure are all contracted in adjustment to the diminished food intake…and thus deflect the purpose for which low calorie diets are prescribed.”

“A more rational form of treatment,” Pennington suggested, would be one that makes fat once again flow readily out of the fat cells, that directs “measures primarily toward an increased mobilization and utilization of fuel” by the muscles and organs. Pennington believed that this is what carbohydrate restriction accomplished and this was why the diets worked. The cells would respond to this increased supply of fuel by accelerating the rate of metabolism—utilizing the fuel. Now the body would have to establish a new equilibrium between the three variables of the energy-balance equation—energy storage, intake, and expenditure. This new equilibrium, however, would be commensurate with a healthy—i.e., uninhibited—flow of fat from the adipose tissue.