Fat calories accumulating in the adipose tissue wouldn’t be available to the cells for fuel. We would have to eat more to compensate, or expend less energy, or both. We’d be hungrier or more lethargic than individuals without such a defect.
Pennington suggested that as the adipose tissue accumulates fat its expansion will increase the rate at which fat calories are released back into the bloodstream (just as inflating a balloon will increase the air pressure inside the balloon and the rate at which air is expelled out of the balloon if the air is allowed to escape), and this could eventually compensate for the initial defect itself. We will continue to accumulate fat—and so continue to be in positive energy balance—until we reach a new equilibrium and the flow of fat calories out of the adipose tissue once again matches the flow of calories in. At this point, Pennington said, “the size of the adipose deposits, though larger than formerly, remains constant: the weight curve strikes a plateau, and the food intake is, again, balanced to the caloric output.”
By Pennington’s logic obesity is simply the body’s way of compensating for a defect in the storage and metabolism of fat. The compensation, he said, occurs homeostatically, without any conscious intervention. It works by a negative feedback loop. By expanding with fat, the adipose tissue “provides for a more effective release of fat for the energy needs of the body.” Meanwhile, the conditions at the cellular level remain constant; the cells and tissues continue to function normally, and they do so even if we have to become obese to make this happen.
This notion of obesity as a compensatory expansion of the fat tissue came as a revelation to Pennington: “It dawned on me with such clarity that I felt stupid for not having seen it before.” By working through the further consequences of this compensatory process, Pennington said, all the seemingly contradictory findings in the field suddenly fit together “like clockwork.”
This defect in fat metabolism would explain the sedentary behavior typically associated with obesity, and why all of us, fat or lean, will become easily fatigued when we restrict calories for any length of time. Rather than drawing on the fat stores for more energy, the body would compensate by expending less energy. Any attempt to create a negative energy balance, even by exercise, would be expected to have the same effect.
Clinicians who treat obese patients invariably assume that the energy or caloric requirement of these individuals is the amount of calories they can consume without gaining weight. They then treat this number as though it were fixed by some innate facet of the patients’ metabolism. Pennington explained that this wasn’t the case. As long as obese individuals have this metabolic defect and their cells are not receiving the full benefit of the calories they consume, their tissues will always be conserving energy and so expending less than they otherwise might. The cells will be semi-starved, even if the person does not appear to be. Indeed, if these individuals are restraining their desire to eat in an effort to curb, if possible, still further weight gain, this inhibition of energy expenditure will be exacerbated.
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
If Pennington was right, a high-protein, high-fat diet that was restricted in carbohydrates but not calories would correct the metabolic fault. The adipose tissue (i.e., energy storage) would shrink, because fat would no longer be trapped in the fat tissue. It would flow out at an accelerated rate, and this would continue until a healthy equilibrium was reestablished between fat storage and fat release. Appetite (i.e., energy in) would adjust downward to compensate for the increased availability of fuel from the fat tissue. Edward Adolph of the University of Rochester and Curt Richter of Johns Hopkins had repeatedly demonstrated that laboratory animals will increase or decrease their food intake in response to the available calories. Slip nutrients into their drinking water or deposit them through a tube directly into their stomachs, and the animals compensate by eating less. Dilute their food with water or indigestible fiber, and the animals compensate by consuming a greater volume to get the same amount of calories. There is no reason to think that this adjustment in caloric intake will not occur if the increase in available nutrients comes from the internal fat stores, rather than external manipulations—no reason to think that the body or its cells and tissues could tell the difference. “Mobilization of increased quantity of utilizable fat, then, would be the limiting factor on the appetite, effecting the disproportion between caloric intake and expenditure which is necessary for weight reduction,” Pennington wrote.
If the fat can be mobilized from the adipose tissue with “sufficient effectiveness,” Pennington suggested, “no calorie restriction would be necessary” on a carbohydrate-restricted diet. A greater share of the energy needs would be supplied by the calories from the fat tissue, and the appetite would naturally adjust. “Weight would be lost, but a normal caloric production would be maintained.” A person would be eating less because his appetite would be reduced by the increased availability of fat calories in his circulation, not because the diet somehow bored, restricted, or revolted him. He would be eating less because his fat tissue was shrinking; his fat tissue would not be
