Good Calories, Bad Calories (64 page)

Pennington considered two facts about obesity to be particularly revealing. One was Hugo Rony’s observation that an obese individual wil spend much of his life in energy balance—in the “static phase” of obesity, to use Rony’s term—just as the lean do. “His caloric intake, like that of people of normal weight, is dictated by the energy needs of his body,” Pennington wrote. “His appetite, far from being uncontrol ed, is precisely and delicately regulated.”

The second fact was that when obese individuals try consciously to eat less—when they go on a low-calorie diet—their metabolism and energy expenditure inevitably decrease, just as they do when lean individuals are semi-starved. Benedict had observed this diet-induced decrease in energy expenditure in his lean subjects in his 1917–18 semi-starvation studies. Frank Evans and Margaret Ohlson had made the same observation of the obese.

Pennington believed, as Benedict, the Cornel nutritionist Graham Lusk, and others had suggested, that this was the natural response to a diminished supply of energy. Less energy is available to the cel s, and so they expend less. On a calorie-restricted diet, Pennington suggested, the obese and the lean become hungry and lethargic for identical reasons—“their tissues are not receiving enough nutriment.”

This presented a dilemma. That the tissues of the lean are semi-starved by calorie restriction is easy to imagine; they don’t have a lot of excess calories to spare. But why would this happen with the obese, who do? Pennington found his answer in a 1943 article by the Columbia University biochemist DeWitt Stetten, who reported that the rate at which fatty acids were released from the fat deposits of congenital y obese mice was significantly slower than it was in lean mice. Stetten had suggested that obesity in these animals was caused by a suppression of the flow of fat from the adipose tissue back into the circulation and its subsequent use by the tissues for fuel.

Pennington proposed that the same thing causes obesity in humans. The adipose tissue amasses fat calories in a normal manner after meals, but it doesn’t release those calories fast enough, for whatever reason, to satisfy the needs of the cel s between meals. This was the metabolic defect that causes obesity, he said, and it could apparently be corrected or minimized by removing carbohydrates from the diet.

By hypothesizing the existence of such a defect, Pennington was able to explain the entire spectrum of observations about obesity in humans and animals simply by applying the same law of energy conservation that other obesity researchers had misinterpreted. The law applies to the fat tissue, Pennington noted, just as it does to the entire human body. If energy goes into the fat tissue faster than it comes out, the energy stored in the fat tissue has to increase. Any metabolic phenomenon that slows down the release of fat from the fat tissue—that retards the “energy out” variable of the equation—wil have this effect, as long as the rate at which fat enters the adipose tissue (the energy in) remains unchanged, or at least does not decrease by an equal or a greater amount. Fat calories accumulating in the adipose tissue wouldn’t be available to the cel s 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 wil increase the rate at which fat calories are released back into the bloodstream (just as inflating a bal oon wil increase the air pressure inside the bal oon and the rate at which air is expel ed out of the bal oon if the air is al owed to escape), and this could eventual y compensate for the initial defect itself. We wil 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 homeostatical y, 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 cel ular level remain constant; the cel s and tissues continue to function normal y, 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, al the seemingly contradictory findings in the field suddenly fit together “like clockwork.”

This defect in fat metabolism would explain the sedentary behavior typical y associated with obesity, and why al of us, fat or lean, wil 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 cel s are not receiving the ful benefit of the calories they consume, their tissues wil always be conserving energy and so expending less than they otherwise might. The cel s wil 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, stil further weight gain, this inhibition of energy expenditure wil be exacerbated.

Consider the kind of young, active men Ancel Keys had employed in his starvation experiments. These men might normal y 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 cel s would be unimpeded by any metabolic defects, and so the cel s 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’l 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 stil 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 cel s, 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 wil further diminish the amount of calories his cel s 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 stil 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 semistarvation 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 al 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 cel s, 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 cel s 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.

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 wil 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 wil 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 cel s and tissues could tel 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 natural y 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 shrinking because he was eating less. “The result would appear to be a ‘negative energy balance,’” Pennington said, “because so much of the energy needs would be supplied from stored amounts.”

Energy expenditure would also increase on such a diet. The now unconstrained flow of fat calories from the adipose tissue would increase the fuel available for cel ular metabolism. The cel s would no longer be undersupplied, as though living in a constant state of semi-starvation, and their metabolism would no longer be inhibited. Metabolic rate would increase, as would the impulse to physical activity—the urge to expend some of the energy now freely available. That such an effect is possible in humans, Pennington said, had been one of the observations reported by Du Bois and his col eagues in their yearlong al -meat-diet experiment with Stefansson and his col eague Anderson. These investigators had measured Stefansson’s and Anderson’s metabolism on a balanced diet and then measured their metabolism repeatedly during the yearlong trial. Both men lost some weight while eating the meat diet; both increased their basal-metabolic rate—7 percent for Stefansson and 5 percent for Anderson. Such an increase in energy expenditure could account for a weight loss of twenty pounds or more over the course of a year. If this change in expenditure went in the other direction when the diet included carbohydrates, it could easily account for the slow development of obesity.

When the obese or overweight go on a carbohydrate-restricted diet, Pennington theorized, there wil be an increase in metabolic and physical activity as their bodies expend this newly available energy, and an attendant weight loss. The naïve assumption would be that the physical activity caused the weight loss, and it would be wrong. They wil final y be burning off their accumulated fat stores and putting that energy to use.

Under these conditions, the energy expenditure of the obese individual might rise to what it otherwise would have been in a healthy state. It was not out of the question, as Frank Evans had reported and Sidney Werner had speculated, that this might be more than four thousand calories a day for someone who was definitively obese. Such an individual might easily eat over three thousand calories a day and stil lose a pound or two a week.