Good Calories, Bad Calories (63 page)

Yudkin was the most prominent advocate of carbohydrate-restricted diets among nutritionists through the 1970s. He also had unconditional faith, however, in the popular misinterpretation of the law of conservation of energy. “The irrefutable, unarguable fact is that overweight comes from taking in more calories than you need,” Yudkin explained in a 1958 diet book entitled This Slimming Business. He reconciled this belief with his advocacy of carbohydrate-restricted diets because he also believed that “much of the extra fat today” in the diet “comes together with carbohydrate in cakes, biscuits, ice cream, and sweetmeats of various sorts.” If we remove the carbohydrates, Yudkin proposed, the fat calories wil come down, too.

In 1960, Yudkin provided experimental evidence to support this statement in a Lancet article entitled “The Treatment of Obesity by the ‘High-Fat’ Diet.”

He had asked four women and two men to consume a carbohydrate-restricted diet for two weeks. They al lost weight, he reported, by consuming significantly less carbohydrates and no more fat than they typical y ate on a balanced diet. The two men ate roughly twenty-nine hundred and thirty-five hundred calories normal y, but reported consuming only fifteen to sixteen hundred when they abstained from carbohydrates. Their fat consumption dropped by two hundred calories a day as wel . This led Yudkin to the “unequivocal” conclusion that “the high-fat diet leads to weight-loss because, in spite of its unrestricted al owance of fat and protein, it is in fact a low-calorie diet….” Weight is lost by restricting calories, even if calorie-restriction is not required by the diet.

Here again, however, Yudkin was confusing an association with cause and effect. Even if Yudkin’s subjects had reduced their calorie consumption on the carbohydrate-restricted diet, which is a common finding in these studies, it does not mean that the reduction in calories caused the weight loss, only that the diet was associated with a reduction in calories as wel as a reduction in weight. The diet could have worked by some other mechanism entirely, but both weight loss and decreased appetite were consequences. The fact that a reduction of appetite associates with weight loss does not mean that it is the fundamental cause.

And, of course, what may have been true, on average, for Yudkin’s seventeen subjects—six in his 1960 study and eleven a decade later—is not necessarily the case for everyone who loses weight on such diets.*105 Even before Yudkin published This Slimming Business, Weldon Walker and the Columbia University physician Sidney Werner had both reported that their subjects lost significant weight while consuming at least twenty-seven hundred and twenty-eight hundred calories a day respectively. In 1954, when the Swiss clinician B. Ril iet discussed his experiences using Pennington’s diet to treat obese patients at the County Hospital of Geneva, he reported that his successes were “numerous and encouraging” with both a twenty-two-hundred-calorie version of the diet and a three-thousand-calorie version. It’s hard to avoid the observation that at least some individuals lose weight on carbohydrate-restricted diets while eating considerably more calories than would normal y be consumed in a semi-starvation diet. This is why Werner speculated that his obese subjects must have typical y been eating four to five thousand calories a day before he set about experimental y reducing them.

But if that is true, why don’t obese patients regularly lose weight on twenty-seven or twenty-eight-hundred calorie balanced diets, and why have clinicians always believed it necessary to semi-starve them with twelve to fifteen hundred calories, or even feed them very low-calorie diets of eight hundred calories or less, to achieve any significant weight loss? Something else is going on here, and it has nothing to do with calories.

The argument that carbohydrate-restricted diets work by the same mechanism as calorie-restricted diets only changes the nature of the dilemma we have to unravel. It does not make it disappear. Even if we accept Yudkin’s notion that al people who lose weight while abstaining from carbohydrates do so because they spontaneously feel the compulsion to eat less, we must then explain why anyone would wil ingly suffer the symptoms of semi-starvation

—hunger, irritability, depression, and lethargy—rather than simply eat another piece of cheese, or steak, or lamb. The standard explanations are that it’s simply too much trouble to do so, or that “al -you-can-eat-diet[s],” as Jane Brody wrote in the New York Times in 1981, “so restrict the dieter’s choices that boredom and distaste automatical y produce a calorie cutback.” But these are unacceptably facile. If the obese end up eating less on this diet, the most likely explanation is that they’re less hungry, in the same way that, if we don’t drink water when water is there for the drinking, we’re probably not thirsty. If we don’t feel or act semi-starved, it’s a reasonable bet that we’re not. “The best definition of food deficiency,” as Ancel Keys and his col eagues wrote in The Biology of Human Starvation, “is to be found in the consequence of it.”

Keys’s starvation studies suggest where the “no bread, no butter” logic wil take us. We know from these studies that if we feed people a carbohydrate-rich diet of fifteen or sixteen hundred calories a day, they wil be obsessed with the “persistent clamor of hunger,” so much so that they might be wil ing to mutilate themselves to escape the ordeal. Meanwhile, if those same people were al owed to consume unlimited calories of only meat, cheese, and eggs, this school of thought dictates, they wil voluntarily restrict their consumption to the same fifteen or sixteen hundred calories—or at least they wil if they’re obese or need to lose ten or twenty pounds—because in this case, as Harvard endocrinologist George Cahil suggested, the “nonappetizing nature” of this meat-egg-and-cheese diet wil overcome the urge to amply satisfy their desire for food. Our subjects wil voluntarily starve themselves, as though hunger itself, and al its regrettable side effects, have been rendered impotent in the face of monotony, which is to say, a diet that these experts define as unappetizing because it does not al ow consumption of starches, flour, sugar, or beer.

But Keys had also severely restricted the choice of foods he fed his subjects. Remember, he had wanted to simulate the foods available during wartime in Eastern Europe and so had al owed his conscientious objectors only bread, potatoes, cereals, turnips, cabbages, and “token” amounts of meat and dairy products. Yet, in the entire fourteen hundred pages of his Biology of Human Starvation, there is not the slightest hint that his semi-starved subjects, or those starving populations he discusses in his comprehensive history of famine, would have turned down more cabbages, bread, or turnips had they been available, not to mention meat, cheese, fish, or eggs. The notion that hunger can be relieved or eliminated simply by limiting the choice of food is exceedingly difficult to embrace.

Over the years, a common way to avoid thinking about the paradox of a diet that al egedly restricts calories but does not induce hunger is to attribute the suppression of appetite to a factor that these authorities consider irrelevant to the bigger picture of weight and health—to ketosis, the condition produced when the liver increases its production of ketone bodies to replace glucose as a fuel for the brain and nervous system. Once ketone bodies are produced, “their appetite-depressing activity takes effect,” as Richard Spark of Harvard Medical School claimed in 1973. “Substances cal ed ketones wil accumulate in your bloodstream [during carbohydrate restriction] and can make you slightly nauseated and light-headed and cause bad breath,” wrote Jane Brody in the New York Times in 1996. “This state is not exactly conducive to a hearty appetite, so chances are you wil eat less than you might otherwise have of the high-protein, high-fat foods permitted on the diet.”

But this, too, fails as a viable explanation. The liver increases ketone-body synthesis only when carbohydrates are unavailable and the body is relying predominantly on stored fat for its fuel. Ketone bodies could be responsible for appetite suppression, as Spark and Brody suggested, but so could the absence of carbohydrates or the burning of fat, or something else entirely. Al of these are associated with the absence of hunger. In fact, the existing research argues against the claim that ketone bodies suppress appetite. Individuals with uncontrol ed diabetes, for example, wil suffer from ketoacidosis, during which ketone-body levels can be tenfold or even forty-fold higher than the mild ketosis of carbohydrate restriction, and yet these people are ravenous. “It is not clear why the sensation of hunger subsides [in starvation studies], but the disappearance is apparently not related to ketosis,” wrote Ernst Drenick in 1964 about his fasting studies at UCLA. Hunger sensations often disappeared in his subjects before ketone bodies could be detected in their blood or urine, “and it did not reappear” in those periods when ketone body levels were low. The same dissociation between ketone bodies and hunger was reported in 1975 by Duke University pediatrician James Sidbury, Jr., in the treatment of obese children.

Another common explanation for the absence of hunger on carbohydrate-restricted diets is that fat and protein are particularly satiating—“these foods digest slowly, making you feel satisfied longer,” as Brody has explained in the Times. (Even those investigators who published studies supporting Yudkin’s idea that carbohydrate-restricted diets work by restricting calories would invariably comment that high-protein, high-fat diets stil induced the least hunger and the greatest feeling of satiation. “There is a good reason to believe that the satiety value of such diets is superior to diets high in carbohydrate and low in fat, and hence, may be associated with better dietary adherence,” the metabolism researcher Laurance Kinsel wrote in an influential 1964 article entitled “Calories Do Count.”) But this is also unsatisfying as an explanation. The statement that fat and protein satisfy us longer is equivalent to the statement that carbohydrates are less satisfying—they either make us experience hunger sooner than fat and protein or perhaps induce hunger, whereas fat and protein suppress it. This leads us back to the now familiar question: what is it about carbohydrates, or about the speed with which we digest them, that accelerates or exacerbates our sensation of hunger and our desire to eat?

Even Yudkin had struggled with the question of why people would wil ingly semi-starve themselves on a carbohydrate-restricted diet. “For reasons I do not clearly understand,” he wrote, there must be something unique about carbohydrates that either stimulates our appetites or fails to satiate us. “It would seem from this that carbohydrate does not satisfy the appetite,” he noted; “it may even increase it….”

This conclusion is simply hard to avoid, considering the half century of experimental observations on these diets. It leaves us with two seemingly paradoxical observations. The first is that weight loss can be largely independent of calories. The second is that hunger can also be. Even if we could establish that weight loss on these diets is universal y attended by a decrease in calories consumed—no bread, no butter—we then have to explain why the subjects of these diets don’t manifest the symptoms of semi-starvation. If they eat less on the diets, why aren’t they hungry? And if they don’t eat less, why do they lose weight?

“It is better to know nothing,” wrote Claude Bernard in An Introduction to the Study of Experimental Medicine, “than to keep in mind fixed ideas based on theories whose confirmation we constantly seek, neglecting meanwhile everything that fails to agree with them.” In the study of human obesity, that fixed idea has been what Yudkin cal ed “the inevitability of calories,” which in turn is based on the ubiquitous misconception of the law of energy conservation. If we believe that conservation of energy—calories in equal calories out—implies cause and effect, then we wil refuse to believe that obese patients can lose significant weight without restricting their energy intake beneath some minimal expenditure. Any reports to the contrary wil be rejected on the basis that they cannot possibly be true. “Claims that weight loss occurs even with high-caloric intake, but no carbohydrate, are absurd,” as the American Medical Association insisted in 1974. “Although authors of popular diet books frequently say that loss of body fat can occur regardless of high-calorie intake, this is not supported by evidence and, in fact, is refuted by the laws of thermodynamics.”

Because such a possibility is not refuted by the laws of thermodynamics, we should take such claims seriously, as Alfred Pennington did. Although several of Pennington’s articles appeared in journals that were widely read, including The New England Journal of Medicine, they would have little influence on the thinking about obesity. A few practicing physicians took his work seriously—George Thorpe and Herman Tal er, a Brooklyn obstetrician who published a 1961 best-sel er based on Pennington’s science entitled Calories Don’t Count—but they only lost professional credibility by doing so.

The great majority of clinicians and nutritionists would not go against the conventional wisdom.

Nonetheless, Pennington was on to something. He set out to understand why his DuPont patients lost weight on a calorie-unrestricted diet that they enjoyed. He knew it contradicted the conventional wisdom but was determined to pursue the evidence. First he read what he cal ed the “voluminous experimental literature on obesity.” He concluded that only “meager and conflicting” evidence existed to support the popular contention that calorie restriction would induce long-term weight loss, or even that it should induce long-term weight loss. He came to believe that experts who invoked the first law of thermodynamics to defend their beliefs did great damage. “These tended to distract the general attention from examination of the evidence on the real question, whether or not common obesity arises from a metabolic defect,” he wrote.

Pennington based his analysis of the obesity problem on one fundamental premise that he adopted from the research on homeostasis in the 1930s and early 1940s: Because fuel is ultimately used by the cel s themselves, the relationship between fuel supply and demand at this cel ular level determines both hunger and energy expenditure. The less fuel available to supply the metabolic demands of our cel s, the greater the hunger and the less energy we wil expend. The greater the fuel available to the cel s, the greater the metabolic activity and perhaps physical activity also. This was something Francis Benedict had suggested in the 1920s and Eugene Du Bois believed. Energy expenditure, wrote Pennington, is an “index of calorie nutrition at the cel ular level.”