Good Calories, Bad Calories

to provide healthy and safe diets.”

This theme of financial rewards for the promoters of these diets would also be echoed repeatedly. A “common factor of reducing regimens is their commercialism—someone stands to make money from their promotion,” wrote George Mann, another veteran of Stare’s nutrition department, in The New England Journal of Medicine in 1974. This didn’t explain those like Pennington, Ohlson, Young, Gordon, or Kekwick and Pawan, who never wrote popular diet books and advocated similar advice to their obese patients, but it was an easy way to dismiss those like Atkins and Taller who did.^*129 They were “instant monetary nutritionists,” wrote Stare, who liked to point out that Atkins made over $1 million in one year from Diet Revolution, while simultaneously treating five hundred patients weekly in his “very lucrative private medical practice.”

But this conflict-of-interest accusation, as we’ve discussed, often cuts both ways. Stare and his Harvard colleagues played the decisive role in ensuring that anyone who claimed that carbohydrates were uniquely fattening would carry the taint of quackery. When White, Mayer, and Stare publicly condemned Herman Taller’s Calories Don’t Count it was a year after the Harvard nutrition department broke ground on a new $5 million building that was paid for largely through private donations. What Stare called the “lead gift” of $1,026,000 came from the General Foods Corporation, the maker of the very carbohydrate-rich Post cereals, Kool- Aid, and Tang breakfast drink. Over the next decade, Stare became the most public defender of sugar^*130 and additives in modern diets, while his department continued to receive significant funding from the sugar industry; from Oscar Mayer, the maker of hot dogs; from Coca-Cola and the National Soft Drinks Association. Would the resident nutritionists in Stare’s department have been more accepting of the efficacy of a diet that restricted refined carbohydrates and sugars if the money had come from another source? If so, would this have effected how other clinical investigators in the field came to interpret the controversy?

The funding of research projects, laboratories, and entire academic centers by the food and pharmaceutical industries is now a fact of life in modern medical research, which is why many journals require that their authors declare potential conflicts of interest. But it raises important questions, just the same. When Science dedicated special issues to obesity research in 1998 and again in 2003, James Hill from the University of Colorado was selected both times to write the review article on diet and lifestyle factors that influence weight gain. In those articles Hill argued that passive overeating and sedentary behavior were the causes of obesity, and he recommended reducing fat in the diet. Hill had long been a defender of the role of carbohydrates and particularly sugar in weight regulation. He even wrote an article, paid for by the Sugar Association, promoting the use of sugar in weight-loss diets, under the assumption that a high-carbohydrate diet, even if loaded with sugar, would “reduce the likelihood of overeating, rather than increasing it, as some popular diet theories purport.” (“The theory that dietary sugar equals high insulin levels equals excess fat deposits is unproven and makes little biological sense,” Hill wrote.) Over the years, as Hill has acknowledged in his conflict-of-interest statements, he has also received consulting fees from Coca-Cola, Kraft Foods, and Mars (makers of Snickers, M&M’s and Mars Bars), companies that would stand to suffer significant setbacks if the notion of the fattening carbohydrate was institutionalized as a fact of science. He has also received over $2 million in what are technically termed “gifts” to his laboratory from Procter & Gamble, the maker of the fat substitute olestra, which has been described in the press as potentially a “dieter’s dream.” Olestra’s only reason for existence is that it will allegedly help us manage our weight by replacing fat in the diet and making it easier for us to consume a low-fat, low-calorie diet. If carbohydrates are the fattening nutrients in human diets rather than fat or all calories, as Atkins suggested, then these diets have no role in weight loss or weight regulation, and olestra’s rationale vanishes.

If the study of weight regulation were a legal issue, rather than a medical and scientific one, the support from Procter & Gamble would have been considered reason enough for Hill to recuse himself from any discussions of the dietary treatment of obesity or participation in any dietary trials that might directly influence Procter & Gamble’s profitability, and thus perhaps Hill’s interests.

In 2002 and 2003, Hill also received over $300,000 a year from the NIH to do a clinical trial testing the Atkins diet against a low-calorie, low-fat diet and, by implication, the justification for olestra as a fat substitute in a weight-reduction diet. And Hill was one of three principal investigators in the follow-up trial of the Atkins diet, for which the NIH provided $5 million. The salient question is whether Hill and the other academics in this pursuit are any less open to having their interpretation of the evidence influenced by financial considerations than Atkins or Taller or any of the other diet-book authors.

“A resolution of the very controversial question of the efficacy of low carbohydrate diets has great practical and theoretical significance,” wrote Donald Novin of UCLA in 1978. Because a generation of obesity authorities were determined to dismiss the practical significance of carbohydrate-restricted diets, they dismissed the potential theoretical significance at the same time. Obesity researchers today say they still have no hypothesis of weight regulation that can explain obesity and leanness, let alone account for a century of paradoxical observations. They insist that obesity is inevitably caused by overeating and thus consuming more calories than we expend, but when asked what causes someone to overeat, they have no answer. Yet the research on insulin and fat metabolism offers one, and it has for several decades.

Chapter Twenty-four

THE CARBOHYDRATE HYPOTHESIS, III: HUNGER AND SATIETY

There is only one way to lose weight, and that is to grow accustomed to feeling hungry. This simple fact, known to most people in affluent countries, seems somehow lost on the authors of the diet, weight-loss, and exercise books that find their lucrative way through the drugstore book racks. Two questions, then: Why do they fail to mention it? And why is it so?

Emory University anthropologist Melvin Konner,

The Tangled Wing, 2003

IN 1975, THE DUKE UNIVERSITY PEDIATRICIAN James Sidbury, Jr., described a “rational basis” for the dietary treatment of childhood obesity, one that would neither torment his young patients with hunger nor rely on pharmaceutical means to prevent it. Such a diet, he wrote, would induce weight loss with a “minimum of anguish and struggle.” Sidbury had an advantage over other investigators treating obese patients in that he had spent his career studying disorders of carbohydrate metabolism and, indeed, had already earned international renown for his development of a diet, still used today, to treat what are called glycogen storage diseases. The same year Sidbury published his description of a “Program for Weight Reduction in Children,” however, he left his clinic at Duke to become director of the National Institute of Child Health and Human Development at NIH. By then, he had written only one short textbook chapter discussing his dietary treatment and one three-page article for an obscure journal called Connecticut Medicine. In them, he described an approach to obesity therapy that differed from Robert Atkins’s only in the details of the application: Sidbury’s diet was very low in both carbohydrates and calories, and Sidbury was writing for medical professionals, not the general public.

He based the design of his diet on several key observations. Fasted children “rarely, if ever, complained of hunger,” Sidbury noted, and the “enzymes of lipogenesis”—insulin—rapidly decrease during fasting. Insulin is chronically elevated in obese patients, and the obese children referred to him in his practice typically consumed a diet dominated by carbohydrates—“crackers, potato chips, French fries, cookies, soft drinks, and the like.” These foods are digested and absorbed as simple sugars, Sidbury explained, “chiefly glucose, which is the most potent