Good Calories, Bad Calories (24 page)

—equivalent to the yearly per-capita consumption recorded in the United States or in the United Kingdom a century earlier.

The remarkable health of the islanders of Crete and Corfu in Keys’s Seven Countries Study—and thus the supposedly salubrious effects of the Mediterranean diet itself—could also be explained by the lack of sugar and white flour. Despite the popularity of the Mediterranean diet today, our understanding of what exactly such a diet is—particularly in Crete and Corfu, where Keys’s study had documented such remarkably low mortality rates

—is based on only two dietary surveys: Keys’s study itself, which analyzed the Cretan diet in 1960, and a Rockefel er Foundation study in 1947.

According to the Seven Countries Study, the Cretan diet circa 1960 included a total of only sixteen pounds a year of sugar, honey, pastries, and ice cream. According to the Rockefel er study, the Cretan diet included only ten pounds a year of sugar and sweets, and the considerable bread consumed was all wholemeal. The reported benefits of the Mediterranean diet, therefore, could be attributed to the fish, olive oil, and vegetables consumed, as it is today, but they could also be due to the minimal quantities of sugar and the absence of white flour.

This lack of concern for any potential health-related difference between vegetables and starches, on the one hand, and refined starches and sugars, on the other, has haunted cancer research as wel . Speculation that dietary fat caused breast, colon, and prostate cancer began in the 1970s, with the same international comparisons that led to the heart-disease hypothesis in the 1950s. Cancer epidemiologists simply compared carbohydrate, protein, and fat contents of diets in different countries with the mortality from various cancers. And these investigators, too, concluded that differences in cancer rates could be explained by differences in fat consumption and animal-fat consumption, particularly between Japan and the United States. They did not serve science wel by ignoring sugar consumption and the difference between refined and unrefined carbohydrates.

These preliminary studies then prompted hundreds of mil ions of dol ars of studies that failed to confirm the initial hypothesis that fat or animal fat led to cancer. (Even in the past few years, similar studies have attributed rising cancer rates in China to the increased consumption of fat, while again paying no attention to sugar or the refinement of the carbohydrates in the diets.) In 1975, Richard Dol and Bruce Armstrong published a seminal analysis of diet and cancer, in which they noted that, the higher the sugar intake in different nations, the higher both the incidence of and mortality from cancer of the colon, rectum, breast, ovary, uterus, prostate, kidney, nervous system, and testicles.*35 Stil , epidemiologists fixated on the fat-cancer hypothesis and made no attempt to measure the refined carbohydrates in the populations they studied. As a result, a joint 1997 report of the World Cancer Research Fund and the American Institute for Cancer Research, entitled Food, Nutrition and the Prevention of Cancer, said this:

The degree to which starch is refined in diets, particularly when the intake of starch is high, may itself be an important factor in cancer risk, as may the volume of refined starches and sugars in diets. Epidemiological studies have not, however, general y distinguished between degrees of refining or processing of starches, and there are, as yet, no reliable epidemiological data specifical y on the effects of refining on cancer risk.

Cleave’s saccharine-disease hypothesis may be intuitively appealing, but it is effectively impossible to test without a randomized control ed trial. If Cleave was right, then epidemiologists comparing populations or individuals with and without chronic disease have to take into account not just sugar consumption but flour, and whether that flour is white or whole-grain, and whether rice is polished or unpolished, white or brown, and even how much beer is consumed compared with, say, red wine or hard liquor. They might have to distinguish between table sugar and the sugar in soft drinks and fruit juices.

Just as fats are now divided into saturated, monounsaturated, and polyunsaturated (and, ideal y, into the various subcategories, including stearic acid and oleic acid), carbohydrates have to be separated into subcategories as wel . It would be easy, Cleave suggested, to gather together the twenty fattest people in any neighborhood and find that “they wouldn’t have a sweet tooth among them, and they wouldn’t like sugar”—they would al be beer drinkers.

“Beer is ful of malt sugar and enormously fattening,” he said.

It may have been these complications that led indirectly to a pared-down version of Cleave’s hypothesis—one that would receive far more publicity

—blaming coronary heart disease, diabetes, and other chronic diseases effectively on sugar alone. So said John Yudkin, who, unlike Cleave, was a prominent figure in the nutrition-research community. In 1953, he had founded the department of nutrition at Queen Elizabeth Col ege in London, the first dedicated department of nutrition in Europe. In the late 1950s, Yudkin began advocating a very low-carbohydrate diet for weight loss and wrote a popular diet book, This Slimming Business. He believed starches and sugars brought nothing of nutritional importance to the diet except calories—sugar was the worst offender—and so they were the obvious nutrient to remove from a weight-loss diet.

Yudkin entered the heart-disease debate in 1957, after Keys published his first series of papers claiming a “remarkable relationship” between fat consumption and coronary heart disease. Yudkin was among those who had taken Keys to task for the limitations of his analysis and his overinterpretation of very limited and unreliable data. Yudkin noted that many factors correlate with heart-disease deaths (not just dietary-fat consumption) one of which happened to be sugar consumption. Yudkin paid attention only to the trends of diet and disease in developed nations, and to heart disease and obesity, rather than the whole slew of chronic diseases, and he decided that sugar itself was the fundamental problem. (Yudkin would distance himself from Cleave by refusing to use the term “refined carbohydrates,” because it “gives the impression that white flour has the same il effects as sugar,” which he considered grossly misleading.) Through the 1960s, Yudkin published the results of a series of experiments implicating sugar in heart disease. He fed sugar and starch to rats, mice, chickens, rabbits, and pigs, and reported that the sugar, depending on the particular animal involved, raised some combination of cholesterol, triglycerides, and insulin levels. Triglycerides are a form of fat molecule found in the blood, and a series of researchers beginning with Pete Ahrens at Rockefel er University and Margaret Albrink of Yale had suggested that triglyceride levels were a better predictor of heart disease than was cholesterol. (Diabetics, as Joslin had noted, al too often died of atherosclerosis, and they, too, inevitably had high levels of triglycerides.) Yudkin also fed high-sugar diets to col ege students and reported that it raised their cholesterol and particularly their triglycerides; their insulin levels rose, and their blood cel s became stickier, which he believed could explain the blood clots that seemed to precipitate heart attacks.

By the early 1970s, the medical-research community was taking Yudkin’s hypothesis seriously. But now the very existence of Keys’s hypothesis was the primary obstacle to the acceptance of Yudkin’s. If one was right, than the other was very likely wrong. The European research community tended to be open-minded on this question. “Although there is strong evidence that dietary fats, particularly the saturated ones, play an important role in the etiology of

[coronary heart disease], there is no proof that they are the only or the main culprit,” wrote Roberto Masironi, an Italian cardiologist who would become president of the European Medical Association. “As regards the relationship of sugars to cardiovascular diseases, it must be borne in mind that these nutrients have common metabolic pathways with fats. Disturbances in carbohydrate metabolism may be responsible for abnormal fat metabolism and may therefore act as a causative factor in the development of atherosclerosis and of coronary disease.”

In the United States, however, Keys’s hypothesis ruled. Keys himself went after Yudkin in a letter that he first distributed widely to investigators in 1970, before it was published in the journal Atherosclerosis. Keys cal ed Yudkin’s arguments for the role of sugar in heart disease “tendentious” and his evidence “flimsy indeed” he treated Yudkin as a figure of ridicule. What made Keys’s critique so ironic, though, is that virtual y every argument that he invoked to criticize Yudkin’s hypothesis had been used in the past as criticism of his own. Most were equal y valid for both, and spoke to the flaws in the epidemiologic evidence—the use of international cause-of-death statistics and food-consumption data or dietary-recal surveys to draw conclusions about cause and effect—rather than to the actual validity of the hypotheses. Keys’s case against Yudkin eventual y came to rest almost entirely on his invocation of the Seven Countries Study as support for his hypothesis. In fact, the Seven Countries Study had been one of the very few studies that had measured sugar consumption in its populations, and sugar indeed turned out to predict heart-disease rates as wel as saturated fat did.

By the early 1970s, Keys’s dietary-fat hypothesis of heart disease, despite the ambiguity of the evidence, was already being taught in textbooks and in medical schools as most likely true. After Yudkin retired in 1971, his hypothesis effectively retired with him. His university replaced him with Stewart Truswel , a South African nutritionist who was among the earliest to insist publicly that Keys’s fat theory of heart disease was assuredly correct and that it was time to move on to modifying the diets of the public at large accordingly. Truswel believed it was more important for the prevention of heart disease to convince the public to eat more onions, for their reported ability to alter the “tendency to thrombosis,” than to eat less sugar.

Yudkin spent his first year of retirement writing a book on his sugar theory, published in 1972 and entitled Pure, White and Deadly in England and Sweet and Dangerous in the American edition. It did not serve to move the medical-research community closer to embracing either Yudkin or his theory.

By the late 1970s, to study the potential y deleterious effects of sugar in the diet, says Sheldon Reiser—who did just that at the U.S. Department of Agriculture’s Carbohydrate Nutrition Laboratory in Beltsvil e, Maryland—and to talk about it publicly, was to endanger your reputation. “Yudkin was so discredited,” says Reiser; “he was ridiculed in a way. And anybody else who said something bad about sucrose, they’d say, ‘He’s just like Yudkin.’”

FIBER

The thing is, it’s very dangerous to have a fixed idea. A person with a fixed idea wil always find some way of convincing himself in the end that he is right.

ATLE SELBERG, winner of the 1950

Fields Medal in Mathematics

THE HYPOTHESIS THAT SUGAR AND refined carbohydrates cause chronic disease peaked as a subject of serious consideration in late April 1973, when George McGovern’s Senate Select Committee on Nutrition and Human Needs held its first hearing on diet and what the committee took to cal ing kil er diseases. The testimony would have little impact on the content of McGovern’s Dietary Goals for Americans, in part because none of the staff members who organized the hearings would stil be working for the committee three and a half years later, when the Dietary Goals would be drafted. Equal y important, neither McGovern nor his congressional col eagues could reconcile what they were hearing from the assembled experts with what they had now come to believe about the nutritional evils of modern diets.

The committee had initial y planned a series of hearings in 1972 on dietary fat, cholesterol, and heart disease, but the plans changed because McGovern ran for president. When the committee returned to the diet-and-chronic-disease issue after McGovern’s defeat, the subject that seemed most urgent—thanks in part to the publication of John Yudkin’s Sweet and Dangerous—was sugar in the diet, diabetes, and heart disease.

The hearings were a surprisingly international affair. Aharon Cohen from Jerusalem testified on diabetes and heart disease among the Yemenite Jews.

George Campbel testified on his studies of diabetes in Zulus and Natal Indians in South Africa. Peter Bennett, an NIH epidemiologist, testified on the Pima Indians of Arizona, who had the highest incidence of diabetes ever recorded at the time: half of the Pima over thirty-five years old were diabetic.

“The only question that I would have,” Bennett said, “is whether we can implicate sugar specifical y or whether the important factor is not calories in general, which in fact turns out to be real y excessive amounts of carbohydrates.” Walter Mertz, chairman of the USDA Human Nutrition Institute, testified, as did his col eague Carol Berdanier, explaining that refined sugar seemed to play particular havoc with health, at least in laboratory rats. It elevated blood sugar and triglycerides, and caused subjects to become diabetic, Berdanier said, “and they die at a very early age.”