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 well. 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 well by ignoring sugar consumption and the difference between refined and unrefined carbohydrates.
These preliminary studies then prompted hundreds of millions of dollars 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 Doll 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 Still, 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
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, generally distinguished between degrees of refining or processing of starches, and there are, as yet, no reliable epidemiological data specifically 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 controlled 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, ideally, into the various subcategories, including stearic acid and oleic acid), carbohydrates have to be separated into subcategories as well. 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 all be beer drinkers. “Beer is full 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 College 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,