In 2002, the Institute of Medicine of the National Academies of Science released its two-volume report on Dietary Reference Intakes (subtitled Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids), and spent twenty pages discussing the possible adverse effects of sucrose and high-fructose corn syrup. It then concluded that there was still “insufficient evidence” to set up an upper limit for sugar consumption in the healthy diet. Nor did the IOM perceive any reason to pursue further research on fructose or sucrose or high-fructose corn syrup and so, perhaps, discover sufficient evidence. In early 2007, the National Institutes of Health was funding at most half a dozen research projects that addressed, even peripherally, the health effects of dietary fructose, meaning sugar and high-fructose corn syrup in the diet.

Over the years, what little research has been done on fructose metabolism has been carried out primarily by biochemists, who have had little motivation, other than perhaps personal health, to pay attention to the nutrition literature—again, an effect of specialization. Their own articles, moreover, are published in biochemistry journals, and have little influence on the nutrition and public-health communities. For this reason, observations on the potential dangers of fructose have managed to remain dissociated from discussions of sugar itself and the role of sucrose and high-fructose corn syrup in modern diets. After the ridicule that John Yudkin received for the work that culminated in his anti-sugar polemic, Pure, White and Deadly—and after the FDA decided that “no conclusive evidence demonstrates a hazard” from sucrose—few researchers have appeared willing even to contemplate the possibility that sugar consumption could have harmful consequences beyond perhaps causing cavities and contributing to obesity.

Chapter 13

Chapter Thirteen

DEMENTIA, CANCER, AND AGING

The bottom line is pretty irrefutable: What is good for the heart is good for the brain.

RUDOLPH TANZI AND ANN PARSON, Decoding Darkness: The Search for the Genetic Causes of Alzheimer’s Disease, 2000

WHEN IT COMES TO THE CAUSE of chronic disease, as we discussed earlier, the carbohydrate hypothesis rests upon two simple propositions. First, if our likelihood of contracting a particular disease increases once we already have Type 2 diabetes or metabolic syndrome, then it’s a reasonable assumption that high blood sugar and/or insulin is involved in the disease process. Second, if blood sugar and insulin are involved, then we have to accept the possibility that refined and easily digestible carbohydrates are as well.

This applies to Alzheimer’s disease and cancer, too, since both diabetes and metabolic syndrome are associated with an increased incidence of these two illnesses. In both cases, critical steps in the disease process have been linked unambiguously to insulin and blood sugar, and the relevant research is now beginning to influence the mainstream thinking in these fields.