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.

Though the characteristic dementia and brain lesions of Alzheimer’s were first described a century ago, the disease only recently captured the attention of the research community. In 1975, when the NIH was supporting hundreds of research projects on atherosclerosis and cholesterol metabolism, it was funding fewer than a dozen on Alzheimer’s and what was then called senile dementia. This number rose gradually through the end of the 1970s. Between 1982 and 1985, the number of Alzheimer’s-related research projects funded by the NIH quintupled.

It took another decade for researchers to begin reporting that heart disease and Alzheimer’s seem to share risk factors: hypertension, atherosclerosis, and smoking are all associated with an increased risk of Alzheimer’s, as is the inheritance of a particular variant of a gene called apolipoprotein E4 (apo E4) that also increases the risk of cardiovascular disease.*59 This in turn led to the notion that what’s good for the heart is good for the brain, but that, of course, depends on our understanding of what exactly is good for the heart. Because Alzheimer’s researchers, like diabetologists, assume that Keys’s fat-cholesterol hypothesis is supported by compelling evidence, they will often suggest that cholesterol and saturated fat play a role in Alzheimer’s as well. But if coronary heart disease is mostly a product of the physiological abnormalities of metabolic syndrome, as the evidence suggests, then this implicates insulin, blood sugar, and refined carbohydrates instead, a conclusion supported by several lines of research that began to converge in the last decade.

A handful of studies have suggested that Alzheimer’s is another disease of civilization, with a pattern of distribution similar, if not identical, to heart disease, diabetes, and obesity. Japanese Americans, for instance, develop a pattern of dementia—the ratio of Alzheimer’s dementia to the stroke-related condition known as vascular dementia—that is typically American; when Japanese immigrate to the United States, their likelihood of developing Alzheimer’s disease increases considerably, while their risk of developing vascular dementia decreases. The incidence of Alzheimer’s dementia in African Americans, according to research published in JAMA in 2001, is twice that of rural Africans, and they are three times as likely to suffer vascular dementia, again suggesting that dietary or lifestyle factors play a role in both dementias.