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,
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,
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
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
Studies in large populations—6,000 elderly subjects in Rotterdam, 1,500 in Minnesota, 1,300 in Manhattan, 800 Catholic nuns, priests, and brothers in the American Midwest, and 2,500 Japanese Americans in Honolulu—have suggested that Type 2 diabetics have roughly twice as much risk of contracting Alzheimer’s disease as nondiabetics. Diabetics on insulin therapy, according to the Rotterdam study, had a fourfold increase in risk. Hyperinsulinemia and metabolic syndrome are also associated with an increased risk of Alzheimer’s disease. And so one interpretation of these results, as the Rotterdam investigators noted in 1999, is that “direct or indirect effects of insulin could contribute to the risk of dementia.”
One complicating factor in this research is that the underlying cause of dementia is exceedingly difficult to diagnose, even on autopsy. For this reason, it’s possible that the research linking diabetes to a higher incidence of Alzheimer’s does so because it confuses the consequences of a known complication of diabetes—vascular dementia—with an apparently increased incidence of Alzheimer’s dementia. These are the two most common causes of dementia, but the actual diagnoses are not clear-cut.
Alzheimer’s dementia is typically perceived as a slow, insidious process that can be identified on autopsy by the presence of neurofibrillary tangles, which are twisted protein fibers located within neurons, and amyloid plaques, which accumulate outside the neurons. Vascular dementia, a recognized complication of diabetes, is perceived as a more abrupt cognitive decline that is caused by small strokes in the blood vessels of the brain. Vascular dementia is usually diagnosed because the dementia appeared shortly after a stroke, or because an autopsy revealed the characteristic stroke-related signs of vascular damage. That vascular dementia is a complication of diabetes means that diabetics are far more likely to be diagnosed someday with vascular dementia than nondiabetics.
In cases of dementia, however, the determination of the actual cause is likely to be arbitrary. Most of us, if we live long enough, will accumulate both vascular damage and Alzheimer’s plaques and tangles in our brains, even if we don’t manifest any perceptible symptoms of dementia. (Similarly, most of us will have plaques in our arteries even if we don’t manifest clinical signs of heart disease.) Vascular dementia and Alzheimer’s dementia appear to coexist frequently, a condition known as
