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CAN DIET PREVENT ALZHEIMERS? (August 2003) Alzheimer Disease is a hideous problem affecting millions of Americans. Ten percent of those over age 65 suffer from this terrible disease that robs them of their personalities and their minds. As our population ages, the problem will get much worse; in the range of 30 percent of those 80 years and older will develop Alzheimers. Obviously, the major goal is to figure out how to prevent the disease. There are lots of tantalizing possibilities, none adequately proved. These include: cholesterol lowering drugs; blood pressure lowering drugs; controlling homocysteine levels; estrogen administration, taking non-steroidal anti-inflammatory drugs, such as aspirin. Then, there are dietary and dietary supplement approaches, including antioxidants and restricting fat or calories in the diet (see Archives article "Can taking antioxidants really prevent Alzheimer Disease"). The August 2002 issue of the journal Archives of Neurology includes an article titled "Caloric intake and risk of Alzheimer Disease". The investigators followed 980 persons, average age 75 years, for four years; during that time, 242 developed Alzheimers. The participants were divided into four groups (quartiles) according to daily calorie and fat intake. This was based on a single dietary determination at the start of the study. Overall, there was no relationship between either fat or total calorie intake and likelihood of developing Alzheimer Disease. However, when the investigators looked at a subgroup with a specific genetic variation, there were some interesting findings. More than one-quarter of the study group had a gene product called apolipo protein E4 that is associated with a cholesterol-carrying protein. Among those with E4, those in the highest quartile of calorie intake were twice as likely to develop Alzheimers; the two highest quartiles of fat intake also had a doubled risk of Alzheimers. Commentary: This is an intriguing preliminary study. It is not the first in the area; two other studies are in general supportive, whereas one is not. It would have been desirable to have carried out more than one dietary questionnaire on each participant. One puzzling feature is that so many (about one-quarter) of the population studied developed Alzheimers during the relatively short (four year) followup period. The total calorie and fat intake was, in general, low, even in the highest quartile. Actually, in this study, the relationship with fat intake was more impressive than that with calories. The E4 genetic variation increases the risk of Alzheimers, but most people who develop Alzheimers do not have that genetic pattern; the study results would not apply to them. Even for those with E4, a low calorie, low fat diet would only (if this study is confirmed) offer moderate protection.
We need several more studies before drawing any conclusions. At present, there is no dietary prescription that has been clearly shown to prevent or reduce the risk of or the severity of Alzheimers. Although there is no known preventive for Alzheimers, there are a lot of interesting possibilities. If it turns out that estrogens do reduce risk, that would go a long way to reverse the very negative reports about the small increased risk of heart disease, stroke, and breast cancer during the first few years of estrogen-progestin treatment among postmenopausal women. If high homocysteine levels, high blood pressure, or high cholesterol levels are risk factors, we have the treatments to control these possible risk factors. If dietary fat or calories increase risk or antioxidants reduce risk, we can change dietary patterns or give appropriate dietary supplements. It would be irresponsible to raise expectations about Alzheimer Disease prevention until we have enough convergent studies to be able to make some specific recommendations. For now, there is reason to be hopeful about the potential for preventing Alzheimers, but, at present, it is just that - a hope, but nothing more. Luchsinger, S.A., et al. Calorie intake and risk of Alzheimer Disease. Archives of Neurology Vol 59 (August) Pgs 1258-1263. 2002.
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