In the wake of studies showing that alcohol had some health benefits, smokers were rabid to find similar good news for cigarettes. An article in the 1991 issue of the International Journal of Epidemiology seemed to offer the evidence that group was after. In that meta-analysis of 11 Alzheimer's Disease (AD) studies, Dr. A. B. Graves determined that alcohol consumption did not increase the risk of dementia, and that smoking actually decreased the risk. Graves makes a very strong statement in the abstract of the article:
A statistically significant inverse association between smoking and Alzheimer's disease was observed at all levels of analysis, with a trend towards decreasing risk with increasing consumption.
While compelling, this observed relationship may have alternate explanations. For example, smokers have lower life expectancy, and rates of dementia double every five years after 65, so many smokers may have died before cognitive problems became apparent.
The smooth graph that Dr. Graves plotted began to break down with the release of the Rotterdam Study, a long-term investigation of age-related diseases among 11,000 elderly citizens. With his suspicion aroused by results in the Rotterdam study that cast doubt on earlier claims of the protective effect of cigarettes, Dr. C. Merchant ran his own study of smokers in Manhattan. He found that current smokers were at higher risk for AD. Interestingly, this risk was ameliorated by the presence of the dreaded APOE-4 allele linked to AD. This fits in with the hypothesis discussed last week that the allele may have some blessing mixed in with the curse. AD genes have also been recently shown to boost memory performance before old-age. The strangest finding was that ex-smokers seemed to have a slightly decreased risk, something that, as of yet, has no explanation.
This month, a study in Neurology goes back to the Rotterdam study and performs a more rigorous analysis of the data. The researchers confirm that current smoking raises the risk of AD by a massive percentage amongst those without the APOE-4 allele. Ex-smokers here were not found to have a decreased risk, but they did not have the elevated risk that one might expect given our previous report that smoking permanently activates many genes. Reuters interviewed one author of the study, Dr. Monique Breteler, about why smoking might increase the risk of AD. She speculated that the correlation might be explained by either the fact that smoking increased the risk of stroke (which is linked to dementia) or that bodies inundated by smoke suffer greater oxidative stress.
Close examination of the Rotterdam Study, backed by additional studies like Dr. Merchant's, deflates the idea that cigarettes offer protection against AD. Early analyses were too quick to jump to conclusions, and it is clear that smoking is detrimental for the average person. There is some room, however, for the possibility that smoking has a different effect on a minority of the population, such as those with the APOE-4 allele. This population difference may account for some of the anomalous findings that cloud the issue. Even if this is the case, smokers will have to look elsewhere for evidence that they are not abusing their bodies. They should look quickly, because life is rarely extended by wishful thinking.
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