The results of a study presented at the American Academy of Neurology’s 60th Anniversary Annual Meeting held April 12–19, 2008 in Chicago suggest that Alzheimer’s patients who supplement with vitamin E may live longer than those who do not use the vitamin.
Valory Pavlik, PhD, of Baylor College of Medicine’s Alzheimer’s disease and Memory Disorders Center in Houston and her colleagues followed 847 men and women with Alzheimer's disease, beginning in 1990 for an average of five years. About two-thirds of the participants consumed 1,000 international units of vitamin E twice per day along with a cholinesterase inhibitor drug commonly used to treat their disease. Fewer than 10 percent of the remaining subjects used vitamin E alone, and 15 percent used neither therapy.
After adjusting for demographics, duration of symptoms at diagnosis, and baseline disease severity, analysis of the data showed that participants who were using vitamin E with or without drug treatment had a 26 percent lower risk of dying than those who did not use the vitamin. Vitamin E used alone was associated with an 18 percent reduction in risk. While those who used a cholinesterase inhibitor drug without vitamin E showed only a 1 percent reduction in mortality compared with those who received no treatment, the study’s results suggest that a combination of the drug and vitamin E appeared to be more effective than either treatment alone.
"Vitamin E has previously been shown to delay the progression of moderately severe Alzheimer’s disease,” Dr Pavlik stated. “Now, we've been able to show that vitamin E appears to increase the survival time of Alzheimer's patients as well. This is particularly important because recent studies in heart disease patients have questioned whether vitamin E is beneficial for survival.”
“The daily amount of vitamin E taken by patients in this study was much higher than what is currently recommended for the general population,” she noted.
"Our findings show that people who took a cholinesterase inhibitor without vitamin E did not have a survival benefit,” Dr Pavlik added. “More research needs to be done to determine why this may be the case.”
Compelling and growing evidence links inflammation and oxidative stress to Alzheimer’s disease. According to the inflammation theory (discussed in dozens of recent clinical trials), inflammatory cytokines gather at the neurons of people who have Alzheimer's. These cytokines set off an inflammatory cascade. The inflammation generates high levels of free radicals that contribute directly to the formation of beta-amyloid plaques. The result is more inflammation, free radicals, and beta-amyloid plaques. Iron has also been linked to the generation of free radicals. Studies have shown that free iron accumulates on the surface of dying neurons, where it generates oxygen-derived free radicals that hasten the spread of the disease (Mandel S et al 2006).
Vitamin E is a powerful antioxidant. Deficiencies of vitamin E in patients who have Alzheimer's disease are associated with increased lipid peroxidation, which appears to cause increased platelet aggregation, a hallmark of Alzheimer's (Ciabattoni G et al 2006). Community studies have shown that high doses of vitamin E, along with vitamin C, may help prevent Alzheimer's disease in the healthy elderly (Landmark K 2006). Combination therapy with vitamins C and E has been shown to reduce lipid peroxidation in people who have mild to moderate Alzheimer’s disease (Galbusera C et al 2004). High doses of vitamin E alone, up to 2000 International Units (IU) daily, slow the mental deterioration of patients who have Alzheimer's disease (Grundman M 2000).
One method by which vitamin E might protect people has to do with its relation to apoE4, which is associated with an increased risk of developing Alzheimer's disease. In people with the apoE4 phenotype, researchers suspect that an impairment in the antioxidant delivery system to neuronal cells may be related to increased oxidative damage (Mas E et al 2006). Another theory suggests that vitamin E might be able to reduce the oxidative damage caused by large amounts of inducible nitric oxide synthase, a pro-oxidant that has been linked to progression of Alzheimer's disease (McCann SM et al 2005).
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