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Title: Vitamin B Supplementation Does Not Slow Cognitive Decline in Patients With Alzheimer's Disease
URL: http://www.pslgroup.com/dg/22ECC6.htm
Doctor's Guide
October 14, 2008


CHICAGO -- October 14, 2008 -- High-dose vitamin B supplementation for patients with mild to moderate Alzheimer's disease (AD) did not slow the rate of cognitive decline, according to a study in the October 15 issue of the Journal of the American Medical Association.

According to the authors, prior studies of B vitamins to reduce homocysteine in AD have not had sufficient size or duration to assess their effect on cognitive decline.

Paul S. Aisen, MD, University of California, San Diego, San Diego, California, and colleagues conducted a clinical trial to determine if reduction of homocysteine levels with high-dose supplementation with folic acid and vitamins B6 and B12 for 18 months would slow the rate of cognitive decline in 409 individuals with mild to moderate AD.

Participants were randomly assigned to 2 groups of unequal size to increase enrolment. Patients were treated with either folate 5 mg/d, vitamin B6 25 mg/d, and vitamin B12 1 mg/d (60%) or placebo (40%).

A total of 340 participants (202 in treatment group, 138 placebo group) completed the trial while taking study medication. Cognitive abilities were measured via testing with the Alzheimer's Disease Assessment Scale (ADAS-cog).

The researchers found that even though the vitamin supplement regimen was effective in reducing homocysteine levels, it had no beneficial effect on the primary cognitive measure. The rate of change in ADAS-cog score did not differ significantly between treatment groups. The authors did find that symptoms of depression were more common in the high-dose supplement group.

"Many studies suggest that relative elevation of homocysteine is characteristic of AD, and laboratory research implicates homocysteine in neurodegenerative mechanisms," the authors wrote.

"High-dose B vitamin supplementation in individuals with normal levels of B vitamins was effective in reducing homocysteine levels. However, our study does not support the treatment of individuals with mild to moderate AD and normal vitamin levels with B vitamin supplements."

In an accompanying editorial, Robert J. Clarke, MD, and Derrick A. Bennett, PhD, University of Oxford, England, United Kingdom, comment on the findings.
"The precise reasons the [study by Aisen and colleagues] failed to detect any beneficial effect of B vitamins on the rate of cognitive decline remain unclear. However, until and unless new data suggest otherwise, there is insufficient evidence to justify routine use of homocysteine-lowering vitamin supplements for the prevention of Alzheimer disease and cognitive decline among individuals with normal vitamin status."

SOURCE: Journal of the American Medical Association

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