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Vitamin B does not slow Cognitive Decline
for Alzheimer Disease Patients
Newswise — High-dose vitamin
B supplementation for patients with mild to
moderate Alzheimer disease did not slow the
rate of cognitive decline, according to a
study in the October 15 issue of JAMA.
Evidence of homocysteine (an
amino acid produced by the body) elevation
in Alzheimer disease (AD) and the
involvement of homocysteine in
neuropathological mechanisms suggest that
reduction of homocysteine may offer an
approach to altering the disease.
B vitamins that influence
homocysteine metabolism have been considered
as a therapeutic option to reduce risk of AD
or slow its progression, according to
background information in the article.
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, M.D., of the
University of California, San Diego, 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 two groups of unequal size to
increase enrollment (60 percent treated with
high-dose supplements [5 mg/d of folate, 25
mg/d of vitamin B6, 1 mg/d of vitamin B12]
and 40 percent treated with identical
placebo).
A total of 340 participants
(202 in active treatment group and 138 in
placebo group) completed the trial while
taking study medication. Cognitive abilities
were measured via testing with the Alzheimer
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.
"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,” the authors conclude.
Editorial: B Vitamins for Prevention
of Cognitive Decline - Insufficient Evidence
to Justify Treatment
In an accompanying editorial,
Robert J. Clarke, M.D., F.R.C.P., and
Derrick A. Bennett, Ph.D., of the University
of Oxford, England, comment on the findings
regarding B vitamin supplementation.
“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,” they write.
“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.”
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