Vitamin E in Diet May Reduce Alzheimer's Disease Risk
July 3, 2002 - A new population-based
study of antioxidants, appearing in the "Journal of the American
Medical Association" ("JAMA"), suggests that a diet rich in foods
containing vitamin E may help protect some people against Alzheimer's
disease (AD). The study is also noteworthy for its finding that
vitamin E in the form of supplements was not associated with a
reduction in the risk of AD. The latest in a series of reports on
vitamin E and dementia, the study findings heighten interest in the
outcome of clinical trials now underway to test the effectiveness of
vitamin E and other antioxidants in preventing or postponing cognitive
decline and AD.
The "JAMA" study was conducted by Martha
Clare Morris, Sc.D., of the Rush Institute for Healthy Aging at
Rush-Presbyterian-St.Luke's Medical Center, Chicago, IL, Denis A.
Evans, M.D., and colleagues. A related study by Morris and colleagues,
"in press" in the July 2002 Archives of Neurology, a "JAMA"
publication, also associates vitamin E with protection against more
general cognitive decline. (Reporting of additional detail on this
study is embargoed for July 14, 2002, 4 p.m. ET.) Both studies were
supported by the National Institute on Aging (NIA) at the National
Institutes of Health.
The June 26 issue of "JAMA" includes
similar findings from scientists in The Netherlands, who also reported
a link between high dietary intake of vitamins C and E and protection
against AD in certain people. In addition, the journal contains an
editorial on the epidemiological study of dietary intake of
antioxidants and the risk of AD by Daniel J. Foley, M.S., of the NIA's
Laboratory of Epidemiology, Demography, and Biometry, and Lon White,
M.D., Pacific Health Research Institute, Honolulu.
"This and a number of important
population studies have pointed to vitamin E as possibly protective
against oxidative damage or other mechanisms associated with cognitive
decline and dementia," says Neil Buckholtz, Ph.D., head of the
Dementias of Aging Branch at the NIA. "The only way this association
can really be tested is through clinical studies and trials now
underway. These will help us determine whether vitamin E in food or in
supplements -- or taken together -- can prevent or slow down the
development of mild cognitive impairment or AD."
It is not recommended, based on current
evidence, that people take high-dose vitamin E supplements or other
antioxidant pills in an effort to prevent mental decline, Buckholtz
says. While population-based studies and animal research have
suggested that antioxidants may be neuroprotective, clinical trials to
test that notion are currently in progress. Little is known about
safety, effectiveness, and dosages of various antioxidant supplements
that are proposed for neuroprotective purposes, Buckholtz emphasizes.
In excessively high doses (above 2,000 International Units daily, or
IU/d), for example, vitamin E may be associated with increased risk of
bleeding, and patients taking anti-coagulant medications may be
especially at risk. Interactions with other medications commonly taken
by older people are also of potential concern. People are advised to
consult with their physicians before taking high doses of supplemental
vitamin E or other antioxidants.
The 815 people participating in the
Morris study were part of the Chicago Health and Aging Project (CHAP),
a study of a large, diverse community of people age 65 and older.
Participants were free of dementia at the start of the study and
followed for an average of 3.9 years. At an average of 1.7 years from
their baseline assessment, participants completed a questionnaire,
asking them in detail about the kinds and quantities of foods consumed
in the previous year.
Some 131 participants had been diagnosed
with AD by the end of the study period, when researchers examined the
relationship between intake of antioxidants, including dietary and
supplemental vitamins E and C, beta carotene, and a multivitamin, and
development of AD. The most significant protective effect was found
among people in the top fifth of dietary vitamin E intake (averaging
11.4 IU/d), whose risk of AD was 67 percent lower when compared to
people in the group with the lowest vitamin E consumption from food
(averaging 6.2 IU/d). (The recommended dietary allowance of vitamin E
is 22 IU/d.) No significant change in risk of AD was found when the
scientists looked at vitamin E supplements, the other antioxidants and
their supplements, or a general multivitamin. There was some evidence,
though not statistically significant, that increased intake of dietary
vitamin C and beta carotene was moving in a "protective direction,"
the researchers said.
The data were also analyzed to see if
age, gender, race, education, or possible genetic risk for AD would
influence the findings. Only the presence or lack of apoE-e4, one form
of a protein associated with increased risk of late-onset AD, seemed
to matter: the protective effect of vitamin E from food was strongest
among people who did not have the apoE-e4 risk factor allele. "Dietary
vitamin E may protect against Alzheimer's disease," says Morris, "but
the protection may only occur among people without the apoE-e4
allele."
Morris suggests that further study in
key areas is needed to confirm and explain some of the study's
findings, including the link with apoE status and the study's striking
distinction between dietary intake of vitamin E and use of
supplements. For example, the lack of a protective effect for the
supplements could be explained by several factors. Some participants
in the study started taking supplements only recently and there may
not have been sufficient time for the supplement to be found
effective. Also, people who believe they have memory problems could be
more likely to take the supplements in the first place. Another
possible explanation might be variations in the forms of vitamin E,
scientists note. Most vitamin E supplements consist of alpha
tocopherol while foods are generally more rich in gamma tocopherol.
These forms of vitamin E scavenge different types of free radicals,
with one possibly more important than another in potentially reducing
risk of cognitive decline. To help determine whether vitamin E might
play a role in preventing AD, or at least in delaying its onset, a
number of clinical trials are now being supported by the NIA. These
include:
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