Vitamin E May Stave Off Lou Gehrig's Disease
Mon Dec 13, 6:10 PM ET
Health - Reuters
NEW YORK (Reuters Health) - In a new study, regular users
of vitamin E were at decreased risk for death from Lou Gehrig'sdisease
(news - web sites), also called amyotrophic lateral sclerosis
(ALS), compared with nonusers.
Given that vitamin E is an antioxidant, the new findings support
the hypothesis that oxidants play a key role in the development
of ALS. Moreover, the results are consistent with earlier findings
showing that increased brain levels of vitamin E seem to delay
the onset of ALS in lab animals. Still, use of another antioxidant,
vitamin C, seemed to confer no protection against ALS, the report
in the Annals of Neurology indicates.
In the study, Dr. Alberto Ascherio, from Harvard School of
Public Health in Boston, and colleagues analyzed data from nearly
1 million subjects enrolled in the American Cancer Society (news
- web sites)'s Cancer Prevention Study II. All of the subjects
were at least 30 years of age when the study began in 1982. Information
on vitamin E use was collected at enrollment and the subjects
were followed from 1989 through 1998.
During follow-up, 525 deaths from ALS were recorded, the investigators
note.
Compared with nonusers, patients who took vitamin E for less
than 15 days per month did not reduce the risk of death from
ALS.
However, patients who used vitamin E for 15 or more days per
month for at least 10 years had a reduced risk of ALS death of
62 percent. As noted, the use of vitamin C, even on a regular
basis for many years, did not protect against ALS.
As to why no benefit was seen with vitamin C, the authors
believe it may be because vitamin C is "a water-soluble
antioxidant with different properties than vitamin E and thus
may not" act the same in the body.
Further studies are needed to confirm the apparent anti-Lou Gehrig's disease, the authors note. Also, because most cases
in the current study occurred spontaneously, it remains to be
determined whether or not a relationship exists for hereditary
ALS, they add.
SOURCE: Annals of Neurology, November 2004.
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