Vitamin E may stave off Lou Gehrig’s disease
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In a new study, regular users of vitamin E were at decreased risk for death from Lou Gehrig’s disease, 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’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-ALS effect for vitamin E, 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.
Revision date: July 6, 2011
Last revised: by Dave R. Roger, M.D.
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