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    Am J Epidemiol. 2011 Mar 15;173(6):595-602. doi: 10.1093/aje/kwq416. Epub 2011 Feb 18.

    Vitamin E intake and risk of amyotrophic lateral sclerosis: a pooled analysis of data from 5 prospective cohort studies.

    Source

    Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts 02115, USA.

    Abstract

    The authors investigated whether vitamin E intake was associated with amyotrophic lateral sclerosis (ALS) in the Nurses' Health Study (1976-2004), the Health Professionals Follow-up Study (1986-2004), the Cancer Prevention Study II Nutrition Cohort (1992-2004), the Multiethnic Cohort Study (1993-2005), and the National Institutes of Health-AARP Diet and Health Study (1995-2005). ALS deaths were identified through the National Death Index. In the Nurses' Health Study and the Health Professionals Follow-up Study, confirmed nonfatal ALS cases were also included. Cohort-specific results were estimated using Cox proportional hazards models and pooled using random-effects models. Among 1,055,546 participants, 805 developed ALS. Overall, using vitamin E supplements was not associated with ALS. However, within cohorts with information on duration of vitamin E supplement use (231 cases), ALS rates declined with increasing years of use (P-trend=0.01). Compared with nonusers, the multivariable-adjusted relative risk was 1.05 (95% confidence interval (CI): 0.60, 1.84) among users for ≤1 year (12 cases), 0.77 (95% CI: 0.33, 1.77) among users for 2-4 years (7 cases), and 0.64 (95% CI: 0.39, 1.04) among users for ≥5 years (18 cases). For dietary vitamin E intake, the multivariable-adjusted relative risk comparing the highest quartile with the lowest was 0.79 (95% CI: 0.61, 1.03); an inverse dose-response was evident in women (P-trend=0.002) but not in men (P-trend=0.71). In this large, pooled prospective study, long-term vitamin E supplement use was associated with lower ALS rates. A possible protective effect of vitamin E deserves further consideration.

    © The Author 2011. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved.

    PMID:
    21335424
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC3105261
    Free PMC Article

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