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Vitamin E Intake and Risk of Amyotrophic Lateral Sclerosis: A Pooled Analysis of Data From 5 Prospective Cohort Studies

By Hao Wang, Éilis J. O'Reilly, Marc G. Weisskopf, Giancarlo Logroscino, Marjorie L. McCullough, Arthur Schatzkin, Laurence N. Kolonel and Alberto Ascherio

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

Topics: Systematic Reviews and Meta- and Pooled Analyses
Publisher: Oxford University Press
OAI identifier: oai:pubmedcentral.nih.gov:3105261
Provided by: PubMed Central
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