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- Martha Clare Morris, Denis A Evans, Julia L Bienias, Christine C Tangney, David A Bennett, Neelum Aggarwal, Robert S Wilson, and Paul A Scherr.
- Rush Institute for Healthy Aging, Rush-Presbyterian-St Luke's Medical Center, 1645 W Jackson, Suite 675, Chicago, IL 60612, USA. mmorris@rush.edu
- JAMA. 2002 Jun 26; 287 (24): 323032373230-7.
ContextOxidative processes have been suggested as elements in the development of Alzheimer disease (AD), but whether dietary intake of vitamin E and other antioxidant nutrients prevents its development is unknown.ObjectiveTo examine whether intake of antioxidant nutrients, vitamin E, vitamin C, and beta carotene is associated with incident AD.Design, Setting, And ParticipantsProspective study, conducted from 1993 to 2000, of individuals selected in a stratified random sample of community-dwelling residents. The 815 residents 65 years and older were free of AD at baseline and were followed up for a mean of 3.9 years. They completed food frequency questionnaires an average of 1.7 years after baseline.Main Outcome MeasureIncident AD diagnosed in clinical evaluations with standardized criteria.ResultsIncreasing vitamin E intake from foods was associated with decreased risk of developing AD after adjustment for age, education, sex, race, APOE epsilon 4, and length of follow-up. Relative risks (95% confidence intervals [CIs]) from lowest to highest quintiles of intake were 1.00, 0.71 (0.24-2.07), 0.62 (0.26-1.45), 0.71 (0.27-1.88), and 0.30 (0.10-0.92) (P for trend =.05). The protective association of vitamin E was observed only among persons who were APOE epsilon 4 negative. Adjustment for other dietary factors reduced the protective association. After adjustment for baseline memory score, the risk was 0.36 (95% CI, 0.11-1.17). Intake of vitamin C, beta carotene, and vitamin E from supplements was not significantly associated with risk of AD.ConclusionThis study suggests that vitamin E from food, but not other antioxidants, may be associated with a reduced risk of AD. Unexpectedly, this association was observed only among individuals without the APOE epsilon 4 allele.
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