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Dietary Intake of Antioxidant Nutrients and the Risk of Incident Alzheimer Disease in a Biracial Community Study
Martha Clare Morris, ScD;
Denis A. Evans, MD;
Julia L. Bienias, ScD;
Christine C. Tangney, PhD;
David A. Bennett, MD;
Neelum Aggarwal, MD;
Robert S. Wilson, PhD;
Paul A. Scherr, PhD,ScD
JAMA. 2002;287:3230-3237.
Context Oxidative 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.
Objective To examine whether intake of antioxidant nutrients, vitamin E, vitamin C, and beta carotene is associated with incident AD.
Design, Setting, and Participants Prospective 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 Measure Incident AD diagnosed in clinical evaluations with standardized criteria.
Results Increasing vitamin E intake from foods was associated with decreased risk of developing AD after adjustment for age, education, sex, race, APOE  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 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.
Conclusion This 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 4 allele.
Author Affiliations: Rush Institute for Healthy Aging (Drs Morris, Evans, Bienias, Bennett, Aggarwal, and Wilson), Rush Alzheimer's Disease Center (Drs Evans, Bennett, Aggarwal, and Wilson), Departments of Internal Medicine (Drs Morris, Evans, and Bienias), Preventive Medicine (Dr Morris), Neurological Sciences (Drs Evans, Bennett, Aggarwal, and Wilson), Clinical Nutrition (Dr Tangney), and Psychology (Dr Wilson), Rush-Presbyterian-St Luke's Medical Center, Chicago, Ill; and Division of Adult and Community Health, Centers for Disease Control and Prevention, Atlanta, Ga (Dr Scherr).
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