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Neurology 2002;59:1161-1169
© 2002 American Academy of Neurology

Intakes of vitamins E and C, carotenoids, vitamin supplements, and PD risk

S.M. Zhang, MD ScD, M.A. Hernán, MD DrPH, H. Chen, MD PhD, D. Spiegelman, ScD, W.C. Willett, MD DrPH and A. Ascherio, MD DrPH

From the Departments of Epidemiology (Drs. Zhang, Hernán, Spiegelman, Willett, and Ascherio), Nutrition (Drs. Chen, Willett, and Ascherio), and Biostatistics (Dr. Spiegelman), Harvard School of Public Health; and the Division of Preventive Medicine (Dr. Zhang) and Channing Laboratory (Dr. Willett), Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA.

Address correspondence and reprint requests to Dr. Shumin Zhang, Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115; e-mail: Shumin.Zhang{at}channing.harvard.edu

Background: Oxidative damage has been implicated in the pathogenesis of PD. Limited and mostly retrospective epidemiologic data suggest a reduction or no change in risk of PD associated with high vitamin E intake.

Objective: To examine prospectively the associations between intakes of vitamins E and C, carotenoids, vitamin supplements, and risk of PD.

Methods: The authors documented the occurrence of PD within two large cohorts of men and women who completed detailed and validated semiquantitative food frequency questionnaires. A total of 371 incident PD cases were ascertained in the Nurses’ Health Study, which comprised 76,890 women who were followed for 14 years, and the Health Professionals Follow-Up Study, which comprised 47,331 men who were followed for 12 years.

Results: Neither intake of total vitamins E or C or use of vitamin E or vitamin C supplements or multivitamins was significantly associated with risk of PD. The risk of PD, however, was significantly reduced among men and women with high intake of dietary vitamin E (from foods only). The pooled multivariate relative risk (RR) comparing individuals in the highest quintile with those in the lowest quintile was 0.68 (95% CI, 0.49 to 0.93). Consumption of nuts was also significantly associated with a reduced risk of PD (for >=5/week vs <1/month, pooled RR, 0.57; 95% CI, 0.34 to 0.95). Intakes of dietary vitamin C and carotenoids were not significantly associated with risk of PD.

Conclusions: Use of vitamin supplements and high intake of carotenoids do not appear to reduce the risk of PD. The reduction in risk of PD associated with high dietary vitamin E intake suggests that other constituents of foods rich in vitamin E may be protective. Alternatively, moderate amounts of vitamin E may reduce risk of PD, but this benefit may be lost with higher intakes.


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