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NEUROLOGY 1996;46:1270
© 1996 American Academy of Neurology

Case-control study of idiopathic Parkinson's disease and dietary vitamin E intake

D. M. Morens, MD, A. Grandinetti, PhD, C. I. Waslien, PhD, C. B. Park, MD, Dr. PH, G. W. Ross, MD and L. R. White, MD

Department of Public Health Sciences, School of Public Health, University of Hawai'i, Honolulu, Hawai'i. (Dr. Morens) (Dr. Grandinetti) (Dr. Waslien) (Dr. Park)
Department of Tropical Medicine, School of Medicine, University of Hawai'i, Honolulu, Hawai'i. (Dr. Morens)
East-West Center, Queen's Medical Center, Honolulu, Hawai'i. (Dr. Grandinetti) (Dr. Park)
Native Hawaiian Health Program, Queen's Medical Center, Honolulu, Hawai'i. (Dr. Grandinetti)
United States Department of Veterans Affairs, Honolulu, Hawai'i. (Dr. Ross)
Honolulu-Asia Aging Study, National Institute on Aging, National Institutes of Health, Honolulu, Hawai'i. (Dr. White)

Address correspondence and reprint requests to Dr. David M. Morens, Epidemiology Program, University of Hawai'i School of Public Health, Biomed D103, 1960 East-West Road, Honolulu, Hawai'i 96822.

A nested case-control study of 84 incident cases of patients with idiopathic Parkinson's disease (PD) detected by June 30, 1994 and 336 age-matched control subjects, compared previously-documented intake of total dietary vitamin E and of selected vitamin E-containing foods. All study subjects had been followed for 27 to 30 years after diet recording in the 8,006-man Honolulu Heart Study cohort. We determined PD outcomes by periodic cohort re-examination and neurologic testing, private physician reports, examination of O'ahu neurologists' office records, and continual death certificate and hospital discharge diagnosis surveillance. Data on vitamin E intake, obtained from three dietary data sets at the time of cohort enrollment (1965 to 1968), included a food-frequency questionnaire and a 24-hour photograph-assisted dietary recall administered by trained dietitians. Although absence of PD was significantly associated with prior consumption of legumes (adjusted OR = 0.27, 95% CI 0.09 to 0.78), a dietary variable preselected for high vitamin E content, neither food categories nor quartiles nor continuous variables of vitamin E consumption were significantly associated with PD occurrence. Though consistent with prior reports of PD protection afforded by legumes, and with speculation on the possible benefits of dietary or supplemental vitamin E in preventing PD, these preliminary data do not conclusively document a beneficial effect of dietary vitamin E on PD occurrence.


Supported by grant NS 30371 of the National Institute of Neurological Disorders and Stroke, National Institutes of Health. The Honolulu Heart Study and the Honolulu-Asia Aging Study, Kuakini Medical Center, Honolulu, Hawai'i are funded, respectively, by the National Heart, Lung and Blood Institute, and the National Institute on Aging, National Institutes of Health.

Received June 14, 1995. Accepted in final form September 22, 1995.




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