, Volume 250, Issue 3 Supplement, pp iii30-iii39

Environmental, life-style, and physical precursors of clinical Parkinson’s disease: recent findings from the Honolulu-Asia Aging Study

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Increased westernization with Japanese migration to the U. S. in the early 20th century is thought to have altered the risk of cardiovascular disease. Whether similar effects include changes in the risk of Parkinson’s disease (PD) is not clear. This report describes the relations between environmental, life-style, and physical attributes and the incidence of PD that have been observed in the Honolulu-Asia Aging Study.


Beginning in 1965, environmental, life-style, and physical attributes were recorded at selected examinations in a cohort of 8,006 Japanese-American men. Subjects were followed for clinical PD.


During 30 years of follow- up, PD was observed in 137 men. Overall incidence (7.1/10,000 person-years) was generally higher than in Asia and similar to rates observed in Europe and the U. S. Precursors of PD included constipation, adiposity, years worked on a sugar or pineapple plantation, years of exposure to pesticides, and exposure to sugar cane processing. Factors showing an inverse association with PD included coffee intake and cigarette smoking. Among dietary factors, carbohydrates increased the risk of PD while the intake of polyunsaturated fats appeared protective. Total caloric intake, saturated and monounsaturated fats, protein, niacin, riboflavin, beta-carotene, vitamins A, B, and C, dietary cholesterol, cobalamin, α-tocopherol, and pantothenic acid showed no clear relation with clinical PD.


Findings suggest that several environmental, life-style, and physical attributes appear to be precursors of PD. Whether patterns of precursors can be used to identify individuals at high risk of future PD or can broaden the scope of early interventions or recruitment into neuroprotective trials warrants further study.

From the Division of Biostatistics and Epidemiology, University of Virginia School of Medicine, Charlottesville, Virginia (RDA); the Pacific Health Research Institute, Honolulu, Hawaii (RDA, GWR, LRW, KHM, JDC, HP); the Department of Veterans Affairs, Honolulu, Hawaii (GWR, LRW, HP); the Kuakini Medical Center and the Honolulu-Asia Aging Study, Honolulu, Hawaii (RDA, GWR, LRW, KHM, JDC, HP); the Departments of Geriatric Medicine and Medicine, University of Hawaii John A. Burns School of Medicine, Honolulu, Hawaii (GWR, LRW, KHM, JDC, HP); the National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, West Virginia (CMB, MK, DSS) and Cincinnati, Ohio (WTS).
Supported by a grant from the U. S. Department of the Army (DAMD17–98–1–8621),by the National Institutes of Health (National Institute on Aging contract N01-AG-4–2149 and grant 1-R01-AG17155–01A1, National Heart, Lung, and Blood Institute contract N01-HC-05102, and a National Institute of Neurological Disorders and Stroke grant 1-R01-NS41265–01), by the National Institute for Occupational Safety and Health (Contract HELD0080060), and by the Office of Research and Development, Department of Veterans Affairs. The information contained in this article does not necessarily reflect the position or the policy of the Government, and no official endorsement should be inferred.