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From the Korea University Genomic Institute (Drs. Park and Abbott) and Department of Neurology (Dr. Park), College of Medicine, Korea University, Ansan-Si, Republic of Korea; and Pacific Health Research Institute (Drs. Ross, Petrovitch, White, Masaki, Nelson, Curb, and Abbott), Department of Veterans Affairs (Drs. Ross, Petrovitch, and White), Kuakini Medical Center and Honolulu-Asia Aging Study (Drs. Ross, Petrovitch, White, Masaki, Curb, and Abbott), and Departments of Geriatric Medicine and Medicine (Drs. Ross, Petrovitch, White, Masaki, Curb, and Blanchette), University of Hawaii John A. Burns School of Medicine, Honolulu, Parkinson’s Institute (Drs. Ross and Tanner), Sunnyvale, CA, and Division of Biostatistics and Epidemiology (Dr. Abbott), University of Virginia School of Medicine, Charlottesville.
Address correspondence and reprint requests to Dr. R.D. Abbott, Department of Health Evaluation Sciences, University of Virginia Health System, PO Box 800717, Charlottesville, VA 22908-0717; e-mail: rda3e{at}virginia.edu
Objective: To examine the relation between milk and calcium intake in midlife and the risk of Parkinson disease (PD).
Methods: Findings are based on dietary intake observed from 1965 to 1968 in 7,504 men ages 45 to 68 in the Honolulu Heart Program. Men were followed for 30 years for incident PD.
Results: In the course of follow-up, 128 developed PD (7.1/10,000 person-years). Age-adjusted incidence of PD increased with milk intake from 6.9/10,000 person-years in men who consumed no milk to 14.9/10,000 person-years in men who consumed >16 oz/day (p = 0.017). After further adjustment for dietary and other factors, there was a 2.3-fold excess of PD (95% CI 1.3 to 4.1) in the highest intake group (>16 oz/day) vs those who consumed no milk. The effect of milk consumption on PD was also independent of the intake of calcium. Calcium from dairy and nondairy sources had no apparent relation with the risk of PD.
Conclusions: Findings suggest that milk intake is associated with an increased risk of Parkinson disease. Whether observed effects are mediated through nutrients other than calcium or through neurotoxic contaminants warrants further study.
Supported by a contract (N01-AG-4-2149) and grant (1-R01-AG17155-01A1) from the National Institute on Aging, a contract (N01-HC-05102) from the National Heart, Lung, and Blood Institute, a grant (1-R01-NS41265-01) from the National Institute of Neurological Disorders and Stroke, and the Office of Research and Development, Medical Research Service, Department of Veterans Affairs, and by the U.S. Department of the Army (DAMD17-98-1-8621).
The information contained in this article does not necessarily reflect the position or the policy of the U.S. Government, and no official endorsement should be inferred.
Received August 24, 2004. Accepted in final form November 23, 2004.
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