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Original Contribution
JAMA. 2000;283(20):2674-2679. doi: 10.1001/jama.283.20.2674

Association of Coffee and Caffeine Intake With the Risk of Parkinson Disease

  1. G. Webster Ross, MD;
  2. Robert D. Abbott, PhD;
  3. Helen Petrovitch, MD;
  4. David M. Morens, MD;
  5. Andrew Grandinetti, PhD;
  6. Ko-Hui Tung, MS;
  7. Caroline M. Tanner, MD, PhD;
  8. Kamal H. Masaki, MD;
  9. Patricia L. Blanchette, MD, MPH;
  10. J. David Curb, MD, MPH;
  11. Jordan S. Popper, MD;
  12. Lon R. White, MD, MPH
  1. Author Affiliations: Department of Veterans Affairs, Honolulu, Hawaii (Drs Ross, Petrovitch, and White); Department of Medicine (Drs Ross, Abbott, Petrovitch, Masaki, Blanchette, Curb, White, and Popper) and Pacific Biomedical Research Center (Dr Grandinetti), University of Hawaii John A. Burns School of Medicine, Honolulu; Division of Biostatistics and Epidemiology, Department of Health Evaluation Sciences, University of Virginia School of Medicine, Charlottesville (Dr Abbott); Pacific Health Research Institute, Honolulu (Drs Ross, Abbott, Petrovitch, Masaki, Curb, and White and Ms Tung); National Institutes of Health, National Institute of Allergy and Infectious Diseases, Bethesda, Md (Dr Morens); The Parkinson's Institute, Sunnyvale, Calif (Dr Tanner); Kuakini Medical Center/Honolulu-Asia Aging Study, Honolulu (Drs Ross, Abbott, Petrovitch, Masaki, Blanchette, Curb, White, and Popper); and University of Hawaii School of Public Health, Honolulu (Ms Tung).

Abstract

Context  The projected expansion in the next several decades of the elderly population at highest risk for Parkinson disease (PD) makes identification of factors that promote or prevent the disease an important goal.

Objective  To explore the association of coffee and dietary caffeine intake with risk of PD.

Design, Setting, and Participants  Data were analyzed from 30 years of follow-up of 8004 Japanese-American men (aged 45-68 years) enrolled in the prospective longitudinal Honolulu Heart Program between 1965 and 1968.

Main Outcome Measure  Incident PD, by amount of coffee intake (measured at study enrollment and 6-year follow-up) and by total dietary caffeine intake (measured at enrollment).

Results  During follow-up, 102 men were identified as having PD. Age-adjusted incidence of PD declined consistently with increased amounts of coffee intake, from 10.4 per 10,000 person-years in men who drank no coffee to 1.9 per 10,000 person-years in men who drank at least 28 oz/d (P<.001 for trend). Similar relationships were observed with total caffeine intake (P<.001 for trend) and caffeine from noncoffee sources (P=.03 for trend). Consumption of increasing amounts of coffee was also associated with lower risk of PD in men who were never, past, and current smokers at baseline (P=.049, P=.22, and P=.02, respectively, for trend). Other nutrients in coffee, including niacin, were unrelated to PD incidence. The relationship between caffeine and PD was unaltered by intake of milk and sugar.

Conclusions  Our findings indicate that higher coffee and caffeine intake is associated with a significantly lower incidence of PD. This effect appears to be independent of smoking. The data suggest that the mechanism is related to caffeine intake and not to other nutrients contained in coffee.

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