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Dietary folate, vitamin B₁₂, and vitamin B₆ and the risk of Parkinson disease

From the Department of Epidemiology & Biostatistics (L.M.L.d.L., J.C.M.W., A.H., M.M.B.B.) and Department of Neurology (L.M.L.d.L., P.J.K.), Erasmus Medical Center, Rotterdam, The Netherlands.

Address correspondence and reprint requests to Dr. Monique M.B. Breteler, Department of Epidemiology & Biostatistics, Erasmus Medical Center, PO Box 1738, 3000 DR Rotterdam, The Netherlands; e-mail: m.breteler{at}erasmusmc.nl

Background: Increased homocysteine levels might accelerate dopaminergic cell death in Parkinson disease (PD), through neurotoxic effects. Higher dietary intakes of folate, vitamin B₁₂, and vitamin B₆ (cofactors in homocysteine metabolism) might decrease the risk of PD through decreasing plasma homocysteine. Moreover, vitamin B₆ might influence the risk of PD through antioxidant effects unrelated to homocysteine metabolism and through its role in dopamine synthesis.

Methods: In the Rotterdam Study, a prospective, population-based cohort study of people aged 55 years and older, the authors evaluated the association between dietary intake of folate, vitamin B₁₂, and vitamin B₆ and the risk of incident PD among 5,289 participants who were free of dementia and parkinsonism and underwent complete dietary assessment at baseline. PD was assessed through repeated in-person examination and continuous monitoring by computer linkage to medical records. Data were analyzed using Cox proportional hazards regression analysis.

Results: After a mean follow-up of 9.7 years, the authors identified 72 participants with incident PD. Higher dietary intake of vitamin B₆ was associated with a significantly decreased risk of PD (hazard ratio per SD, 0.69 [95% CI 0.50 to 0.96]; for highest vs lowest tertile, 0.46 [0.22 to 0.96]). Stratified analyses showed that this association was restricted to smokers. No association was observed for dietary folate and vitamin B₁₂.

Conclusions: Dietary vitamin B₆ may decrease the risk of Parkinson disease, probably through mechanisms unrelated to homocysteine metabolism.

This study was supported by a grant (M.M.B.B., grant no. 015.000.083) from the Netherlands Organization for Scientific Research (NWO). The Rotterdam Study is supported by the Erasmus Medical Center and Erasmus University Rotterdam; the Netherlands Organization for Scientific Research (NWO); the Netherlands Organization for Health Research and Development (ZonMw); the Research Institute for Diseases in the Elderly (RIDE); the Ministry of Education, Culture and Science; the Ministry of Health, Welfare and Sports; the European Commission (DG XII); and the Municipality of Rotterdam. The sponsors of the study had no role in study design, data collection, data analysis, or writing of the report.

Disclosure: The authors report no conflicts of interest.

Received November 29, 2005. Accepted in final form March 22, 2006.