Vitamin D levels associated with Parkinson's disease risk

Individuals with higher levels of vitamin D appear to have a reduced risk of developing Parkinson's disease, according to a report in the July issue of Archives of Neurology, one of the JAMA/Archives journals. Vitamin D is known to play a role in bone health and may also be linked to cancer, heart disease and type 2 diabetes, according to background information in the article. "Recently, chronically inadequate vitamin D intake was proposed to play a significant role in the pathogenesis of Parkinson's disease," the authors write. "According to the suggested biological mechanism, Parkinson's disease may be caused by a continuously inadequate vitamin D status leading to a chronic loss of dopaminergic neurons in the brain."

Paul Knekt, D.P.H., and colleagues at the National Institute for Health and Welfare, Helsinki, Finland, studied 3,173 Finnish men and women age 50 to 79 who did not have Parkinson's disease at the beginning of the study, in 1978 to 1980. Participants completed questionnaires and interviews about socioeconomic and health background, underwent baseline examinations and provided blood samples for vitamin D analysis.

Over a 29-year follow-up, through 2007, 50 of the participants developed Parkinson's disease. After adjusting for potentially related factors, including physical activity and body mass index, individuals in the highest quartile (one-fourth of the study population) of serum vitamin D levels had a 67 percent lower risk of developing Parkinson's disease than those in the lowest quartile of vitamin D levels.

"Despite the overall low vitamin D levels in the study population, a dose-response relationship was found," the authors write. "This study was carried out in Finland, an area with restricted sunlight exposure, and is thus based on a population with a continuously low vitamin D status. Accordingly, the mean [average] serum vitamin D level in the present population was about 50 percent of the suggested optimal level (75 to 80 nanomoles per liter). Our findings are thus consistent with the hypothesis that chronic inadequacy of vitamin D is a risk factor for Parkinson's disease."

The exact mechanisms by which vitamin D levels may affect Parkinson's disease risk are unknown, but the nutrient has been shown to exert a protective effect on the brain through antioxidant activities, regulation of calcium levels, detoxification, modulation of the immune system and enhanced conduction of electricity through neurons, the authors note.

"In intervention trials focusing on effects of vitamin D supplements, the incidence of Parkinson disease merits follow up," they conclude.

(Arch Neurol. 2010;67[7]:808-811. Available pre-embargo to the media at www.jamamedia.org.)

Editor's Note: This work was supported by a National Institutes of Health grant. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

Editorial: Findings Add to Research on Neurological Effects of Vitamin D

"The study by Knekt et al in this issue of the Archives is the first longitudinal analysis of vitamin D status as a risk of incident Parkinson's disease and examines a cohort of more than 3,000 participants from the Mini-Finland Health Survey," writes Marian Leslie Evatt, M.D., M.S., of Emory University, Atlanta, in an accompanying editorial.

"A growing body of basic research lends plausibility to a role for adequate vitamin D status protecting against development of Parkinson's disease," Dr. Evatt writes. "Knekt and colleagues' study provides the first promising human data to suggest that inadequate vitamin D status is associated with the risk of developing Parkinson's disease, but further work is needed in both basic and clinical arenas to elucidate the exact role, mechanisms and optimum concentration of vitamin D in Parkinson's disease."

"With the animal data showing a U-shaped curve for neuroprotective effects of vitamin D, it seems prudent to confirm the findings presented in this issue and investigate whether the apparent dose-response relationship observed in the current study maintains its slope, levels off or becomes negative with higher 25-hydroxyvitamin D concentrations. In the interim, data from interventional studies of fractures and falls appear to justify optimizing vitamin D levels to greater than 30 to 40 nanograms per milliliter."

(Arch Neurol. 2010;67[7]:795-797. Available pre-embargo to the media at www.jamamedia.org.)

Editor's Note: Please see the article for additional information, including author contributions and affiliations, financial disclosures, funding and support, etc.

Source: JAMA and Archives Journals