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Vitamin D Insufficiency Common in Parkinson's Patients

By Brian Chorley
November 2008

Neurologist and lead author Marian Evatt
Neurologist and lead author Marian Evatt (Photo courtesy of Emory University)

A team of investigators at the Emory University School of Medicine, funded by an NIEHS grant (http://www.niehs.nih.gov/research/supported/centers/parkinsons/index.cfm) and grants from other NIH institutes, recently reported that a significant portion of Parkinson's patients suffer from vitamin D insufficiency. Their findings were published in the October issue of Archives of Neurology. Marian Evatt, M.D., assistant professor of Neurology at Emory and assistant director of the Movement Disorders Program at Wesley Woods Geriatric Hospital, was first author of the paper.

Parkinson's disease is a neurodegenerative disorder in which substantia nigra, the locus of dopamine-producing nerve cells in the brain, dies or becomes impaired. Dopamine shortage causes difficulty with muscle coordination and control, the hallmark symptoms of Parkinson's disease. Approximately 1.5 million Americans are affected by this disease.

In this study (http://www.ncbi.nlm.nih.gov/pubmed/18852350?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum) Exit NIEHS, insufficiency was defined as 30 nanograms or less of the storage form of vitamin D, 25-hydroxyvitamin D, per milliliter of blood. Deficiency was defined as 20 nanograms per milliliter or less. The researchers reported that 55 percent of a Parkinson's cohort exhibited vitamin D insufficiency. Insufficiency was noted in only 36 percent of healthy subjects, a significantly lower percentage. In addition, 23 per cent of the Parkinson's patients exhibited vitamin D deficiency, compared to 10 percent in the control group.

Vitamin D, a fat soluble pro-hormone, has been linked to maintaining physiologic function as well as preventing diseases, such as bone, cardiovascular, autoimmune and, notably, neurologic disorders. Synthesis occurs in the skin with UV-B radiation exposure, primarily from sunlight. Diet, such as fortified foods and certain fish, can also provide minor amounts of vitamin D. Deficiency can result from inadequate sun exposure, metabolism or absorption disorders, and other genetically influenced factors.

The researchers recognized that patients with chronic neurodegenerative disease commonly exhibited risk factors for vitamin D insufficiency, including advanced age, obesity and decreased sun exposure. The study limited potentially confounding effects of these factors by selecting individuals who resided in sunny southern locales, had paler complexion and were being treated in an outpatient clinic — making them more likely to have increased UV-B exposure.

Additionally, age was not a criteria inclusion, thereby minimizing age-related confounding effects. Intriguingly, Parkinson's patients were also more likely to exhibit vitamin D insufficiency than patients with another neurodegenerative disorder, Alzheimer's disease, 55 percent versus 41 percent. Although Evatt and colleagues suggested that a potential reason for this difference may be due to increased mobility issues more common in Parkinson's patients, they did not see a correlation between 25-hydroxyvitamin D insufficiency and symptom duration in either group. The investigators suggest that this phenomenon may therefore be unique to Parkinson's disease.

This study adds to the growing body of evidence in support of the notion that vitamin D deficiency may contribute to the pathogenesis of Parkinson's. Vitamin D regulates multiple cellular processes known to be abnormal in Parkinson's disease, including cellular differentiation, proliferation and apoptosis. Additionally, vitamin D receptor and activating enzyme are enriched in hippocampal and substantia nigra cells in the brain, problematic regions in Parkinson's patients. Evatt and her colleagues at Emory are currently researching the role of vitamin D in Parkinson's development and progression, as well as the therapeutic potential of vitamin D supplementation.

These findings could have immediate clinical implications. Potential risk of bone disorder, cancer and autoimmune diseases, such as diabetes mellitus, are associated with vitamin D deficiency. Evatt suggests that Parkinson's patients should be checked more regularly for low 25-hydroxyvitamin D levels as a strategy for minimizing further complications of an already debilitating neurodegenerative disease.

Citation: Evatt ML, Delong MR, Khazai N, Rosen A, Triche S, Tangpricha V. (http://www.ncbi.nlm.nih.gov/pubmed/18852350?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum) Exit NIEHS 2008. Prevalence of vitamin D insufficiency in patients with Parkinson disease and Alzheimer disease. Arch Neurol 65(10):1348-1352.

(Brian Chorley, Ph.D., is a postdoctoral fellow in the NIEHS Laboratory of Molecular Genetics Environmental Genomics Group.)



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