 | July 16, 2010 | Low vitamin D levels can predict Parkinson's disease | | In yet another study to reveal the far-reaching benefits of vitamin D, researchers at the National Institute for Health and Welfare in Finland report in the July, 2010 issue of the AMA journal Archives of Neurology the finding of a correlation between reduced blood levels of vitamin D and an increased risk of developing Parkinson's disease. The study included 3,173 participants in the Mini-Finland Health Survey who were free of Parkinson's disease between 1978 and 1980. Frozen blood samples obtained during this period were analyzed for serum 25-hydroxyvitamin D. Over the 29 year follow-up period, 50 subjects were diagnosed with Parkinson's disease. Average vitamin D levels among the participants were approximately half of current recommended levels, which is most likely attributable to Finland's higher latitude. Those whose serum vitamin D levels were among the top 25 percent of the subjects at 50 nanomoles per liter or greater had one-third the adjusted risk of developing Parkinson's disease than that of subjects whose vitamin D levels were among the lowest fourth at less than 25 nanomoles per liter. The investigation is the first longitudinal study to demonstrate an association between insufficient vitamin D levels and the subsequent development of Parkinson's disease. In their commentary, the authors explain that, although the exact mechanisms by which vitamin D helps protect against Parkinson's disease are not understood, the vitamin has shown neuroprotective effects via antioxidative mechanisms, immunomodulation, enhanced nerve conduction and other means. "The vitamin D receptors and an enzyme responsible for the formation of the active form 1,25-hydroxyvitamin D have been found in high levels in the substantia nigra, the region of the brain affected most by Parkinson disease," they note. "This raises the possibility that chronic inadequacy of vitamin D leads to the loss of dopaminergic neurons in the substantia nigra region." "In intervention trials focusing on effects of vitamin D supplements, the incidence of Parkinson disease merits follow up," they conclude. | |  |
| Parkinson’s disease is a devastating brain disorder that gradually robs people of the ability to control their own movements. While the causes and cure of this affliction remain elusive, progressive scientists are continuing to unravel this disease. During Parkinson’s, cells in the parts of the brain that control movement and regulate mood are gradually destroyed. The primary defect in Parkinson’s is a loss of dopaminergic neurons (such as dopamine-producing neurons) in a part of the brain called the substantia nigra. Dopamine is a neurotransmitter that modulates movement (Purves D et al 2001). In Parkinson’s disease, the dopamine-producing nerve cells are destroyed by high levels of oxidative damage (Atasoy HT et al 2004; Ross GW et al 2004). There is evidence that this oxidative damage is, in turn, caused by defects in the cells’ mitochondria, or power-generating centers. The ideal treatment for Parkinson’s disease would be a neuroprotective agent— a treatment that protects the brain. While no neuroprotective prescription agent has been found, studies suggest that high-dose coenzyme Q10 (CoQ10), a natural agent, may have neuroprotective properties. CoQ10 is known to support mitochondria by enhancing energy levels in the brain, as well as by acting as a powerful antioxidant. In one phase 2 clinical trial, CoQ10 significantly slowed the progression of Parkinson’s disease (Beal MF 2003). Conventional therapy for Parkinson’s disease focuses on increasing the production and utilization of dopamine. Levodopa, which is the precursor to dopamine, has been the mainstay of Parkinson’s disease therapy since its discovery in the early 1960s. Today, levodopa remains the foundation of Parkinson’s therapy. However, after 5 years, levodopa begins to lose its effectiveness in patients with Parkinson’s disease. If used as the sole treatment, levodopa must then be prescribed in higher and higher doses, leading to more adverse effects and more intense symptoms. Other drugs that target other parts of dopamine production and the utilization cascade are now increasingly prescribed. When used early enough, these drugs can help postpone levodopa therapy. |
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