While I don’t know the exact mechanism about how vitamin D works in alleviating neurological diseases like MS, autism, and others, I strongly suspect it has to do with our run away immune system which attacks our normal nerve fibers including those in the brain. For example, the chance of a young kid living up to the age of 15 when nerve and brain development progresses most rapidly increase their chance of MS is 100%.
One of the most important roles for vitamin D is to control our immune system and activate our T-Cells so when real infections occur, they send the T-Cells to the source of the infection so our immune system can go into action.
Since every cell in our body has a receptor for vitamin D activated in the cell, we should take enough vitamin D3 and sun to get our level of non-active metabolite of vitamin D3 which is stored in our fat tissues, as high as we are comfortable in doing. The 25-hydroxy vitamin D inactive metabolite should be at levels of 75 or higher for you if your doctor says you are susceptible.
Ask him or her why they predict Parkinson’s?
I suspect you need to start at 50,000 IU of vitamin D3 a week for two or three months to catch up. Do it now after seeing your doctor. Don’t let them measure the active vitamin D or 1,25 dihydroxy vitamin D. It does not mean much because it various so much. Mine is about 73 nanograms/milliliter.
People feel good when they go into the sun without sunscreen because producing vitamin D3 also keeps us from being depressed. The longer we are depressed, the smaller our hippocampus becomes making coming out of depression harder. Shock Therapy under a sedative works faster too.
Jim Kawakami, Dec 5, 2010, http://jimboguy.blogspot.com
ScienceDaily (July 13, 2010) — http://www.sciencedaily.com/releases/2010/07/100712162624.htm 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.
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."
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