Objective: Higher latitude, lower ultraviolet exposure, and lower serum 25-hydroxyvitamin D (25OHD) correlate with higher multiple sclerosis (MS) prevalence, relapse rate, and mortality. We therefore evaluated the effects of high-dose vitamin D2 (D2) in MS.Methods: Adults with clinically active relapsing-remitting MS (RRMS) were randomized to 6 months' double-blind placebo-controlled high-dose vitamin D2, 6,000 IU capsules, dose adjusted empirically aiming for a serum 25OHD 130-175 nM. All received daily low-dose (1,000 IU) D2 to prevent deficiency. Brain MRIs were performed at baseline, 4, 5, and 6 months. Primary endpoints were the cumulative number of new gadolinium-enhancing lesions and change in the total volume of T2 lesions. Secondary endpoints were Expanded Disability Status Scale (EDSS) score and relapses.Results: Twenty-three people were randomized, of whom 19 were on established interferon or glatiramer acetate (Copaxone) treatment. Median 25OHD rose from 54 to 69 nM (low-dose D2) vs 59 to 120 nM (high-dose D2) (p = 0.002). No significant treatment differences were detected in the primary MRI endpoints. Exit EDSS, after adjustment for entry EDSS, was higher following high-dose D2 than following low-dose D2 (p = 0.05). There were 4 relapses with high-dose D2 vs none with low-dose D2 (p = 0.04).Conclusion: We did not find a therapeutic advantage in RRMS for high-dose D2 over low-dose D2 supplementation.Classification of evidence: This study provides Class I evidence that high-dose vitamin D2 (targeting 25OHD 130-175 nM), compared to low-dose supplementation (1,000 IU/d), was not effective in reducing MRI lesions in patients with RRMS.
It is believed that vitamin D3 from oral supplements, which is unsulfated, cannot be converted to D3 sulfate, and may therefore not have the identical health benefits as the vitamin D your skin synthesizes
lyndacarol wrote:According to the following article:
http://articles.mercola.com/sites/artic ... _DNL_art_1It is believed that vitamin D3 from oral supplements, which is unsulfated, cannot be converted to D3 sulfate, and may therefore not have the identical health benefits as the vitamin D your skin synthesizes
Perhaps it is the sulfur that makes the difference?
My hypothesis: excess insulin (hyperinsulinemia) plays a major role in MS, as developed in my initial post: general-discussion-f1/topic1878.html "Insulin – Could This Be the Key?"
Dental caries has been shown to be inversely related to total sun exposure, with those living in sunnier areas having about half as many cavities as those living in less sunny areas.
Increasing your and your family’s vitamin D levels appears to be a much better option compared to drinking fluoridated water, as there are many additional health benefits of vitamin D, and a number of adverse effects of water fluoridation, including dental fluorosis and potential reduction in IQ.
There are multiple connections between your oral health, heart disease, and vitamin D status, and higher vitamin D levels have been found to prevent health problems related to your mouth, heart, and cardiovascular system.
Vitamin D may also play a crucial role in cancer. Grassroots Health is now implementing the world’s first cancer prevention project and study to evaluate vitamin D as a preventive strategy against breast cancer. Participants are being sought.
Conclusion/Significance: Twelve week supplementation of high dose vitamin D3 in RRMS patients was well tolerated and
did not induce decompensation of calcium metabolism. The skewing towards an anti-inflammatory cytokine profile
supports the evidence on vitamin D as an immune-modulator, and may be used as outcome measure for upcoming
randomized placebo-controlled trials.
Therefore, we speculate that the rise in IL-10+CD4+ T cells might
reflect expansion of inducible regulatory Tr1 cells. The finding of
an altered profile of pro- and anti-inflammatory CD4+ T cells
conforms to observations in experimental studies  and further
supports the assessment of vitamin D3 as a natural immune
modulator in MS .
Results: Twenty-three people were randomized, of whom 19 were on established interferon or glatiramer acetate (Copaxone) treatment. Median 25OHD rose from 54 to 69 nM (low-dose D2) vs 59 to 120 nM (high-dose D2) (p = 0.002). No significant treatment differences were detected in the primary MRI endpoints. Exit EDSS, after adjustment for entry EDSS, was higher following high-dose D2 than following low-dose D2 (p = 0.05). There were 4 relapses with high-dose D2 vs none with low-dose D2 (p = 0.04).
Conclusion: We did not find a therapeutic advantage in RRMS for high-dose D2 over low-dose D2 supplementation.
Conclusion:D3 is approximately 87% more potent in raising and maintaining serum 25(OH)D concentrations and produces 2- to 3-fold greater storage of vitamin D than does equimolar D2. For neither was there evidence of sequestration in fat, as had been postulated for doses in this range. Given its greater potency and lower cost, D3 should be the preferred treatment option when correcting vitamin D deficiency.
It seems that Vitamin D has a direct effect on the regulatory T lymphocyctes known as Tr1 cells. These cells keep the Th1 imnflamitory response from getting out of control.
Here is a good description of this process:
Here are some recent articles from the imunological community on the effect of Vitamin D on the immune system;
Here is a company developing cell therapy for Tr1 cells:
It appears that the immunologist are way ahead of the game in terms of a cure for MS. Vitamin D and Tr1 regulatory cells seem to be the key.
Unfortunately, it does not seem like much research or attention is being focused on this in the U.S.
goodtotalk wrote:Can you tell me where to find documented proof of that fact please if you would be so kind
While 8,000 IU's of vitamin D3 per day is a general recommendation that appears to be beneficial for most people, vitamin D experts from around the world are in agreement that the most important factor is your vitamin D serum level. There's no specific dosage level at which "magic" happens. So the take-home message is that you need to take whatever dosage required to obtain a therapeutic level of vitamin D in your blood.
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