I take 70,000IU and 600mg per day for 6.5 months already. When do you think my problems with magnesium should start? what was your first symptom if you recall? ;)
My search criteria: multiple sclerosis + vitamin D + 10,000. Go to this link:
http://www.ncbi.nlm.nih.gov/pubmed/?ter ... D+10%2C000
Search found 19 results as of today.I sorted results by publication date. Let's look at all trials starting from the oldest, I skipped trials which doesn't have conclusions/results:
We conclude that large numbers of patients with MS and TM in our cohort are deficient in vitamin D. HDE significantly elevated 25(OH)D levels in MS patients and was more effective at increasing 25(OH)D levels than LDC. Prospective studies are required to determine appropriate dosing regimen to achieve optimal levels in the majority of MS patients and to ascertain the safety, immunological response, and ultimately the clinical efficacy of vitamin D replacement therapy.
Our findings are consistent with a protective immunomodulatory effect of ambient UV radiation on the onset of WG and CSS. We discuss possible mechanisms, including the effect of vitamin D on the immune system.
High-dose vitamin D (approximately 10,000 IU/day) in multiple sclerosis is safe, with evidence of immunomodulatory effects.
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.
Multiple sclerosis (MS) is an inflammatory disease in which the myelin sheaths around the axons of the central nervous system are damaged. The damage leads to demyelination and scarring as well as a broad spectrum of signs and symptoms. The epidemiological data suggest a possible influence of vitamin D as an immunomodulatory agent on multiple sclerosis susceptibility as well as on clinical course of the disease. We investigated the effects of short-term vitamin D3 therapy on Iranian patients with MS. In a prospective randomized controlled trial study, 62 MS patients received 300,000 IU/month vitamin D3 or placebo as intramuscular injection for 6 months. Our results showed no significant difference between the treatment and the control groups in the expanded disability status scale scores and number of gadolinium-enhancing lesions during the 6-month treatment period. After 6 months, the levels of cell proliferation in the vitamin D treatment group were significantly lower than the control group. Also, the levels of transforming growth factor-beta and interleukin-10 in the vitamin D treatment group were significantly higher than the control group. This result suggests that vitamin D therapy may help prevent the development of MS and could be a useful addition to the therapy.
Sun exposure and vitamin D status may have independent roles in the risk of CNS demyelination. Both will need to be evaluated in clinical trials for multiple sclerosis prevention.
The reported prevalence and incidence figures in our study were higher than in our previous report of 2007, in which the prevalence and incidence of MS were reported to be 43.8 and 3.64 per 100,000, respectively. This dramatic increase in the prevalence of MS puts Isfahan amongst the regions with the highest prevalence of MS in Asia and Oceania and is mostly due to changing environmental factors, amongst which vitamin D deficiency seems an important factor in our population.
At 12 months, mean serum 25-hydroxyvitamin D [25(OH)D] concentrations were 83 ± 35 nmol/liter and 179 ± 76 nmol/liter in control and treated participants, respectively (paired t, P < 0.001). Serum 1,25(OH)(2)D did not differ between baseline and 1 yr. In treated patients, 12-month PBMC proliferative responses to neuron antigens myelin basic protein and exon-2 were suppressed (P = 0.002). In controls, there were no significant changes in disease-associated PBMC responsiveness. There were no significant differences between groups in levels of selected biomarkers.
MS-associated, abnormal T cell reactivities were suppressed in vivo by cholecalciferol at serum 25(OH)D concentrations higher than 100 nmol/liter.
A causative role for CYP27B1 in MS is supported; the mutations identified are known to alter function having been shown in vivo to result in rickets when 2 copies are present. CYP27B1 encodes the vitamin D-activating 1-alpha hydroxylase enzyme, and thus a role for vitamin D in MS pathogenesis is strongly implicated.
Although vitamin D deficiency is considered an environmental factor in multiple sclerosis (MS), the immunological and clinical effects of vitamin D supplementation remain unclear. We performed a pilot study of the immunomodulatory effects of vitamin D in healthy individuals (n=4), who took 5000-10,000 IU/day of vitamin D over 15 weeks. After 15 weeks of vitamin D supplementation, serum 25(OH) vitamin D levels rose significantly from baseline, with a corresponding increase in IL-10 production by peripheral blood mononuclear cells and a reduced frequency of Th17 cells. These data provide a strong rationale for randomised trials to assess the clinical effects of vitamin D supplementation in MS.
We showed increased serum latency activated peptide (LAP) of TGF-β levels in MS patients treated with vitamin D3. The immune regulatory effects of TGF-beta may play a role in the improved MRI outcomes that we observed earlier in the vitamin D treated group of patients.
I left this one as the last. http://www.ncbi.nlm.nih.gov/pubmed/22354743
Supplementation with 20,000 IU vitamin D(3) weekly did not result in beneficial effects on the measured multiple sclerosis-related outcomes.
This study was not powered to address clinical outcomes, but none of the results were suggestive of an effect in this unselected population of fully ambulatory persons with multiple sclerosis.
So 20,000IU per week (~3000IU per day) DID NOT RESULT in beneficial effects on the measured multiple sclerosis-related outcomes.
Isn't interesting, that the amount of vitamin D usually recommended doesn't have any effect?