Results from the first trial of vitamin D for MS


A randomized trial of high-dose vitamin D2 in relapsing-remitting multiple sclerosis.

Stein et al, Neurology, October 25, 2011

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.

“This study is the first published randomised double blind controlled trial of vitamin D supplementation in MS. Disappointingly it did not show that taking higher doses of vitamin D can protect against MS disease activity. However, several features of this study mean that further work is still needed to test whether vitamin D is an effective treatment or not. This study was very small (20 patients- as compared to trials such as Alemtuzumab using 500- the more patients you have the more likely you are able to see whether a treatment works); both groups of patients were taking more vitamin D than the UK Government recommend per day (6000IU of vitamin D a day versus 1000IU) so the control group may have had some protection as well; the study was run for 6 months which is thought to be too short to really say whether there is a meaningful effect of treatment, and the investigators used vitamin D2 instead of the more active D3. All of this being said, the study raises the question of whether vitamin D deficiency is only involved in triggering MS and not in how the disease progresses; but we need to test this appropriately.”

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  • Why did the researchers choose D2 rather than D3? It seems to be a poor bit of research (23 people) to base a conclusion on.

  • Agreed! To be honest, there is little point to this study. When performing a clinical trial, a genetic or an epidemiological study researchers need to decide on what the power of the study needs to be (i.e. how many people need to be investigated). For clinical trials it is probably more than 500, for genetic studies this needs to be thousands. Better trials for vitamin D on their way.

By Ram



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