Vitamin D in Optic Neuritis Trial fails

Salari M, Janghorbani M, Etemadifar M, Dehghani A, Razmjoo H, Naderian G.Effects of vitamin D on retinal nerve fiber layer in vitamin D deficient patients with optic neuritis: Preliminary findings of a randomized, placebo-controlled trial.
J Res Med Sci. 2015;20(4):372-8

BACKGROUND:There is accumulating evidence for a possible protective role of vitamin D in the development and disease course of multiple sclerosis. Whether vitamin D is also effective in treating patients with optic neuritis (ON) is not known. The aim of this study was to evaluate the effect of oral vitamin D on the thickness of retinal nerve fiber layer (RNFL) in vitamin D deficient patients with ON by optical coherence tomography.
MATERIALS AND METHODS: A Phase II placebo-controlled randomized clinical trial conducted between July 2011 and November 2012 included 52 patients with confirmed unilateral ON aged 15-38 years and low serum 25-hydroxyvitamin D levels. The main outcome measures were changes in thickness of RNFL and macula 6 months after treatment. Patients were randomly allocated to receive 6 months of treatment with adding either 50,000 IU/week vitamin D or placebo.
RESULTS: In the 27 patients treated with vitamin D, the mean (standard deviation [SD]) thickness of RNFL decreased from 111.3 (18.9) μm at baseline to 91.4 (13.3) at the end of study period (P < 0.001). Correspondingly, in the 25 patients treated with placebo, the mean (SD) thickness of RNFL decreased from 113.7 (21.5) μm at baseline to 96.1 (12.3) at the end of study period (P < 0.01). In both groups, the mean thickness of the macula did not changed (P > 0.05). Average thickness of RNFL at the end of trial did not differ between groups.
CONCLUSION: Adding vitamin D to routine disease therapy had no significant effect on the thickness of RNFL or macula in patients with ON. This trial is registered on (ID NCT01465893).
This study says that if you start taking vitamin D when you get optic neuritis, then there is no effect of saving retinal nerves and so the writing is on the wall for other CIS doing the same thing.

To me, this comes as no real surprise as I would have expected this.
OK, I accept that I could not know the answer unless the study has been done. However, I can have opinions and this is just one and may be a wrong one.

First, the treatment window from onset to drug treatment was up to one month, which is probably too long even for a drug that was going to work. Animal studies show us that damage is accumulated in the first few days and but interpolation a few weeks at most.

Next, the outcome is based on neuroprotection rather than an anti-inflammatory/immunomodulatory effect. All the rhetoric built up has been about vitamin D being an anti-inflammatory and stopping susceptibility. However, the inflammation has occurred when the optic neuritis has started.

Next, it is a nutriceutical that has few side effects….this suggests that it is not going to be a potent immunosuppressive. If it is not potent the chances of having a major effect is limited

Every MS Society will have had an application to do a trial of vitamin D and many have been funded? 

How many are looking at using vitamin D to prevent disease after it has started, compared to vitamin D as risk factor. If we think that vitamin D can have the potency of Alemtuzumab and Natalizumab then someone needs to look at our brains, as I believe we are deluding ourselves. 

We are getting an array of active drugs, but in the UK at best one can use a low efficacy drugs….maybe we should be trying to “nip it in the bud”. 

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  • I take vitamin D3 every day since my blood tests showed she was very low, less than 30 nmol / L , 5.000 ui every day…. But still sometimes I wonder if the Low vitamin D3 dosage would be one of the possible causes or a consequence of the activity of MS … Something like "which came first, the chicken or the egg?" …

  • Active arm received around 7000 ui of vitamin D daily.
    This is definitive too little.
    Vitamin D council says there no trouble taking 10000 ui daily in normal people, so I don't understand how 7000 should / could be curative in autoimmunity.
    Anyway first Vitamin D trials where using 600 ui daily supplementation, so at least we are starting to see increasing doses trials nowadays.

  • The patients receiving the vitamin D had one single dose a week of 50000 iu. I would of thought a daily lower amount of 7000 iu might absorb better.

  • I have tried Vit D3 in various doses and then tried sunlight and my take is that the immodulatory effect is very small – I had relapses in March and in August and inbetween despite supplementation and despite spending a big amount of time sunbathing.

    Yes, go outside cos it won't do you any harm to have higher Vit D levels and get a nice skin colour but as a therapy I predict the studies to fail or to show only a small difference.

  • I would argue that vitamin d is not anti inflammatory but that a lack of vitamin d can lead to stronger active immune response. The difference is that adding more, once the body is replete, will have no effect.

    My other point is you cannot fix a gearbox that failed due to lack of oil by adding more oil, it is too late. It is likely that any effects are before birth (epigenetic), or stop the problem before it starts, say keeping Epstein Barr infected B cells hibernated.

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