“The following is my presentation from yesterday’s Clinical Trials Network meeting. I had to provide an overview of the vitamin D as a disease-modifying treatment for MS. I started by making the point that there is little difference between prevention and a DMT as both strategies modify the course of MS. Clearly the burden of proof for MS prevention is an order of magnitude higher than that for modifying the course of established MS. The issue of whether or not vD is a DMT is an important one and I agree the current data set is not convincing. The main issue is reverse causation, i.e. cells involved in inflammation consume vD therefore inflammation itself is the cause of low vD levels. Data supporting reverse causation from outside the field of MS is extensive. However, there are clues that suggest low vD levels may be linked to MS activity as part of the causal pathway. At the end of the day we can argue about the roll of vD in MS until the cows come home; unless we do an randomised interventional study will not resolve the issue.”
“I spent a lot of time focusing on the dose of vitamin D, which is something that has generated a lot of discussion on this blog; particularly among the cynics. I don’t think we can use the general population to generate a normal level of vD and to define specific cut-offs for vD insufficiency and vD deficiency. Why? Because the majority of population may be deficient hence this may result in a spuriously low set of normal values. I therefore used Reinhold Vieth’s evolutionary medicine perspective to argue for a level of greater than 100nmol/L as being normal. This is based on circulating vD levels in the great apes and hunter-gatherer societies in Africa, for example the Maasai, and levels in people working outdoors, for example lifeguards and farmers. I also stressed that blood vD levels are also determined by genetic factors therefore in an ideal world we would titrate levels of supplementation based on blood levels. This latter approach at a population level is too expensive and logistically impossible hence the adoption of EFSA’s or the Vitamin D Council’s recommendations. I made the point that the current RDA (recommended daily allowance) is based on the prevention of rickets in the cod liver oil era. 400U is the magic amount of vD in a teaspoon of cod liver oil and that is how the RDA was set. It is clear that this is too little and needs to be adjusted upwards. This with all the cultural changes that are lowering vD levels in the population may be driving up the incidence of MS and other diseases. This is why it is so important to tackle the issue of vD supplementation in MS urgently and generate the necessary evidence to guide clinical practice.”
“The purpose of the meeting yesterday was to start the discussion and kick-start a group tasked with coming up with some concrete recommendations regarding a clinical trial tackling the issue of vD in MS.”
“I am still hoping to get Bruce Hollis an Internationally renowned vD expert to do a guest post on the rationale for the 5,000U per day recommendation from the vD Council.”
Vitamin D as a disease-modifying therapy
Oh No! Not another vD post. #MSBlog #MSResearch #ClinicSpeak
The only known toxic effect of vitamin d is high blood calcium. This starts, for some, when blood 25(OH)D goes above 500nmol/L. The supplement dose that has never been seen to cause adverse events in 10,000IU a day. So give then 10,000IU a day and check their blood calcium levels, it is much cheaper than a vitamin d test. If the supplement is from Amazon or the like it is also very cheap. If it has no effect on MS at least their bones will be stronger and they will not get secondary hyperparathyroidism. It is worth remembering that 25(OH)D is basically inert and is acting as a reservoir so the levels are not carefully controlled by the body. It is also worth noting that consumption goes up with supply and the relationship between supplement level and 25(OH)D is not linear.
Would not it be possible to do a clinical trial the way GrassRootsHealth is conducting their clinical trial(s). MSers are highly motivated, so if given the right instructions they will no doubt cooperate.
Do we really need more trials in MS on vitamin D? On clinical trials.gov there are 29 studies in MS, some recruiting and over 2000 other ones. Are they all of such poor quality that they need repeating? If they are of poor quality why were they done in the first place?If the outcome of supplementation is so great, do you not think that you would have seen it as there are plenty of MSers taking high doses. Or is it just an incremental thing. The trials cost a lot, would the money be better spent on health promotion?
Reinhold Vieth gives compelling evidence that the Lowes Observed Averse effect Level or LOAEL is 40k/day. I took this amount for two years before being diagnosed with MS. It didn't stop my conversion from ADEM to MS but I felt it was worth a try. Never the less I keep my vitamin D levels up because there is ample evidence that it produces adaptive Tregs. Vitamin D or probably won't halt MS, but I suspect it may help reduce damage when an attack occurs. This is because aTregs HP shutdown out of control immune responses whereas natural Tregs (nTregs) are thought to prevent autoimmunity.
Thank you, I've never thought that my low Vitamin D levels are the cause of my MS although my mother constantly thinks its because I didn't much milk as a kid. This report is great and will be shared on my website.
what if people with MS volunteered to register in their own trial? I like the idea of a grass roots style trial.