Vitamin D in Mice


High dose vitamin D exacerbates central nervous system autoimmunity by raising T-cell excitatory calcium

As you know we have posted on this paper already and we were rather critical of the paper, because the refereeing was frankly rubbish. However what do we know? This study in mice has been picked as Editors choice in the journal Brain and it got a special mention in ECTRIMS2019. The home message that too much vitamin D was going to make your MS worse. I am sure this headline gets the journalists going

We said the central problem was that in constrast to what is said in the abstract and results, there was no effect of standard dose vitamin D, saying why bother with vitamin D in the first place?

Throughout the manuscript it says vitamin D makes things better and then in the figure and in the discussion saying it was not-significant. Meaning there was no effect of vitamin D. Mice live in holes and come out in the dark and so their vitamin D evolution is not going to be the same as human stuff.

However, there was a question mark raised by MD2, because vitamin D is the active ingredient in rat poison. It hardens the blood vessels of the rodents due to calcium deposition. In this study were fed mouse poison at a 10th of an acutely lethal dose for 12 weeks and so was the apparent worsening, because some of the mice had pegged-it (died). S

Well the authours had stated that one could have access to the data for a reasonable request. DrLove make one or two and eventually an excel sheet was produced and she gave it me blinded (So I didn’t know what is what) to have a look at. But now I can say that our initial thoughts did not seem to correct as most of the beasts made it to the end of the experiment, so they didn’t snuff it (die). If the data was deposited at the time of submission that could have been reported with the initial report.

However, I also have to say that with the actual data, if I compare the disease occurence, the maximum severity of disease and time of onset disease then there are actully no statisitically significant effects of either the standard or high dose of vitamin D. The apparent reduction in severity is largely mediated by one animal that really didn’t get EAE, it had mild signs for a day. remove this from the analysis and it makes the reduction even smaller (graph on right)

Re- working of data removing the one non-susceptible animals. Black turns out to be a high dose , red is the standard vitamin D response.

So if we equated this to how it would transpire in humans , as a relapse or not, then there would be no effect of vitamin D. I bet profG would beg to differ.

The apparent worsening is due to some of the animals remaining paralysed rather than recovering. Will that prevent some of you from taking mega doses of vitamin D? That would probably be a good thing as there is no evidence that mega doses are needed. But there are plenty of people who have taken mega doses and did it make MS worse..I think we know the answer. Enough said

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  • Hmm… Vitamin D in mice… Who cares? Irrelevant rodent research? I mean, chocolate is poisonous to dogs…

  • The real problem is that mice don’t get MS. So I doubt this tells us anything about MS. If a consistently higher vitamin d level (normal for people with high sun exposure) affects how the Epstein Barr virus interacts with B cells then this mechanism will never be seen in mice.

  • The human body has a storage mechanism for vitamin d in the form of 25(OH)D bound to vitamin d binding protein in the blood. In this form it is stored and delivered as needed to cells where it is converted into an active form and then it has an effect. This is why the body can function over a wide range range of 25(OH)D level, but it requires 1,25(OH)D to be precisely controlled. The body functions poorly when there is not enough vitamin d and when the storage system is overloaded. What they are doing with the rats is overloading this storage system and that is why the system is no longer working correctly. In adults overloading occurs at sustained (about 6 months) intakes of over about 40,000IU a day, it will depend on body volume and the variations in binding protein.

    However, what has not been considered is the ability of viruses to detect the rising and falling of 25(OH)D levels as a trigger for the reawakening of latent viruses. Then the effect of latitude on MS is about consistent vitamin d levels not absolute levels.

  • I’m also considering so called Coimbra Protocol – high doses of Vit D. There seems to be a correlation between EBV and Vit D metabolism. People with specific VDR gene (vitamin d receptor) polymorphism seems to be in this group.
    According to Coimbra, Vit D should be given at high doses to saturate the body.
    I have just sent my probe for DNA tests in UK to check if I have Fok I or Apa I polymorphisms.

    There are few groups on fb, where members shares great stories. Seems to good to be true.. but why not to try?

    1) Epstein-Barr virus encoded EBNA-3 binds to vitamin D receptor and blocks activation of its target genes:
    2) Variation in the vitamin D receptor gene is associated with multiple sclerosis in an Australian population.

    • At levels below 10,000IU a day for fair sized adults vitamin d is food. At these levels it is a pharmaceutical drug. Get your blood calcium levels check frequently, high levels of vitamin d are toxic.

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