A study shows that Multiple Sclerosis (MS) treatment by Interferon-Beta  improves  the ability of the MS patient to produce vitamin D by exposure of their skin to the sun

The research was done at the Australian facility  Menzies Research Institute Tasmania

Quoting the article [1]:

“…In this study, we found that IFN-β therapy is associated with greater production of vitamin D from sun exposure…Not only did we find that persons taking interferon-beta had higher vitamin D levels than those not taking it, we also found that this increase in vitamin D was due to an enhancement of the association between sun and vitamin D, with persons on interferon-beta having nearly three-times as much vitamin D from similar amounts of sun exposure to those not taking interferon-beta, [said Menzies's Dr Simpson]”

If an MS treatment can improve the body’s ability to use sun rays to have the skin manufacture vitamin D, the converse should be true : MSers  untreated by Interferon-Beta, should have  an impaired capacity of producing vitamin D, and have less of it in their blood serum.

Some comments about this:

  1. We published a post on a recent study [3] questioning the ability of Interferon Betas to slow down MS as measured by  disability progression scales
  2. We also published a post on a study [5] questionning the ability of high vitamin D to improve MS over low doses, as measured by brain lesions displayed by Magnetic Resonance Imaging (MRI).  However, another study, referenced in  [4], showed that rising vitamin D blood serum levels did decrease the relapse frequency 49 ± 22 nmol/l to 110 ± 26 nmol/l on average :
    “…every 10 nmol increase in 25-OH-D level was associated with a reduction in the relapse incidence rate of 13.7%. …” So some vitamin D can slow the relapse frequency, up to a point.
If Interferons-beta do not slow MS disability, but improve vitamin D levels, what does that tell  us about vitamin D ? Probably that vitamin D supplementation cannot slow the MS disability progression. Granted
The  Menzies result thus further shows, in an indirect way,  that improving vitamin D serum level does not necessarily slow MS disability progression.
Note: The  authors Niall Stewart, Steve Simpson Jr, claim  that the higher level of Vitamin D will decrease the relapse frequency of Relapsing Remitting Multiple Sclerosis (RRMS):  Hence the title of the publication: “ Interferon-β and serum 25-hydroxyvitamin D interact to modulate relapse risk in MS”  That seems to a suggestion only since they say further : “…suggesting part of the therapeutic effects of IFN-β on relapse in MS may be through modulation of vitamin D metabolism…”
At any rate, there is no contradiction with the findings of (3,4).  That is because there are several ways to measure the efficacy of an MS treatment:
  • By reducing the relapses of RRMS
  • By slowing down the disability progression
  • other…
One could decrease the relapse frequency, without slowing the disability progression . That has to do with the duality inflammation/neurodegeneration of the disease. That complex topic of will be another post of ours.
However, it seems that disability progression should trump relapse frequency in the great scheme of things. But that is for every MSer to answer…
What can be understood then of the study done at the U. Of California, San Francisco (UCSF), also  published in Neurology [6]. It states:
“……Higher vitamin D levels are associated with less subsequent disability and reduced loss of gray matter volume. Vitamin D may be an important contributor to neurodegeneration in MS…”
First of all let us say upfront that we do not have any stake one way or the other. One could infer from study [1] that vitamin D does not help disability.
Since this statement seems to be contradicted by [6], let us look a little further into this:
The Menzies work shows that Interferon Beta raises the level of vitamin D in MS patients’s blood. The UCSF shows that patients with a higher level of 25-hydroxyvitamin D3 have less disability.
The obvious question is of chicken vs. egg type: Did the patients have higher level of 25-hydroxyvitamin in the UCSF study because their MS was less disabling  or that the vitamin D countered the disabling tendency of MS?
This is the old quandary: Association is not necessarily causation
Not to say that  vitamin D levels should not be also improved for the sake overall health of any MS patients, RRMS or Progressive MS.

MSers : Why don’t you run this by your Doctor or Clinical Nutritionist!

 

Update 8/01/12:

 

Sources:

  1. UTAS ; “New link found between MS treatment and vitamin D” ; July 2012
  2. Neurology ; “”Interferon-β and serum 25-hydroxyvitamin D interact to modulate relapse risk in MS” ;  July 2012
  3. medinewsdigest ; “MND BRIEF: Multiple Sclerosis: Beta interferons (β-IFNs) might not slow disability progression” July 2012
  4. Therapeutic Advances In Neurological Disorders ; “Relationship between 25-OH-D serum level and relapse rate in multiple sclerosis patients before and after vitamin D supplementation.” ; 2012
  5. medinewsdigest; “In Brief: High Doses of Vitamin D Not Very Helpful in Treating Multiple Sclerosis”; May 2012
  6. Neurology ; “Vitamin D Levels Are Associated with Disability and Brain Volume in Multiple Sclerosis” ; April 2012
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