ResearchSpeak: vitamin D and disease progression

Should we be prescribing vD supplements to all of our patients with MS? #ResearchSpeak #MSBlog

“The study below shows no correlation with low baseline vD levels and future disability progression. However, it did show a correlation with relapses in young pwMS. I am not surprised by this data as it is becoming increasingly clear in established MS that low levels of vD levels may be due to reverse causation, i.e. inflammatory disease activity lowers vD levels rather than the low vD levels driving inflammatory disease activity. The latter is called the consumptive vD hypothesis. Please note this interpretation does not apply to disease susceptibility, i.e. low vD levels are an important risk factor for developing MS. To test the latter hypothesis we need to population-based prevention studies.”

“You may ask, based on my interpretation of this data, why do we recommend vD supplementation to people with an established diagnosis of MS? We do this as part of our holistic approach to the management of MS and do it for bone and general health. I tell my patients that based on the current evidence we can’t support the use of vD as a DMT in MS. There are ongoing trials addressing this question; we will need to wait to see the results.”

Muris et al. Vitamin D Status Does Not Affect Disability Progression of Patients with Multiple Sclerosis over Three Year Follow-Up. PLoS One. 2016 Jun 8;11(6):e0156122.

BACKGROUND AND OBJECTIVE:  The risk of developing multiple sclerosis (MS) as well as MS disease activity is associated with vitamin D (25(OH)D) status. The relationship between the main functional disability hallmark of MS, disability progression, and 25(OH)D status is less well established though, especially not in MS patients with progressive disease.

METHODS: This retrospective follow-up study included 554 MS patients with a serum baseline 25(OH)D level and Expanded Disability Status Scale (EDSS) with a minimum follow-up of three years. Logistic regressions were performed to assess the effect of baseline 25(OH)D status on relapse rate. Repeated measures linear regression analyses were performed to assess the effect on disability and disability progression.

RESULTS: Baseline deseasonalized 25(OH)D status was associated with subsequent relapse risk (yes/no), but only in the younger MS patients (≤ 37.5 years; OR = 0.872, per 10 nmol/L 25(OH)D, p = 0.041). Baseline 25(OH)D status was not significantly associated with either disability or disability progression, irrespective of MS phenotype.

CONCLUSION: Within the physiological range, 25(OH)D status is just significantly associated with the occurrence of relapses in younger MS patients, but is not associated with disability or disability progression over three years follow-up. Whether high dose supplementation to supra physiological 25(OH)D levels prevents disability progression in MS should become clear from long term follow-up of supplementation studies.

6 thoughts on “ResearchSpeak: vitamin D and disease progression”

  1. Agree completely Prof. G.When I was diagnosed no sign of deficiency at all.What was explored was family history, my dad passed from ALZ. I am EBV+.I spent much time in sunlight, always have taken a multivitamin for daily requirements.Whilst back then I never knew the extreme rates of MS in western NY I was well aware there was quite a bit here. In fact, its the one thing scared me no end while I was in college working towards my RN degree. I thought once I was passed 40 was no longer something I needed worry of in my own health. BAM!Why would this small little region of the globe have massive VD deficiency?We are on Lake Ontario… Lots of great lakes, other cities dont have the rates in this region.I need go on a HUNT! What are the Lupus rates, Parkinsons, ALZ, and other neurological/immuno numbers in this region. Took me nearly 8 months to finally get an MS number and that is active cases. It doesnt touch upon those who have passed who endured MS as for many many years the NMSS here listed Rochester NY on of less than a handful of hotspots. Why?I REALLY wish I could find a way to touch all patients in this region and get some data. I found your former post in relation to urban rates .vs. rural (and here we have suburban) fascinating. Would love try to gather data in that respect in this hotspot region.If I *WERE* to try pursue this exactly what should I be looking for? Lets say I take on that task. I'd need know all info need be sought and perhaps I can get it some traction.

  2. The problem with this research is it does not address the idea that there are two reasons why a person may have higher vitamin d. One is supply and the other is consumption. It is quite possible that two people with the same vitamin d level may have that level for two different reasons. The first may have higher intake but the second may be switching off uses of vitamin d. Vitamin d is used to control calcium and do something in the immune system, the ability to turn off non calcium uses of vitamin d as the levels drop would be a evolutionary advantage as it makes it easier to get through the winter without serious problems. If one of the systems that turns off protects against MS, then those with low intakes and somewhat higher blood levels may be the most susceptible. It is basically how far down the barrel can you scrape.

    1. I would have thought the other uses of vitamin d simply turn back on as vitamin d levels rise, but how high you have to go for them to switch on probably varies between people. This would explain why there is not a linear relationship between supplementation and 25(OH)D blood levels and why for the same supplement intake/sun exposure individuals have widely varying 25(OH)D levels. How full a bath is depends both on the size of the tap and the size of the plug hole. The problem is we do not know, but simplistic analysis like that in this paper does not help. We do not know fully how vitamin d is used by the immune system (although it is not an immune suppressant). We do not even know if there is a difference between a daily, weekly or monthly dose, although my instinct is that having your 25(OH)D levels cycling up and down is probably not good and this would occur with a monthly dose. The only way I can see to test the idea that uses of vitamin d by the immune system switch off would be to supplement at a relatively high level say 20,000IU a day, while monitoring blood calcium levels (for safety) and see what happens. This is probably less unreasonable now that the RDA for vitamin d has been shown to be miscalculated by a factor around 6 to 8 times. The RDA should be about 5000IU to 8,000IU a day not 400IU a day.

  3. Would it not be sensible globally for neurologists as new entry patients to MS arise that a VD test be done immediately. Its an inexpensive and simple test. While that may not result in anything related to why's it would definitively show that some link truly exists statistically or not. If so, then perhaps deeper research might be granted and pursued?

    1. Exactly, that's what I would say. They don't do the test when the investigation could be MS or not, then it is very difficult to establish this causal link VD. And where it fits the 4 genes are linked to the VD deficiency?

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