The Vitamin D-bate
Previously I have posted on nutrition and MS disease management. Researching that was, quite frankly, fairly fruitless in terms of yielding conclusive results. (On the plus side, it means I feel absolutely no remorse about my “everything in moderation” diet. I also got to unleash my quirky sense of humour and let it run amok on the various food groups.)
What I touched on only briefly within that post was the issue of dietary supplements and MS causality, disease progression and symptom management. Given the hot-off-the-press results on Vitamin D from researchers across the ditch at Johns Hopkins, it seemed timely to revisit this topic to provide a “D-briefing”, if you will, in this instance more comprehensively (and less comically).
D-sease mechanisms- a brief history
Vitamin D’s first claim to fame was in relation to bone health, and in particular, rickets. What was originally a rare condition in the 1600s, had become widespread between 1700 - 1900, mainly in heavily polluted European cities where people spent most of their time indoors. A combination of research and D-tective work revealed that either eating foods rich in vitamin D (e.g. cod liver oil) or exposure to sufficient sunlight could prevent rickets.
However, it wasn’t until the early 1900s that we gained an appreciation of the existence of vitamins (compounds obtained in small quantities via our diet and required by the body for normal growth). Relatively soon afterwards, in the 1930s, the chemical compound for vitamin D was identified. The researcher who led the team of over 50 scientists later received the Nobel prize for his work, so you could say it was a big D-eal. [Purists will note that vitamin D is in fact a steroid hormone, but the misnomer remains in play.]
Fast forward to the beginning of the new millennium, and that’s roughly when vitamin D resurfaced in the scientific spotlight. This time it was in relation to a whole range of potential health benefits, which is when the waters were muddied with a number of conflicting reports.
The devil is in the D-tails
Vitamin D is measured in International Units. (Don’t ask me why. It just is.) A low dose supplement is generally 400-1000 IU/day. Higher doses, such as in the recent JHU study, would be 10,000-20,000 IU a day, although some folks go all out and take up to 240,000 IU in one go. Egads!
Furthermore, vitamin D exists in a number of different states. Vitamin D3 (aka cholecalciferol) from supplements and sun exposure is biologically inactive. Via a series of reactions, the liver converts it firstly to 25(OH)D (aka calcidiol) and then the kidneys kick in to produce the active metabolite 1,25(OH)2D (aka calcitriol). These both circumnavigate their way around the body via the bloodstream.
The former, 25(OH)D, has a long halflife and this compound is what is measured to D-termine Vitamin D status. However, it’s the latter 1,25(OH)2D which is the active compound. Among other roles, it assists in regulating levels of calcium and other micronutrients.
A true D-ficiency?
If you peruse the literature on supplements, the first stumbling block is how to D-fine the thresholds for vitamin D deficiency (i.e. when a level is considered too low), toxicity (i.e. when a level is considered too high) and what is considered optimal (i.e. just right). It may even vary from person to person. In short, the scientific community has yet to reach a consensus, so in the interim we are flying blind.
Moreover, it is possible to end up with much higher levels of serum 25(OH)D via supplementation than from via sunlight. There are currently no results on longterm studies of vitamin D supplementation, so this adds to the D-lemma. Thankfully, as MStranslate reported, there are currently clinical trials underway to gauge the efficacy, safety and tolerability of vitamin D in MS, which should shed some light when they are published.
Finally, there’s the conundrum of how to interpret the conflicting claims about vitamin D – particularly its role in chronic diseases such as MS. There have been many, many studies of the effects of vitamin D on chronic disease and the overall trend seems to be that vitamin D-deficiency may predispose to certain conditions, but an excess of vitamin D appears to be harmful as well.
The recent results of the JHU study crew appear to suggest that in a small group of patients over a short time frame, high levels of vitamin D reduce the levels of a type of immune cell that is linked with disease progression. The reduction in the number of these cells was not seen in the cohort of patients given a lower dose of vitamin D. While both promising and enlightening, there was no difference in relapse rates between the two groups.
Thus in summary, with regards to MS and vitamin D, the scientific community is still D-liberating on whether the drug is D-leterious or D-sirable, and in the meantime, it’s quite a D-lemma whether to D-mand or D-sist it.