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Abstract
This article briefly introduces the basics of multiple sclerosis’ (MS) clinical hallmarks and pathophysiology. Vitamin D is presented, including its metabolism and effects on the immune system. The epidemiological observations linking vitamin D to MS range from a half century old findings of latitude gradients and migrational risk patterns to modern, nested, case–control biobank studies. These observations show an association without doubt although causation has yet to be proven. Vitamin D as a treatment for MS is an emerging concept and both current and anticipated data will be covered. Lastly, we discuss future challenges, ideas on how to move from association to causation, and the prospect of primary prevention of this disabling disease.
Financial & competing interests disclosure
J Salzer has received financial support from Biogen Idec, Merck Serono, Sanofi-Aventis and The Swedish Association of Neurologically Disabled, has received honoraria from Merck Serono, Biogen Idec, Teva Pharmaceuticals and Genzyme/Sanofi for lectures, and has received support to travel to scientific meetings from Biogen Idec and Merck Serono. P Sundström served on the scientific advisory board for Novartis and has received support to travel to scientific meetings from Biogen Idec and Novartis. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending or royalties.
No writing assistance was utilized in the production of this manuscript.
Key issues
Multiple sclerosis (MS) is an inflammatory disease of the central nervous system.
Vitamin D is a steroid prohormone that is produced in the skin upon ultraviolet B radiation, and it has immunomodulatory, mainly anti-inflammatory effects.
Vitamin D can also be ingested, both as supplements and through the diet.
There is no consensus as to what serum levels of 25 hydroxyvitamin D (25[OH]D) are to be viewed as normal or optimal. However, for immunomodulatory effects, at least ≥75 nmol/l is probably required, and few in the Western world have such levels today.
Observational data support a link between vitamin D levels and MS risk. These data include geographical prevalence patterns, migrational data, ultraviolet B exposure data and data from studies on 25(OH)D levels in prospectively collected biobank samples.
Observational data also suggest the use of vitamin D as a therapeutic agent in MS. These data include seasonal variations in relapse rates and associations between serial measurements of 25(OH)D levels and relapse rates.
Data from randomized controlled trials using vitamin D to treat MS are so far inconclusive, but several large trials are in progress, and results from these will appear over the next few years.
Primary prevention of MS with vitamin D supplementation may be possible, but randomized controlled trials to test this are not feasible. Instead, we have to rely on observational studies, and therefore such studies need to be very carefully designed so that no erroneous conclusions on causality are drawn.
To move further from association toward causation, large, well-matched prospective biobank case–control studies assessing all potential biomarkers of interest, and genetic Mendelian randomization studies, may be useful.