Chicken or egg? There are numerous studies showing a seasonal variation in blood vD levels that appear to be associated with MS disease activity. Many people interpret this as causal, i.e. low vD levels are responsible for MS disease activity. Another interpretation is that MS disease activity causes low vD levels, i.e. the immunological cascade responsible for triggering MS disease activity consumes vD and simply lowers blood levels.
How do we sort out the causation vs. association? What we need is an adequately powered double-blind placebo-controlled trial to answer this question. The problem is who is going to pay for the trial and what dose of vD do we use? Another issue is that many in the vD field think that blood vD levels are simply a proxy for sunlight exposure and that is more important than vD; in other words we need to do a trial of ultraviolet (UV) light exposure rather than simply supplementing vD. How does UV light come into the equation? There is good data that UV light modulates T-cells function as they get exposed to light in the skin. This is in fact a well accepted treatment for autoimmune skin diseases.
I have been to so many ‘vD in MS meetings’ and we never reach consensus on how to take things forward. I suspect long after I have retired and moved onto other things the next generation of MS researchers will be having the same discussions and debates. Sad, but likely to be true.
Hartl et al. Seasonal variations of 25-OH vitamin D serum levels are associated with clinical disease activity in multiple sclerosis patients. DOI: http://dx.doi.org/10.1016/j.jns.2017.01.059
•25-(OH)-D serum concentrations showed seasonal variations in patients with multiple sclerosis.
•the nadir of vitamin D serum concentrations in winter preceded the peak in prevalence of relapses in spring by two months.
•an increment of 10 ng/ml 25-(OH)-D resulted in 20% reduction in the prevalence of relapse at visit.
Background: Low 25-hydroxy vitamin D (25-[OH]-D) serum concentrations have been associated with higher disease activity in multiple sclerosis (MS) patients.
Methods: In a large cross-sectional study we assessed the vitamin D status in MS patients in relation to seasonality and relapse rate. 415 MS-patients (355 relapsing-remitting MS and 60 secondary-progressive, 282 female, mean age 39.1 years) of whom 25-(OH)-D serum concentrations were determined at visits between 2010 and 2013 were included in the study. All clinical data including relapse at visit and expanded disability status scale were recorded in a standardized manner by an experienced neurologist. Seasonal variations of 25-(OH)-D serum concentrations were modelled by sinusoidal regression and seasonal variability in the prevalence of relapse by cubic regression.
Results: The mean 25-(OH)-D serum concentration was 24.8 ng/ml (range 8.3–140 ng/ml) with peak levels of 32.2 ng/ml in July/August and nadir in January/February (17.2 ng/ml). The lowest modelled prevalence of relapse was in September/October (28%) and the highest modelled prevalence in March/April (47%). The nadir of 25-(OH)-D serum concentrations preceded the peak in prevalence of relapses by two months.
Conclusion: In summary, seasonal variation of 25-(OH)-D serum levels were inversely associated with clinical disease activity in MS patients. Future studies should investigate whether vitamin D supplementation in MS patients may decrease the seasonal risk for MS relapses.