Boosting vitamin D levels in patients with early signs of multiple sclerosis may retard disease progression according to new research published in JAMA Neurology this month.
During a five year follow-up period, the researchers found multiple sclerosis (MS) patients with serum 25-hydroxyvitamin D (25(OH)D) concentrations greater than or equal to 50 nmol/L had a four times lower change in T2 lesion volume and a two-fold lower rate of brain atrophy and lower disability than those whose blood levels were below 50 nmol/L.
“Because the prevalence of vitamin D insufficiency is high, supplementation could potentially benefit a large proportion of patients with MS,” the researchers, led by Alberto Ascherio, M.D. PhD., of the Harvard School of Public Health, Boston, write.
The Betaferon/Betaseron in Newly Emerging multiple sclerosis For Initial Treatment (BENEFIT) study included almost 500 patients from 18 European countries, as well as Israel and Canada, whose blood 25(OH)D levels were measured as part of a randomised trial originally designed to study patients given interferon beta-1b treatment for MS.
As part of this study, the researchers examined whether blood concentration of 25(OH)D was associated with MS disease activity and progression in patients with a first episode suggestive of MS.
Almost all patients enrolled had at least one 25(OH)D measurement. Patients were followed for up to five years with magnetic resonance imaging.
Increases of 50-nmol/L in average blood 25(OH)D levels within the first 12 months were associated with a 57 percent lower risk of new active brain lesions, 57 percent lower risk of relapse, 25 percent lower yearly increase in T2 lesion volume and 0.41 percent lower yearly loss in brain volume from months 12 to 60.
“Among patients with MS mainly treated with interferon beta-1b, low 25(OH)D levels early in the disease course are a strong risk factor for long-term MS activity and progression,” the study authors write.
They add that the “profound association of 25(OH)D levels with MRI measures of disease activity and progression is of particular clinical relevance for patients with [clinically isolated syndrome] in whom the prognostic value of MRI pathology for the development of long-term disability has been demonstrated”.
In MS patients the term “clinically isolated syndrome” is used to describe a first neurologic episode that lasts at least 24 hours, and is caused by inflammation/demyelination in one or more sites in the central nervous system (CNS).
The authors also argue that the robustness of their results in analyses leaving a one year lag time between the last serum 25(OH)D measurement and assessment of MS outcomes “provides evidence that low vitamin D was not a consequence of the disease process itself but rather its predictor”.
This is an important finding and one which directly contradicts a recent systematic review published in the Lancet Diabetes & Endocrinology (link), which contends that a low blood level of vitamin D is a result, rather than the cause, of many diseases.
The JAMA study authors conclude that their results provide evidence supporting a protective effect of vitamin D on the diseases process underlying MS and the importance of correcting vitamin D insufficiency.
JAMA Neurology Published online January 20, 2014. doi:10.1001/.jamaneurol.2013.5993.
Editor’s Note: Authors made conflict of interest disclosures. This study was supported by the National Institute of Neurological Diseases and Stroke and the National Multiple Sclerosis Society. The BENEFIT study was sponsored by Bayer.
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