The Clinical Efficacy of Vitamin D and Ms

Multiple Sclerosis(MS) is a chronic inflammatory disease(Kirbas et al, 2012, p. 43), whereby the body's own immune system attacks the protective myelin sheath of the central nervous system (CNS). It is generally accepted that MS is an autoimmune process (Multiple Sclerosis Australia, 2013).

During an attack of MS, T-Lymphocytes cross the blood brain barrier into the CNS, attacking cells that are responsible for the myelin sheath. This leads to inflammation and scarring (lesions) of the myelin sheath. This inflammatory phase, also known as a relapse, interferes with nerve impulses of the CNS. Relapses lead to a progressive loss of neural function (Payne 2001, p. 349).

The cause of MS is still unknown. It is believed that genetic and environmental factors are the leading aetiological factors. Vitamin D (VITD) is suggested to have an immunomodulatory role in the CNS, thus being targeted as important in the treatment of autoimmune disease (Riccio 2011, p. 228).

Hypovitaminosis D is currently one of the most studied environmental factors for MS, many believing that it has great clinical implications (Kirbas et al, 2012, p. 43). MS patients have increased levels of proinflammatory cytokines and decreased levels of anti-inflammatory cytokines. It is hypothesised that by increasing the levels of VITD, it may be possible to alleviate the disease symptoms (Mark et al, 2006, p. 420).

This review will examine the clinical efficacy of VITD and the evidence available.

VITD can have its origin in UV synthesis or diet. VITD is transported to the liver where it is hydroxylated. Further hydroxylation occurs in the kidneys, resulting in the active form 1,25 -dihydroxyvitamin D (calcitriol). The VITD status of a person is assessed by using 25-hydroxyvitamin serum levels-[25(OH)D] (Mark et al,2006, p. 418). Recommended normal levels have recently been revised to 75-250nmol/L (Overcoming Multiple Sclerosis, 2013).

Studies of VITD in the treatment of MS are rare and limited. Pierrot-Diseilligny (2009, p. 1474) makes note of treatments ranging from 6 months to two years with VITD. The daily dose ranged from 100 IU/d to 14,000 IU/d. The treated patients showed a reduction in the predicted number of relapses. In one treatment patients also showed a significant increase in TGF-beta1 levels (an anti-inflammatory cytokine affected by VITD). It is also worth noting, that overall patients did not show noticeable side effects from the high dosages of VITD (Pierrot-Diseilligny, 2009, p. 1474). Whilst these treatments are encouraging, control groups were not employed in some of the trials and the treatment groups were small ( no more than 40 patients). Also the dosage range was broad, leaving the question of what is the appropriate therapeutic dosage.

Two recent trials were found that explored the benefits of VITD in the treatment

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