Vitamin D and multiple sclerosis.

Department of Exercise and Nutrition Science, School of Public Health and Health Professions, University at Buffalo, Buffalo, NY 14214, USA.
Critical reviews in food science and nutrition (Impact Factor: 5.55). 11/2012; 52(11):980-7. DOI: 10.1080/10408398.2010.516034
Source: PubMed

ABSTRACT Multiple sclerosis (MS) is an inflammatory disease of the central nervous system and characterized by neurological and cognitive manifestations. The disease is more common in populations living in high altitudes with low sun exposure, women more than men, and certain ethnic backgrounds more than others. The etiology of MS is yet unknown, although several factors have been implicated in its development. These include genetic factors and environmental factors as well as dietary components and their interactions. Among the dietary components that have recently attracted the attention is vitamin D. This mini-review summarizes current knowledge on the potential use of vitamin D in the protection and treatment of MS. In addition, the mechanism(s) by which vitamin D plays a role in the development and/or protection from MS are discussed.

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    • "The relationship of vitamin D with the immune system is being intensely discussed. It has been shown that vitamin D induces immune tolerance [Weiss, 2011], vitamin D deficiency being related to the development of autoimmune diseases, such as multiple sclerosis [Ho et al. 2012; Holmøy et al. 2012, Weinstock-Guttman et al. 2012], "
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    ABSTRACT: The extraskeletal effects of vitamin D have attracted considerable interest. Vitamin D deficiency appears to be related to the development of diabetes mellitus type 2 and the metabolic syndrome. Vitamin D may affect glucose homeostasis, vitamin D levels having been found to be inversely related to glycosylated hemoglobin levels in gestational diabetes mellitus. In addition, vitamin D appears to protect from the development of gestational diabetes mellitus. The aim was to study levels of 25-hydroxy vitamin D3 [25(OH)D3] and the relationship between 25(OH)D3 levels and glycemic control in patients with diabetes mellitus type 2. Glycosylated hemoglobin (HbA1c) and 25(OH)D3 levels were measured in a group of 120 diabetes mellitus type 2 patients. The same measurements were performed in a group of 120 control subjects of the same age and sex. 25(OH)D3 was measured by radioimmunoassay and glycosylated hemoglobin (HbA1c) was measured by high-performance liquid chromatography. 25(OH)D3 levels were lower in the diabetes mellitus type 2 patients than in the control group, being 19.26 ± 0.95 ng/ml and 25.49 ± 1.02 ng/ml, in the patient and control groups, respectively (p < 0.001, Student's t-test). 25(OH)D3 levels were found to be inversely associated with HbA1c levels in the diabetic patients (p = 0.008, r (2) = 0.058, linear regression). 25(OH)D3 levels were found to be inversely associated with HbA1c when the patient and control groups were analysed together (p < 0.001, r (2) = 0.086). Vitamin D levels appeared to be lower in diabetes mellitus type 2 patients than in the control group, vitamin D levels being related to glycemic control in diabetes mellitus type 2. These findings may have therapeutic implications as cautious vitamin D supplementation may improve glycemic control in diabetes mellitus type 2.
    Therapeutic advances in endocrinology and metabolism 08/2013; 4(4):122-8. DOI:10.1177/2042018813501189
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    ABSTRACT: This paper reviews the recent data on the role of vitamin D (VD) in the genesis of various immunological disorders. It inhibits immune reactions in general, but it enhances the transcription of 'endogenous antibiotics' such as cathelicidin and defensins. VD inhibits the genesis of both Th1- and Th2-cell mediated diseases. The pleiotropic character VD-induced effects are due to the altered transcription of hundreds of genes. VD supplementation in most related studies reduced the prevalence of asthma. Th1-dependent autoimmune diseases (e.g., multiple sclerosis, Type 1 diabetes, Crohn's disease, rheumatoid arthritis and so on) are also inhibited by VD due to inhibition of antigen presentation, reduced polarization of Th0 cells to Th1 cells and reduced production of cytokines from the latter cells. VD seems to also be a useful adjunct in the prevention of allograft rejection. Last but not least, VD supplementation may be useful in the prevention or adjunct treatment of chronic obstructive pulmonary disease.
    Expert Review of Respiratory Medicine 12/2012; 6(6):683-704. DOI:10.1586/ers.12.57
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    ABSTRACT: Background: An association between multiple sclerosis (MS) prevalence as well as MS mortality and vitamin D nutrition has led to the hypothesis that high levels of vitamin D could be beneficial for MS. The purpose of this systematic review is to establish whether there is evidence for or against vitamin D in the treatment of MS. Methods: Systematic literature searches were performed to locate randomized, placebo-controlled, double-blind trials measuring the clinical effect of vitamin D on MS in human participants. Data were extracted in a standardized manner, and methodological quality was assessed by the Jadad score. Results: Five trials were located that met the selection criteria. Of the 5 trials, 4 showed no effect of vitamin D on any outcome, and 1 showed a significant effect, namely by a reduction in the number of T1 enhancing lesions on brain magnetic resonance imaging. Three studies commented on adverse effects of vitamin D, with gastrointestinal adverse effects being the most frequently reported. The literature is limited by small study sizes (ranging from 23 to 68 patients), heterogeneity of dosing, form of vitamin D tested (vitamin D3 in 4 trials and vitamin D2 in 1) and clinical outcome measures. Therefore, a meta-analysis was not performed. Conclusions: The evidence for vitamin D as a treatment for MS is inconclusive. Larger studies are warranted to assess the effect of vitamin D on clinical outcomes in patients with MS. We further encourage researchers to also test the effect of vitamin D on the health-related quality of life experienced by patients and their families.
    Neuroepidemiology 12/2012; 40(3):147-153. DOI:10.1159/000345122 · 2.48 Impact Factor
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