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Multiple sclerosis and vitamin D: an update.
Eur J Clin Nutr 2004; 58(8):1095-109EJ

Abstract

MS is a chronic, immune-mediated inflammatory and neurodegenerative disease of the central nervous system (CNS), with an etiology that is not yet fully understood. The prevalence of MS is highest where environmental supplies of vitamin D are lowest. It is well recognized that the active hormonal form of vitamin D, 1,25-dihydroxyvitamin D (1,25-(OH)(2)D), is a natural immunoregulator with anti-inflammatory action. The mechanism by which vitamin D nutrition is thought to influence MS involves paracrine or autocrine metabolism of 25OHD by cells expressing the enzyme 1 alpha-OHase in peripheral tissues involved in immune and neural function. Administration of the active metabolite 1,25-(OH)(2)D in mice and rats with experimental allergic encephalomyelitis (EAE, an animal model of MS) not only prevented, but also reduced disease activity. 1,25-(OH)(2)D alters dendritic cell and T-cell function and regulates macrophages in EAE. Interestingly, 1,25-(OH)(2)D is thought to be operating on CNS constituent cells as well. Vitamin D deficiency is caused by insufficient sunlight exposure or low dietary vitamin D(3) intake. Subtle defects in vitamin D metabolism, including genetic polymorphisms related to vitamin D, might possibly be involved as well. Optimal 25OHD serum concentrations, throughout the year, may be beneficial for patients with MS, both to obtain immune-mediated suppression of disease activity, and also to decrease disease-related complications, including increased bone resorption, fractures, and muscle weakness.

Authors+Show Affiliations

Department of Molecular Cell Biology and Immunology, VU Medical Center, Amsterdam, The Netherlands. b.m.van.amerongen@inter.nl.netNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

15054436

Citation

VanAmerongen, B M., et al. "Multiple Sclerosis and Vitamin D: an Update." European Journal of Clinical Nutrition, vol. 58, no. 8, 2004, pp. 1095-109.
VanAmerongen BM, Dijkstra CD, Lips P, et al. Multiple sclerosis and vitamin D: an update. Eur J Clin Nutr. 2004;58(8):1095-109.
VanAmerongen, B. M., Dijkstra, C. D., Lips, P., & Polman, C. H. (2004). Multiple sclerosis and vitamin D: an update. European Journal of Clinical Nutrition, 58(8), pp. 1095-109.
VanAmerongen BM, et al. Multiple Sclerosis and Vitamin D: an Update. Eur J Clin Nutr. 2004;58(8):1095-109. PubMed PMID: 15054436.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Multiple sclerosis and vitamin D: an update. AU - VanAmerongen,B M, AU - Dijkstra,C D, AU - Lips,P, AU - Polman,C H, PY - 2004/4/1/pubmed PY - 2004/11/2/medline PY - 2004/4/1/entrez SP - 1095 EP - 109 JF - European journal of clinical nutrition JO - Eur J Clin Nutr VL - 58 IS - 8 N2 - MS is a chronic, immune-mediated inflammatory and neurodegenerative disease of the central nervous system (CNS), with an etiology that is not yet fully understood. The prevalence of MS is highest where environmental supplies of vitamin D are lowest. It is well recognized that the active hormonal form of vitamin D, 1,25-dihydroxyvitamin D (1,25-(OH)(2)D), is a natural immunoregulator with anti-inflammatory action. The mechanism by which vitamin D nutrition is thought to influence MS involves paracrine or autocrine metabolism of 25OHD by cells expressing the enzyme 1 alpha-OHase in peripheral tissues involved in immune and neural function. Administration of the active metabolite 1,25-(OH)(2)D in mice and rats with experimental allergic encephalomyelitis (EAE, an animal model of MS) not only prevented, but also reduced disease activity. 1,25-(OH)(2)D alters dendritic cell and T-cell function and regulates macrophages in EAE. Interestingly, 1,25-(OH)(2)D is thought to be operating on CNS constituent cells as well. Vitamin D deficiency is caused by insufficient sunlight exposure or low dietary vitamin D(3) intake. Subtle defects in vitamin D metabolism, including genetic polymorphisms related to vitamin D, might possibly be involved as well. Optimal 25OHD serum concentrations, throughout the year, may be beneficial for patients with MS, both to obtain immune-mediated suppression of disease activity, and also to decrease disease-related complications, including increased bone resorption, fractures, and muscle weakness. SN - 0954-3007 UR - https://www.unboundmedicine.com/medline/citation/15054436/Multiple_sclerosis_and_vitamin_D:_an_update_ L2 - http://dx.doi.org/10.1038/sj.ejcn.1601952 DB - PRIME DP - Unbound Medicine ER -