Vitamin D and multiple sclerosis

Colleen E. Hayes, Faye E. Nashold, Christopher G. Mayne, Justin A. Spanier, Corwin D. Nelson

Research output: Chapter in Book/Report/Conference proceedingChapter

11 Scopus citations

Abstract

Multiple sclerosis (MS) is a genetically and immunologically complex neurodegenerative disease that often strikes in young adulthood and causes significant disability in individuals who are afflicted. Although there is no doubt that genetic risk factors and other environmental factors contribute to MS etiology, the evidence supporting an inverse association between vitamin D3 and MS risk and severity is sufficiently strong and diverse to nearly satisfy the criteria for asserting that a causal relationship exists between insufficient vitamin D3 and MS disease risk and severity. Vitamin D3 and MS hypothesis provides a coherent explanation for several puzzling facts of MS natural history and biology in women. Specifically, this hypothesis provides some explanation as to why the disease course commonly shows a relapsing-remitting pattern that later becomes progressive, why there is a rapidly increasing female sex bias, and why the disease remits during pregnancy. Seasonal fluctuations in UVL and vitamin D supplies in high latitude regions may contribute to the relapsing-remitting pattern. Moreover, the emerging concept of synergy between the vitamin D3 and E2 endocrine systems suggests that increasing prevalence of vitamin D insufficiency may adversely affect women more than men, contributing to the growing female sex bias. The increases in estriol and 1,25(OH)2D3 during pregnancy may reduce MS disease activity, whereas the decreases in E2 production at menopause may undermine the vitamin D3 protective effects and accelerate MS disease. These insights are banked upon to suggest new approaches to alter the MS disease course in women.

Original languageEnglish (US)
Title of host publicationVitamin D
PublisherElsevier Inc.
Pages1843-1877
Number of pages35
ISBN (Print)9780123819789
DOIs
StatePublished - 2011
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2011 Elsevier Inc.

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