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Active form of vitamin D directly protects the blood–brain barrier in multiple sclerosis – Aug 2017

Clinical and Experimental Neuroimmunology, First published: 22 August 2017, DOI: 10.1111/cen3.12398
Shiori Takahashi, Toshihiko Maeda, Yasuteru Sano, Hideaki Nishihara, Yukio Takeshita, Fumitaka Shimizu, Takashi Kanda

Objectives
The active form of vitamin D, 1α,25-dihydroxyvitamin D3 (1α,25-[OH]2D3), is reported to have protective effects for multiple sclerosis (MS), but the precise mechanisms of this effect on MS remain unclear. We hypothesized that 1α,25-(OH)2D3 has protective effects on the blood–brain barrier (BBB) in MS.

Methods
The expression of vitamin D receptor in a human brain microvascular endothelial cell line (HBMEC) was examined. The effects of 1α,25-(OH)2D3 on HBMEC after stimulation with tumor necrosis factor-α were observed. In addition, we assessed the effects of sera from MS patients, including those in the acute and stable phase of relapse–remitting MS or secondary progressive MS, on the BBB property in the presence or absence of 1α,25-(OH)2D3.

Results
HBMEC were found to express the vitamin D receptor at both the mRNA and protein level. Pretreatment of HBMEC with 1α,25-(OH)2D3 attenuated the decrease of zonula occludens-1 and claudin-5, and the increase of intercellular adhesion molecule-1 (ICAM-1) induced by tumor necrosis factor-α. In addition, nuclear factor kappa B activation mediated by tumor necrosis factor-α was decreased after incubation with the activated vitamin D. Furthermore, incubation with 1α,25-(OH)2D3 attenuated the increase of vascular cell adhesion molecule-1 and anti-phospho-nuclear factor kappa B in HBMEC after exposure to sera from patients with relapse-remitting MS and secondary progressive MS, and restored the decrease of zonula occludens-1 and claudin-5 in HBMEC after incubation with sera from the acute phase of relapse–remitting MS patients.

Conclusions
Treatment with 1α,25-(OH)2D3 prevents BBB disruption caused by both relapse–remitting MS and secondary progressive MS sera through upregulation of tight junction proteins and downregulation of cell adhesion molecules in HBMEC, suggesting that 1α,25-(OH)2D3 might have the direct protective effects on the fragile BBB in MS patients.

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Normally Vitamin D is activated in the body (by kidneys and paracrine system)
The activated vitamin D apparently helps protect the blood-brain barrier from MS
One excellent treatment for MS is to get lots of Vitamin D, which would result in getting much more BBB protection

Getting Vitamin D into your body shows many ways

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Note

There are 10 sources of vitamin D
Note: Magnesium and Omega-3 both increase the active vitamin D getting to the cells
Reasons for low response to vitamin D ~40 reasons as of Aug 2017

Searched PubMed for “vitamin d” “blood-brain barrier” Aug 2017, here are 2 of the results

See also VitaminDWiki

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