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
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.
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.
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.
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.
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
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
- Serotonin regulated by Vitamin D – part 1 autism – Feb 2014 which is in VitaminDWiki
- Multiple sclerosis and air pollution exposure: Mechanisms toward brain autoimmunity March 2017
“However, recent evidence suggests that major mechanisms involved in MS pathogenesis, such as inflammatory factors expression, free radicals overproduction, the blood brain barrier (BBB) breakdown . . . “
Publlisher wants $36 for the PDF
- Multiple Sclerosis: number needed to treat with vitamin D may be as low as 1.3 – Meta-analysis Oct 2013
- Vitamin D has already cleared 100 percent of lesions from over 1,000 MS patients in Brazil
- Multiple Sclerosis more likely if poor vitamin D genes - 22nd study – Aug 2017
- Multiple Sclerosis suppressed by an Ultraviolet wavelength not associated with Vitamin D (mice) – Nov 2016