I usually hang out in the UC forum, but occasionally post here.
I have a big thread on the radical induction theory time to re-visit.
Anyway here perhaps is what is really going on with Vitamin D,taken from my thread.
Old Mike
Peroxides strongly inhibit the VDR, if the VDR's are not working,then believe you can load up on as much vitamin D as possible but it will not activate the receptor.
http://www.jbc.org/content/277/15/13294.full.pdf
From the first paper I posted the VDR is knocked down by peroxides/inflammation.
From this paper we see what is going on in UC and Crohns where the VDR is low in gut tissue, regardless of vitamin D serum status.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3754241/
Important statement from the paper:
Epidemiological studies have shown that low vitamin D status is common in IBD. Since the major source of vitamin D comes from UV light–driven photosynthesis and dietary components, vitamin D is thought to be an environmental factor that might affect the development of IBD. Studies have suggested that high vitamin D intake is associated with a reduced risk of CD (35), and there are also reports that vitamin D can inhibit colitis in some animal models (40–42); however, whether vitamin D status plays a causative role in the pathogenesis of human IBD is unclear. In this study, we observed very low vitamin D status in one cohort of IBD patients (Shenyang) that did not use vitamin D supplementation and observed relatively normal serum vitamin D levels in another cohort (Chicago) that was routinely supplemented with vitamin D. These results neither include nor exclude low vitamin D status as a causative factor in human IBD. In fact, high serum 1,25-dihydroxyvitamin D status has been reported in a subset of CD patients (56). Future prospective studies are needed to address this issue more conclusively. Despite different serum vitamin D levels, one common feature of these two cohorts is a marked reduction of mucosal epithelial VDR expression. Thus, reduced VDR status in the lesion appears to be an intrinsic characteristic of IBD that is independent of serum vitamin D status. What drives down VDR expression remains to be resolved, but our ongoing preliminary studies suggest that local inflammation is a critical factor in VDR downregulation. In fact, few studies have examined VDR status in the IBD population, but the colonic VDR appears to directly linked to colonic inflammatory status.
Looks like butyrate can also be important.
http://www.ncbi.nlm.nih.gov/pubmed/25080448
also we can have a genetic risk, which might mean difficult to correct
http://onlinelibrary.wiley.com/doi/10.1002/ibd.22966/abstract
here is the complete thread,lots of info on free radicals and IBD
https://www.healingwell.com/community/default.aspx?f=38&m=3322927
Post Edited (Old Mike) : 6/9/2015 6:57:04 AM (GMT-6)