Here perhaps is what is actually going on.
Peroxides irreversibly inhibit the VDR. So if the VDR is inhibited
you can take all the Vitamin D you want, and have high serum vitamin D level
but, its action will be inhibited due to lack of VDR.
http://www.jbc.org/content/277/15/13294.full.pdf
From this paper below we see what is going on in UC and Crohns where the VDR is low in gut tissue, regardless of vitamin D serum status.
So knocking down peroxides with R Lipoic acid,Butyrate and anything else that
can knock down peroxides, will allow for VDR upregulation,then also take
Vitamin D.
Old Mike
http://www.jci.org/articles/view/65842
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