"ME, my bed, and I"

Borrowed from a new friend on myspace, whose site is a "ME-CFIDS-PVFS-FMS-MS-RA-Lyme-Lupus and related diseases support page". She goes by the name "ME, my bed, and I". I asked her if I could borrow this since so many of us Cushing's and post-op Cushing's patients are Vitamin D deficient. She graciously agreed:

Vitamin D metabolism and Th1 inflammation1,25-D is manufactured in the cytoplasm of Th1 activated macrophages by enzymatic conversion of 25-D to 1,25-D. The P450 enzyme involved is CYP-27B1, and the conversion occurs in the mitochondria of the activated macrophages. This conversion is catalysed 30-fold by the presence of Interferon-gamma, the cytokine characteristic of a Th1 immune reaction. The mitochondria do not have significant quantities of the enzyme CYP-27A1, which is necessary for 1,25-D to be produced directly from 7-dehydro-cholesterol, which is most probably the pathway that the body preferentially uses when one is isolated by geography or season from ingesting food with Vitamin-D in it. The Vitamin D ingested is converted to 25-D, and it then directly fuels the out-of-control production of 1,25-D in the mitochondria of the Th1 activated macrophages. Production of 25-D when exposed to sunlightThe keratinocytes of the skin can, by comparison, make 1,25-D directly from 7-dehydro-cholesterol, and they do this when exposed to sunlight. Because the final stage of this reaction is also catalyzed by any Interferon-gamma from any inflammation paracrine to the keratinocytes, any and all 25-D which is made from sunlight is energetically converted to 1,25-D (OK, well, NEARLY all ). Thus sunlight is not usually a significant contributor to the 25-D levels of Th1 patients. It is ingested Vitamin D which primarily fuels the over-production of 1,25-D in activated macrophages, and which exerts the immunosuppressive action upon the host. Ipso facto, when 1,25-D is elevated because a Th1 patient is ingesting Vitamin D, the immune system cannot kill the intraphagocytic bacteria, there is less cytokine release, and the patient feels better and may even become less symptomatic - in the short term. Of course, as far as we know, the bacteria are now (slowly, chronically) multiplying, unhindered, in the cytoplasm of the phagocytes. Dr. Trevor Marshall, PhDMacrophages also produce Vit. D in response to UV light (not just keratinocytes) 4/9/2007UVB-induced 1,25(OH)2D3 production and vitamin D activity in intestinal CaCo-2 cells and in THP-1 macrophages pretreated with a sterol Delta7-reductase inhibitor."In conclusion, preconfluent CaCo-2 cells and THP-1 macrophages are able to induce vitamin D activity upon UVB irradiation and hence combine all parts of the vitamin D photoendocrine system, a characteristic which is therefore not keratinocyte specific."Fish make Vitamin D in the absence of UV light See for example "Cloning of a functional vitamin D receptor from the lamprey (Petromyzon marinus), an ancient vertebrate lacking a calcified skeleton and teeth"http://endo.endojournals.org/cgi/content/full/144/6/2704I personally believe that UV light is not necessary for for Homo sapiens either. Mankind has been hung up on the "sunshine" concept, and has not gone looking for the enzyme which allows the electrocylic cleavage of the sterol ring. So they haven't found itStandard human logic has failed to understand the steroidal nature of Vitamin D. Biologists are now publishing an average of one paper a day describing the steroidal actions of Vitamin D. But nobody in clinical medicine seems to notice. (VDR pubmed results)..Trevor..Read more on the Vitamin D Tutorial at the Marshall Protocol Study Site