Type: Abstract presentation
Presented by: Trevor Marshall, PhD
Conference: Days of Molecular Medicine 2006
Location: Karolinska Institute
Date: 2006
Additional content: PDF of Poster
The VDRThe Vitamin D Receptor. A nuclear receptor located throughout the body that plays a key role in the innate immune response. Nuclear ReceptorIntracellular receptor proteins that bind to hydrophobic signal molecules (such as steroid and thyroid hormones) or intracellular metabolites and are thus activated to bind to specific DNA sequences which affects transcription. is at the heart of the human innate immunityThe body's first line of defense against intracellular and other pathogens. According to the Marshall Pathogenesis the innate immune system becomes disabled as patients develop chronic disease., responsible for TLR2A receptor which is expressed on the surface of certain cells and recognizes native or foreign substances and passes on appropriate signals to the cell and/or the nervous system., TLR4, CAMP TACO and IL2 expression [1]. During Th1 immune challenge, the VDR is activated by the endogenous secosteroid 1,25 dihydroxyvitamin D. We have previously described how intra-phagocytic bacterial pathogens are responsible for much chronic inflammatory disease [2,3], and our phase 2 study results have confirmed this pathogenesis. In order to induce recovery from chronic inflammatory disease, it is necessary to restore VDR function by removing all exogenous sources of the secosteroid we call ‘Vitamin-D,’ and dampen down over-exuberant VDR activity, for example with the ARBA drug which is an angiotensin receptor blocker. One of the ARBs is olmesartan (Benicar). Not all ARBs activate the Vitamin D Receptor. OlmesartanMedication taken regularly by patients on the Marshall Protocol for its ability to activate the Vitamin D Receptor. Also known by the trade name Benicar. [1]. This enables the immune system to recognize the pathogens.
RESULTS: To date we have demonstrated recovery from Hashimoto’s Thyroiditis, Rheumatoid Arthritis, Sarcoidosis, and an assortment of chronic inflammatory diagnoses. This breakthrough is the result of a collaboration between molecular scientists and a disparate group of innovative physicians, facilitated by the Internet. However, the widespread application of this pathogenic understanding will require meticulous translation of the molecular science into conventional clinical precepts.