The immune system attacks itself, instead of the invader, causing a strain on white blood supply, and greatly increases the inflammation. This can cause a GI trac infection that spreads. Routine Supplementation of Immune vitamins, Rosehip seed tea, magnolia bark extract, and Chaparral will stop this genetic transcription error in the DNA. Once your immune system is regulating correctly, fighting your infection is easier. I would take up to 4 capsules of magnolia bark, 4 cups of rosehip seed tea, and 2 capsules of Chaparral, twice a day. Very Very Powerful. Also keep in mind that Stinging Nettle root robs fungus of chitin. The stuff that makes the shell of the fungus, up to 6 caps per day really weakens fungal infections.
33% of people have the defective Gene.
Psora goes back thousands of years.
Look up Psora, it is just now receiving some attention.
One of Psora body types biggest problems is in the behavior of FXR, the regulation of ornathine, and the removal of ammonia from the body.
FXR Farnesoid x receptor:
The bile acid receptor (BAR), also known as farnesoid X receptor (FXR) or NR1H4 (nuclear receptor subfamily 1, group H, member 4) is a nuclear receptor that is encoded by the NR1H4 gene in humans.
It plays roles in:
FXR is expressed at high levels in the liver and intestine. Chenodeoxycholic acid and other bile acids are natural ligands for FXR. Similar to other nuclear receptors, when activated, FXR translocates to the cell nucleus, forms a dimer (in this case a heterodimer with RXR) and binds to hormone response elements on DNA, which up- or down-regulates the expression of certain genes.
One of the primary functions of FXR activation is the suppression of cholesterol 7 alpha-hydroxylase (CYP7A1), the rate-limiting enzyme in bile acid synthesis from cholesterol. FXR does not directly bind to the CYP7A1 promoter. Rather, FXR induces expression of small heterodimer partner (SHP), which then functions to inhibit transcription of the CYP7A1 gene. In this way a negative feedback pathway is established in which synthesis of bile acids is inhibited when cellular levels are already high. FXR has also been found to be important in regulation of hepatic triglyceride levels. Studies have also shown the FXR to regulate the expression and activity of epithelial transport proteins involved in fluid homestasis in the intestine, such as the cystic fibrosis conductance transmembrane regulator (CFTR)
Farnesoid X receptor has been shown to interact with:
Peroxisome proliferator-activated receptor gamma coactivator 1-alpha and
Retinoid X receptor alpha.
Demand for immune stability is enhanced using:
The Farnesoid X Receptor (FXR) is a member of the nuclear receptor superfamily of ligand-activated transcription factors, which plays crucial role in bile acid, cholesterol, lipid and glucose metabolism, as well as in the development of atherosclerosis, intestinal bacterial growth and liver regeneration. FXR is also involved in the pathogenesis of cholestatic diseases, non-alcoholic fatty liver disease and inflammatory bowel disease. Recent evidence further suggests a key role for FXR in apoptosis and cancer. Notably, FXR deficiency promoted intestinal inflammation and tumorigenesis, suggesting that FXR activation might be a promising strategy in the treatment of colon cancer. FXR deficiency in mice led to the development of spontaneous hepatocarcinomas, while FXR inhibition might represent a novel therapeutic approach in Barett's esophagus. In Breast Cancer cell lines, FXR agonists down-regulated the Breast Cancer target gene aromatase. FXR inhibited Leydig tumor growth and progression, supporting evidence that FXR may be an important regulator of androgen homoeostasis. Further studies are required in order to establish possible antitumor effects of this nuclear receptor. Either reactivating or inhibiting FXR expression may represent promising therapeutic strategies in the treatment of certain types of human cancer.
The farnesoid-X receptor (FXR), also known as the chief regulator of bile acid metabolism, is thought to play a role in some hepatobiliary and gastrointestinal disorders. In a study published in The American Journal of Pathology, researchers demonstrated dysfunctional intestinal FXR-signaling in a rat model of cholestatic liver injury, accompanied by intestinal bacterial translocation (BTL) and increased permeability and inflammation.