Polyenylphosphatidylcholine + Tauroursodeoxycholic acid
There are many types of liver injury, but only one is normally associated with the use of oral androgens -- cholestasis. This condition is defined as a failure of normal bile to reach the duodenum, which may be due to a number of different pathological states between the hepatocyte and the ampulla of Vater. When one takes oral androgens (typically methylated at C17a) the physical structure of the hepatocyte is altered -- microfilaments and canaliculi become less contractile. Disruptions in the canalicular bile salt export pump may also occur. This leads to impaired bile flow and the retention of highly cytotoxic hydrophobic bile salts. At low concentrations, these retained bile salts cause apoptosis; at higher concentrations, necrosis and severe liver damage.
This is where AEGIS comes into the picture. It was designed with users of oral androgens in mind, and brings together the best anti-cholestatic ingredients available.
-Can prevent apoptosis during cholestasis. Toxic bile acids produce apoptosis Via fas- and TRAIL- death receptor mediated pathways. Both are, to some degree, dependent on the translocation of the 'bax' pro-apoptoic molecule from the cytosol of hepatocytes to the cell mitochondria. TUDCA prevents bax translocation, strongly stabilizes mitochondrial membranes, and activates the MAPK pro-survival pathway in hepatocytes. (1) These effects protect hepatocytes from bax-related apoptosis.
-Is a hydrophilic bile acid, and its presence markedly shifts the bile pool towards hydrophilicity, which, to some extent, detoxifies it. When used consistently, especially at pharmacological doses, TUDCA (along with UDCA) eventually becomes the predominant bile acid in the liver and in general circulation. (2)
-Directly stimulates bile secretion via modulating cellular signalling pathways in hepatocytes, such as ERK, src, PKC and others. These signalling pathways generally phosphorylate, or activate, the bile salt export pump (BSEP) and other processes involved in bile export/secretion. (For example, PKC-alpha-mediated secretion of HCO3-.) (3, 4, 5)
-Stabilizes cellular membranes and dilates bile canaliculi. This former effect has been shown to protect human cells from hydrophobic bile salt induced apoptosis (6), and the latter may serve to counteract the reduction in contractility seen in androgen-induced cholestasis. (7)
-Oral androgen administration may decrease hepatic Na+, K+-ATPase, Ca2+, Mg2+-ATPase and F-actin levels --- all of which may be restored, and even raised, by polyenylphosphatidylcholine administration. (8)
-Is secreted into bile by hepatocytes, where it serves as a major component of the micelles in which bile acids are emulsified. Increased levels of biliary phosphatidylcholine reduces the cytotoxicity of bile acids, whereas phosphatidylcholine-secretion impairment (as is often seen in ABCB4 disease) is characterized by extremely severe cholestatic liver disease. (9)
To summarize: Aegis is highly-potent, highly-specific liver protection for people taking hepatotoxic oral androgens. Superior protection cannot be bought, nor should it be needed.
Reduce steroid and drug-related toxicity.
Support optimal liver health and bile flow.
High-potency blend of two cytoprotective ingredients.
Ideal for people exposed to environmental toxins or hepatotoxic oral androgens.
- Reduce steroid and drug-related toxicity.
- Support optimal liver health and bile flow.
- High-potency blend of two cytoprotective ingredients.
- Ideal for people exposed to environmental toxins or hepatotoxic oral androgens.
BUY AEGIS NOW
1. Joana D. Ameral, Ricardo J. S, Viana, Rita M. Ramalho, Clifford J. Steer, and Cecília M. P. Rodrigues (2009), "Thematic Review Series: Bile Acids: Bile acids: regulation of apoptosis by ursodeoxycholic acid", J. Lipid Res, 50(9) 1721-1734. doi: 10.1194/jlr.R900011-JLR200
2. Trauner and Graziadei (1999), "Review article: mechanisms of action and therapeutic applications of ursodeoxycholic acid in chronic liver diseases". Aliment. Pharmacol. Ther, 13: 979–995. doi: 10.1046/j.1365-2036.1999.00596.x
3. Dieter Häussinger, Anna Kordelia Kurz, Matthias Wettstein, Dirk Graf, Stephan Vom Dahl, Freimut Schliess (2003), "Involvement of integrins and Src in tauroursodeoxycholate-induced and swelling-induced choleresis ", Gastroenterology,124(5), 1476-1487
4. Ulrich Beuer (1997), "Effects of Bile Acids on Hepatocellular Signaling and Secretion", YJBM, 70, 341-346
5. Frank Dombrowski, Bruno Stieger and Ulrich Beuers (2006), "Tauroursodeoxycholic acid inserts the bile salt export pump into canalicular membranes of cholestatic rat liver", Laboratory Investigation, 86, 166–174. doi:10.1038/labinvest.3700371
6. Häussinger D, Kurz AK, Wettstein M, Graf D, Vom Dahl S, Schliess F (2003), "Involvement of integrins and Src in tauroursodeoxycholate-induced and swelling-induced choleresis", Gastroenterology, 124(5), 1476-1487
7. Kolde G, Kessler E, Van Husen N, Themann H (1978), "Ultrastructural-morphometric analysis of polyenylphosphatidylcholine [PPC] treated cholestatic rat liver", Z Gastroenterol, 16(10), 625-639
8. Françoise Chanussot and Liliane Benkoël (2003), "Prevention by dietary (n-6) polyunsaturated phosphatidylcholines of intrahepatic cholestasis induced by cyclosporine A in animals", Life Science, 73(4), 381–392
9. Gonzales E, Davit-Spraul A, Baussan C, Buffet C, Maurice M, Jacquemin E (2009), "Liver diseases related to MDR3 (ABCB4) gene deficiency", Front Biosci., 14, 4242-425