by Ed Barillas, Staff Writer
Around all the campfires it is known that 17-alpha alkylated steroids are liver toxic. There are, however, various opinions about the whys and hows and it all basically boils down to the person using the steroid, the steroid being used, dose and duration of use. The most common toxicity experienced is intrahepatic cholestasis, which is an occurrence where bile flow is stopped when oral anabolics enter the liver. The aftermath is that bile is released into the small intestine where its main job is to assist in the absorption of fats and fatlike substances. This blockage stops the bile salts from being released into the bile duct, which causes a buildup inside the hepatocyte. This occurring buildup becomes toxic to the hepatocytes. One ill effect is that it causes jaundice, which is a yellowing of the eyes and skin and is kin to cholestasis. This happens because bilirubin, which is a derivative of red blood cell breakdown, is usually eliminated through the bile. This is clinically categorized as, bland cholestasis since inflammation is not present and is completely reversible when the drug causing the problem is no longer used.
Aside from cholestasis, there are other ill side effects such as hepatic adenoma and peliosis hepatis – the onset of blood filled cavities in the liver. This is very rare and many believe that peliosis hepatis is caused because of liver blood outflow obstruction at the junction of centrilobular and sinusoids veins. Many also believe that with AAS users, the blockage happens because of the prolapse of hyperplasic hepatocytes into the hepatic venule wall, which is good because if cholestasis can be avoided then so can peliosis hepatis. The occurrence of Hepatic adenoma is very rare and happens only after months or years of constant use.
The liver had many crucial functions in the body but its main function is to metabolize drugs and secretions and excretions of bicarbonate and bile salts for digestion. When testosterone has been orally ingested, it is absorbed in the small intestine and is carried to the liver by way of the portal vein where it is metabolized to a 17-keto steroid by the enzyme 17-hydroxy steroid dehydrogenase. This interaction is very fast, and only when high levels of testosterone are ingested does the enzyme system get super saturated, which permits some of the testosterone to get by unchanged.
The conversion of 17-hydroxy to 17-keto is prevented with these types of steroids. This is crucial since the basic difference between 17-aa/s and a regular steroid is that one retains a free 17 hydroxyl group and the other does not when passing through the liver. 17-aa’s are toxic because the free hydroxyl is permitted to merge with glucuronic acid which creates a D-ring 17-glucuronide. It is important to note here that it is not the 17 (a steroid that is liver toxic ) but rather the 17-glucuronide metabolite and its metabolizing process which causes them to be toxic.
This can also be attributed to non-alpha alkylated steroids, 17-alpha alkylated, estrogens and androgens.
So after all this harm that can be done to the liver by these substances, what drugs can be considered liver friendly? Well take oxandrolone, which is another orally adminstered C17 alpah-alkylated AASs. The main part of oxandrolone confers a resistance to liver metabolism and marked anabolic activity. Its also good to note that oxandrolone does not show the dramatic hepatotoxic results like jaundice, hepatis, neoplasms, hyperphasias, and cholestatic which is blamed on C17 alpha-alkylated AAS’s’. One could say that its resistance to 17-glucuronidation (metabolism) is the reason for its not being toxic.