[/U] Correct! Perhaps your thinking, well how about this drug? Nope!
The effects of Ursadiol on patients with primary biliary cirrhosis (these unfortunate patients develop "scaring" of the bile ducts which allows the bile to accumulate) while initially encouraging, because it DID improve transaminase levels, does NOT effect mortality!
Is the frequency of AAS associated liver disease any higher than that of alcohol, I suspect not. However what we do know FOR SURE is the longer someone drinks and the more extensive the exposure the greater the likelihood of developing evidence of hepatic injury as evidenced thru elevated transaminase enzyme levels.
More importantly much like the genetic basis for alcohol related cirrhosis, there are those whom appear predisposed to severe liver injury with CHRONIC AAS exposure (based on case reports) consequently the notion of running a continuous "multi drug oral cycle" especially absent periodic enzyme assays is asking for trouble and must be avoided.
However as CBS (who is this guy anyway?) mentioned the hepatic insult occurs (or may be identifiable by increased enzymes) after a latent period of several weeks. This occurrence is not at all unusual with most hepatic toxins and still provides enough time to discontinue AAS use once detected. As an aside, any significant increase of bilirubin above the precycle baseline warrants an IMMEDIATE cessation of the offending agent!!!
Finally as many VETS have already mentioned most of this discussion is much to do about nothing primarily because the liver is our toxic waste dump and has a truly REMARKABLE capacity to heal itself, which is just another reason why hepatic supplements only add cost to an already expensive endeavor.
Best
jim
