liver enzymes will recover pretty drastically after the discontinuation of any methyl steroid... Even after a cycle of superdrol, most pple's liver enzymes recover within 4-6 weeks
Blood work taken while "on" cycle would def be the best indicator of how liver toxic the epithio compound really is... but that being said it's still good to know that after 3 weeks, levels return to the normal range
however, I find it hard to believe that the hepatoxicicity of superdrol compares to that of epistane
And as for the post about Nolva being hepatoxic... that claim is highly exaggerated IMO, i'v had bloodwork several times only days after discontinuing nolva and haven't had elevated liver enzymes as a result
From an article which I found very interesting...from another forum but the Dr.Skeptik said he has researched Nolvadex for 25 years...
"Schwarzenegger wrote:
Nolvadex is metabolized by the liver, so it can cause hepatotoxicity. However, nolvadex has been shown to protect against alcohol-induced liver damage and estrogen-related hepatic injury (think xeno-estrogens, etc.) I'd say it's pretty safe within the bounds of it's prescribed dosing range. There's no interaction with alcohol or AAS. The only real danger would be huge doses and prolonged exposure, much as anything else that would cause permanent liver damage. I can't give an estimate of what this number could be, but I'm sure you wouldn't reach it with typical bodybuilding use.
Dr. Skeptik wrote:
Not quite.
Tamoxifen is the most studied drug ever released. There is about 50 million patient years of experience--in studies--in women for guidance.
Historically, liver dysfunction was most reported in Scandinavia in the early 1970's; but there the standard dose was 40 mg per day, rather than 20 mg which became standard in the early 1980's. On that dose, liver dysfunction is exceedingly rare.
Other points:
The tamoxifen protective effects are seen in rats and mice which have a different metabolism of it than do humans. I would not count on a hepato-protective effect.
Liver dysfunction occasionally associated with tamoxifen may be due to fattly liver, or "non-alcohol steatic hepatitis (NASH)" It may not be causative, but permissive; i.e., it uncovers the metabolic tendency toward NASH in middle-aged women. (And cirrhosis due to tamoxifen must be so rare as to be reportable.)
Prolonged dosing does not increase the risk of liver dysfunction.
But you are correct: doses of 20 mg per day in men is almost as safe as a peanut butter sandwich, and probably safer than tylenol with beer.
Contrary to Schwarzenegger's objection,just because something is metabolized in the liver does not predict that it is hepatotoxic. Direct hepatotoxicity is exceedingly rare and I offered the explanation from the Scandinavian experience.
Dysfunction, or steatosis, does not seem to rise in incidence after the first 6 months; this rare finding is not a cumulative risk over time, but it is sporadic, and may be influeced by diet and lipid levels. (The data are available from randomized trials of tamoxifen taken for 5 years versus 10 years.). And while there may be greater authorities in SERM pharmacology, I have been involved in this research for 25 years."
I find this quite interesting to say the least...what do you guys think???