Thanks for the replies folks. I see this thread has some real entertainment potential and 20 mg/day of oxandrolone has been studied and associated with mild hepatic effects:
https://www.physiology.org/doi/full/10.1152/japplphysiol.00808.2003
Seems like oxandrolone’s reputation for “mildness” is related to dosage and individual’s genetic response. Running 50-100 mg/day of oxandrolone probably ain’t gonna give the same result as 20 mg/day so just wanted to daylight the obvious. I don’t think anyone is doing histology on the kidneys while trial participants are running oxandrolone but perhaps that’s another place to look.
I was just genuinely curious why oxandrolone is dispensed from legitimate pharmacies via troche when its oral (delivery via digestive system) bioavailability is so high. Seems like a hammer in search of a nail. What was I missing? Hence I thought about avoiding liver damage. But, just because the drug doesn’t get delivered to liver/circulation via portal system doesn’t mean it can’t come back to the liver/kidney via serum for additional metabolism. Seems to me a troche’s strength is to get molecules (which have low oral bioavailability) into circulation by increasing bioavailability (avoid digestive system) and not to minimize end-organ metabolism damage. I can’t find an example of the latter in the literature.
Now, with regard to the delivery systems mentioned by you guys, would be an interesting experiment to test these different delivery modes on CMP/SHBG, lipids (hepatic lipase etc.). Appears to be a challenge for some to keep serum T levels reasonable (even with exogenous T usage) while also running oxandrolone since SHBG heads toward zero.
CONCLUSIONS: Patients had erectile dysfunction in association with low testosterone and SHBG, in spite of exogenous testosterone replacement. Discontinuation of oxandrolone led to the normalization or improvement of testosterone levels in all three patients with symptomatic improvement in one patient. First pass metabolism of orally administered oxandrolone may decrease hepatic synthesis of SHBG, allowing exogenously supplied testosterone to be excreted. Further work is necessary to elucidate the relationship.
I understand you guys may not be concerned with oxandrolone’s safety in particular, but think about this concept with respect to other hepatotoxic 17-AA AAS as @iron_yuppie mentions and ability to decouple anabolic effect from SHBG hit, significant hepatic lipase rise which ain’t good for some vulnerable populations. Wishful thinking, theory vs practice? I admire your ruthless efficiency @zeek1414.