“Note: Contrary to finasteride, which is highly selective for the type II isoform of the 5-ar enzyme, dustasteride, which has been found to reduce circulating DHT levels by >90% is a pan-5-ar inhibitor. It is thusly no wonder that 0.5mg/day of dustasteride prevented the increase in lean mass in female-to-male transsexuals who were treated with 1,000mg testosterone-undeconate for 54 weeks (Meriggiola. 2008).
Although testosterone and not DHT appears to be the major hormonal driving force of actual increases in muscular size (not strength!), the results of the Meriggiola study, where the total (>90%) blockade of all three of the 5-ar isoforms by dustasteride (see red box, above) inhibited the muscle-building effects of 1,000mg testosterone-undeconate clearly suggest that the reduction of at least small amounts of testosterone to dihydrotestosterone is a necessary prerequisite for the testosterone-induced increases in lean muscle mass. Whether a critical threshold as for circulating DHT levels exists, or whether it was the dustasteride induced blockade of the local reduction of testosterone to DHT by 5-ar type III right in the skeletal muscle that was responsible for this effect will yet have to be established in future studies.”
I maintain the belief that this condition can be treated with Dihydrotestosterone AND Testosterone, I have yet to hear of anyone on here who has used both together. Also, Dihydrotestosterone used long term with Testosterone, at least for 6 months to a year in non-responsive individuals. I came upon the above study doing some research tonight, since so little is written about Avodart (and I am only 2 weeks off and it has a 5 weeks half-life, second longest half life of any drug).
The only research I have found with significance is the above study done on transsexuals, often Avodart is used for female to male transsexuals (I can see why). I maintain the view that we are genetically pre-disposed to respond to these drugs stronger than others. The key to a treatment to this disorder lies with designer DHT drugs, designer DHT drugs work differently than DHT and through a different pathway than DHT. So for those who do not respond to DHT, they may respond to a synthetic DHT, anyone have any thoughts?