what an unfortunate series innacuracies.
1. people report suppressed libido because of suppressed oestrogen
2. people get gyno because they are using superdrol and other "designer steroids" which are mostly progestins which do not aromatize, using an AI with progestin is not all that useful. Some of these compounds may also have oestrogenic metabolites from sulfation and downstream of 5alpha reduction. also the oral bioavailability issues and the fact that one entire batch of rebound XT was not actually ATD, but instead an incomplete synthesis may have played roles in other cases.
3. homosexual preference among rats is common with all aromatase inhibitors.
4/5. it is nearly retarded logic to assume that because aromatase inhibition in rats causes homosexual preference that it will cause libido problems for the same reason.
6. AGAIN, reduced libido is a normal side effect of significant oestrogen suppression.
7. this study was done prior to the understanding of the impact of aromatase inhibitors, hence some very erroneous conclusions are made, both aromasin and ATD bind to the AR at .2% affinity of DHT as would your 17 hydroxylated and methlyated version, though affinity might be different it would still bind without activity. Now how effective it would bind to aromatase is another question, one which there is no data on. Unless you would like to provide it.
as a note- many of these studies used silastic implants which deliver ATD to the brain, hence very significant oestrogen suppression in the brain. With oral(250mg at 3 times per day), injected and transdermal suppression of oestrogen plasma oestrogen is comparable to aromasin. between 90-95% of plasma oestrogen suppression.