The phenomenon specifically that is observed with 1-androstenes is a decrease in excretion of 17-keto steroids (inactive) and increased excretion of 17beta-hydroxyl steroids. This is either due to a shift in the 17beta-HSD equilibrium towards the formation of hydroxyl steroids, or to an inhibition of excretion of the hydroxyl steroids. Or maybe a combination of both. I dunno, for practical purposes it doesn't really matter what the mechanism is as long as the net result is that more 17beta-hydroxyl is formed.
True, but the efficacy isn't on trial here. Noone is going to deny 1AD is a powerful and effective hormone. Only trying to determine whether the urinary excretion can be an accurate measure for comparative oral activity, especially considering its arbitrary.
But I guess its futile to discuss these matters. Seems like matter for future studies. Thanx for answering though.