What counts as elevated? The presence of oestrogen alone is perhaps enough? Anyway I think I've expressed my thoughts on gyno a few times, but for the record there can be no true consensus, because there is scarce (any?) controlled research into the condition in AAS using bodybuilders.
Many hormones are seriously out of normal alignment when using AAS, and in the periods of recovery. Not just in total, but their ratios, and their non-physiological fluctuations. We know that gyno is a complex condition that can be influenced by numerous hormones and growth factors and very likely their interaction as well. It's doubtful it's just about the behaviour of a single factor, whether it be androgens/DHT, oestrogen, prolactin, progesterone, IGF-1, GH or whatever.
Much cleverer minds than my own have chipped in with many different and seemingly robust models of gyno development in AAS users, but none of them are complete without clinical studies (and that won't happen), and some seem maybe a little myopic in scope. The fact that idiopathic gynecomastia can occur without elevations of oestrogen or progesterone is evidence enough that estradiol/oestrogen is evidently not the whole story. But they are well worth reading for their insights (eg Peter Van Mol has written quite a few times among others) and you can make your mind up yourself.
However, for most bodybuilders, it would appear that if you control oestrogenic activity at root, coupled with some strong androgenic (eg DHT) effect, you do control the gyno proliferation/differentiation/apoptosis. This has been anecdotally demonstrated a million times over, and I think quite rightly it's promoted as the first course of action for anyone with difficulties.
The time to accommodate other options is only when that appears to fail, perhaps because you're particularly susceptible to the effects of AAS activiting ER via AR, or because your aromatase activity is difficult to control (especially with increasing bodyfat), or more commonly when the side-effects of suppressing oestrogen become too severe (joints, lipids etc) and you can't tolerate stronger DHT-derived AAS. I'm sure there are probably a myriad of other reasons as well, many not yet fully understood.
But what this means in effect is that the automatic tendency to promote DA agonists (eg Caber/Prami) on any cycle with tren etc, is frowned upon because we tend to (rightly or wrongly) believe prolactin has its effect further up the chain in gyno promotion and development. DA agonists also have health-related side-effects that should be considered worse than suppression of oestrogen for the majority of men until the contraindicating factors I mentioned above have been experienced.
So, to summarise my thoughts:
(1) I am not a guru and I don't have the answers
(2) control oestrogen
(3) don't polypharmacy without good reason
(4) consider other meds only when you've exhausted the straightforward options
(5) once you know yourself, use what works for you
(6) don't pretend it's a binary right-wrong, yes or no thing and that we/you have all the answers*
*which is the hardest thing to write on bodybuilding forums, since the IQ is sometimes low and the desire for simple answers that soon become parroted fact high
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