interesting, can you elaborate a bit on your theories of how masteron relates with estrogen in the body ?
Im not referring to a theory at all. Back in the 1970s before the development of hormone receptor technology it was noted female breast CA patients fared better than controls when Masteril was used. Why? Well it the responsible mechanism was thought to be Mesteron's ability to bind and antagonize the E-2 receptor. After all that must be the ONLY receptors in female breast tissue, right? NOT
All that made sense then BUT now it's well known female breast tissue has MANY hormonal ligands including E-2, TT AND DHT receptors.
Moreover its also been established there's a dichotomy of sorts in the forms of hormonal therapy which may be used to "treat" breast CA. One can either bind /antagonize the E-2 foci, bind an agonist to the TT or DHT receptor or a combination of the two.
Having said that, E-2 antagonists therapy has been proven more effective than TT agonism treatment, overall.
Sorry about the digression, so the bottom line is THE REASON BREAST CA PATIENTS IMPROVED ON MASTERON was it's agonist effect on the TT/DHT receptor, rather than it acting as an E-2 antagonist.
The latter is why some "bros" claim Masteron antagonizes the effects of E-2, lowering the need for AI's or SERMS.
Retrospectively it seems the researches in the 1970s completely ignored the more likely cause Masteron was benefical in breast CA patients, because androgenic side effects were a trite occurance in these patients and also the number one reason "AAS therapy" (w TT, Nandrolone, or Master) was discontinued.
regs
jim