Movin_weight
Active member
I see what you're saying here Movin'. I'm still having a hard time grasping the increase in est receptor sites in an area that it is antagonist to. (I'm a chemist NOT an MD)![]()
I'm going to throw this to a couple Doc's to get there response/explanation and I'll be sure to throw it over here.
I'm gyno prone myself. First cycle Dbol back in the 80's with no gyno. Pushed the envelope on the second cycle with double dosing and WHAM, gyno left nip.(No post cycle therapy back then.)
Then the 90's with PH's... 19Nor 5diol great size, but off cycle WHAM gyno right nip.
Year 2007- Now I'm on Epi and seeing a decrease(not elimination) in gyno and sensitivity with GREAT gains. Going into post cycle therapy soon with above mentioned SERMS to choose from.
This cycle was completely based on gyno response with PH used. Epi seemed to have the best results as far as gyno goes, so I jumped on this train. Now to avoid the gyno during and after PCT....
Yeah that would be good to here somethin straight from a doc... I just read alot and anylyze what i read to the best of my ability so it should all be taken for piece of mind more than anything since i am not an MD either.
however when i say an increase in receptors i do not mean that the drug itself increases receptors in the breast area.
You are 100% correct that SERMs are antagonists in breast tissue which means that they block or depress the actions of the estrogen receptor sites in breast tissue plain and simple
However the human body is extremely complex and versitile and whenever an external drug is introduced to the body, the body has a reaction to maintain it's homeostasis
The body does not want something to come in and block all it's estrogen receptors in breast tissue, as this does not maintain the natural balance of hormones... so in reaction to the drug doing this, the body increases receptors in order to try and give the estrogen somewhere to bind... basically it then becomes a foot-race between the SERM and estrogen as to who reaches the receptor first, and with high doses the SERM will usually win (unfortunately i have failed to find studys that have been done regarding this action, but we are talking about a drug that was used to block estrogen in cancer cells, not neccessarily to cure gyno or come off a cycle)
But this is also why we taper off SERMS, so the body gradually allows the binding of estrogen to return to normal without a big surge in estrogen binding (what we call rebound) even with the long half life of SERMs of you go from taking 60mg ed to nothing, your going to experience some serious issues
Another example of the body trying to maintain homeostasis is when we take androgens/steroids... the bodys reacts to these drugs by shutting down natty test production... and then eventually if the drugs are taken for a long period of time, the body will down-regulate androgen receptors which is why we don't continue to see gains for an infinite amount of time