Matsuo Munefusa.
Bluelighter
There is a myth within the bodybuilding community that nolvadex, what could be termed a synthetic estrogen or an estrogen blocker (selective estrogen receptor modulator, ie SERM) depending on the perspective, can increase PGR activation when used in conjunction with progesterone AAS (ie trenbolone, nandrolone). The myth holds that using tamoxifen with nandrolone or trenbolone will worsen gyno symptoms.
I'd like in this post to point out why this myth was started and why this myth is false. I'd also like to add anecdotal information of my own at the end.
There were a few studies of tamoxifen noting how this drug increased PGR activation. [somebody have time to find these studies search pubmed: tamoxifen estrogen agonist endometrium].
The flaw is that tamoxifen is a mixed agonist/antagonist. In endometrial tissue (ie the cells of the uterus) the drug is an agonist, meaning it activates the estrogen receptor in similar way that estrogen itself does. Big surprise, there are estrogen receptors in the lining of the uterus! Also PGR receptors. Activating estrogen receptors is important cascade step in activating PGR receptors. Remember, no activation of estrogen receptors means no activation of PGR.
In breast tissue however, the drug is an antagonist, meaning it 'blocks' the receptor from being activated (by estrogen or an analogue). This is why the drug is primarily used to treat breast cancer in women (as well as for our purposes). If the estrogen receptor is blocked in breast tissue then the PGR receptor will not be activated despite the presence of progesterone AAS such as nandrolone (deca, NPP).
treatment for any type of gyno symptoms should include nolvadex therapy. Estrogen levels should be controlled by an aromatase inhibitor as a first line defense.
I'd like in this post to point out why this myth was started and why this myth is false. I'd also like to add anecdotal information of my own at the end.
There were a few studies of tamoxifen noting how this drug increased PGR activation. [somebody have time to find these studies search pubmed: tamoxifen estrogen agonist endometrium].
The flaw is that tamoxifen is a mixed agonist/antagonist. In endometrial tissue (ie the cells of the uterus) the drug is an agonist, meaning it activates the estrogen receptor in similar way that estrogen itself does. Big surprise, there are estrogen receptors in the lining of the uterus! Also PGR receptors. Activating estrogen receptors is important cascade step in activating PGR receptors. Remember, no activation of estrogen receptors means no activation of PGR.
In breast tissue however, the drug is an antagonist, meaning it 'blocks' the receptor from being activated (by estrogen or an analogue). This is why the drug is primarily used to treat breast cancer in women (as well as for our purposes). If the estrogen receptor is blocked in breast tissue then the PGR receptor will not be activated despite the presence of progesterone AAS such as nandrolone (deca, NPP).
treatment for any type of gyno symptoms should include nolvadex therapy. Estrogen levels should be controlled by an aromatase inhibitor as a first line defense.
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