In that case, I hope Jacob will come out and defend his comment. He said "it does not activate the AR" and I am simply asking him how he came to that conclusion. Very simple question, asked without a personal attack or hidden agenda...
Of course you are not. I apologize if you feel you are being accused.
However, I am unsure if you are referring to or understanding "activating the AR" as I am. By "activating the AR" I am assuming you are referring to a genomic activation of the AR whereby an androgen binds to its associated receptor, resulting in transcription, mRNA synthesis, and the production of muscle-specific proteins.
However, I am assuming that is
not how you have understood the term! After reading the thread over, I believe you understand "activating the AR" to mean a suppression of natural testosterone production. When it was said it does not cause any natural suppression, and you continued with your line of questioning, I then assumed you understood "activating the AR" in the manner I described above; in the case of PRIME, this would result in PRIME being a SARM [selective androgen receptor modulator]. This, however, is a highly unlikely scenario, which is why I said:
We do not. However, we do know that it is not causing any hormonal suppression.
That was to say: "We cannot be sure that PRIME is not having some non-suppressive AR action, but suggesting anything of the like is mere conjecture. We do know through blood tests, however, that it is not suppressive in anyway."
I hope we are both on the same page here, as there seems to be some confusion. Hopefully this post has clarified the situation slightly; if it has not, hopefully you will clarify your use of the terms!
