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ConkerTheKing
New member
Which is the stronger hpta feedback loop, estrogen receptors not being activated or androgen receptors being activated?
I'm running Formestane at the moment as a standalone aromatise inhibition cycle, to try and optimise my relatively poor T:E ratio. Essentially, I share the same concern that many others do over the possibility of formestane being suppressive.
It got me thinking though - which is the stronger feedback loop in the brain? Formestane is a fairly powerful AI, so it's going to knock out a significant amount of estrogen. This would normally result in HPTA UP regulation. However, as it also coverts to 4-HT, an androgen, it has been suggested that it could also suppress the HPTA by activating enough androgen receptors that the hypothalamus would presume there's too much testosterone being naturally produced.
So if you're in a situation in which aromatase is being inhibited enough to tell the HPTA to make more testosterone so that it can be aromatised, but enough androgen receptors are being activated to tell the HPTA to make less testosterone, which signal is going to "win"? Will the ultimate result be up or down regulation? Does the body consider it more important to avoid having too much testosterone or to avoid having too little estrogen?
I'm running Formestane at the moment as a standalone aromatise inhibition cycle, to try and optimise my relatively poor T:E ratio. Essentially, I share the same concern that many others do over the possibility of formestane being suppressive.
It got me thinking though - which is the stronger feedback loop in the brain? Formestane is a fairly powerful AI, so it's going to knock out a significant amount of estrogen. This would normally result in HPTA UP regulation. However, as it also coverts to 4-HT, an androgen, it has been suggested that it could also suppress the HPTA by activating enough androgen receptors that the hypothalamus would presume there's too much testosterone being naturally produced.
So if you're in a situation in which aromatase is being inhibited enough to tell the HPTA to make more testosterone so that it can be aromatised, but enough androgen receptors are being activated to tell the HPTA to make less testosterone, which signal is going to "win"? Will the ultimate result be up or down regulation? Does the body consider it more important to avoid having too much testosterone or to avoid having too little estrogen?
