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ConkerTheKing
New member
Clomid is the go-to drug for guys intending to restart their HPTA after it has been shut down for one reason or another. It does this apparently by binding to estrogen receptors in the hypothalamus itself, or perhaps in the pituitary gland (several studies have failed to reach a consensus on which is responsible).
Unusually, Clomid inhibits estrogen activity at both estrogen receptors, A and B. Many SERMS, on the other hand, either inhibit one and have no effect on the other, or even sometimes inhibit one and actually have an activating, estrogenic effect on the other.
Essentially I'm wondering whether anybody knows which receptor, A or B, is responsible for telling the HPTA to shut down when there's an over-abundance of estradiol. The reason I'm asking here is because I've read several medical studies on the subject and they all seem to give conflicting answers, or inconclusive answers, to this question - and as at present I do not have access to clomid, I'm looking into other modulators which have well known opposing effects - inhibiting one receptor while weakly activating the other.
Obviously in this scenario, I'm looking to figure out which receptor I need to block in order to block the estrogenic feedback loop which inhibits production of LH. For instance, one OTC serm I've been looking at is known to have a blocking effect at ER beta, but a weak estrogenic effect at ER alpha. Apparently this makes it optimal for use in fighting on-cycle gyno, but what sort of effects would such a modulator have on LH and test production?
It's entirely possible that nobody will have a clear answer on this as the medical literature available certainly seems to have a genuine lack of consensus, but I thought it would be worth asking nonetheless.
Unusually, Clomid inhibits estrogen activity at both estrogen receptors, A and B. Many SERMS, on the other hand, either inhibit one and have no effect on the other, or even sometimes inhibit one and actually have an activating, estrogenic effect on the other.
Essentially I'm wondering whether anybody knows which receptor, A or B, is responsible for telling the HPTA to shut down when there's an over-abundance of estradiol. The reason I'm asking here is because I've read several medical studies on the subject and they all seem to give conflicting answers, or inconclusive answers, to this question - and as at present I do not have access to clomid, I'm looking into other modulators which have well known opposing effects - inhibiting one receptor while weakly activating the other.
Obviously in this scenario, I'm looking to figure out which receptor I need to block in order to block the estrogenic feedback loop which inhibits production of LH. For instance, one OTC serm I've been looking at is known to have a blocking effect at ER beta, but a weak estrogenic effect at ER alpha. Apparently this makes it optimal for use in fighting on-cycle gyno, but what sort of effects would such a modulator have on LH and test production?
It's entirely possible that nobody will have a clear answer on this as the medical literature available certainly seems to have a genuine lack of consensus, but I thought it would be worth asking nonetheless.
