conkertheking
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Hey folks, last minute question before I begin my Letrone & Rebirth log tomorrow:
I'm having a very hard time finding any definitive answers to this question, but I feel it's an important one before I finally commit to taking both of these products at the same time as opposed to consecutively. What I'm trying to find out is, do we know which estrogen receptor - alpha or beta - is responsible for telling the hypothalamus to stop producing GnRH or the pituitary to stop producing LH, when E2 gets too high?
The reason I ask is because one of the compounds in Rebirth, ellagic acid, is known to completely antagonise (block) ER beta, but slightly agonise (activate) ER alpha (the scientific studies cite it as "a small but significant estrogenic effect"). This is perfect for preventing gyno and other estrogen related sides, which is well documented, but what about the HPTA feedback loop? My concern is the possibility that the slight agonistic effect of Ellagic Acid on ER alpha will lessen the effects of the massive estradiol reduction expected with Letrone, if - and only if - it's the alpha receptor which controls the HPTA rather than the beta receptor.
Frustratingly, I've spent the last several days looking for medical studies on this and all I can find are papers which contradict eachother. So in other words, nobody seems to know for sure which receptor tells the HPTA when to shut itself down, . And I'm inclined to trust Rebirth on this because we've seen other logs of Rebirth during PCT in which LH and FSH had significant rises over the period, even after extraordinary heavy androgen cycles, so my instinct is to just go with it and stop asking questions
But obviously if there's a chance that Ellagic Acid's agonistic effect on the alpha receptor will lessen the effect of Letrone, that's something I should take into account.
Obviously aside from all this, there's E.Cottoni which could well be an antagonist of both receptors and therefore neutralise this issue altogether - there doesn't seem to be any research examining specifically which receptors E.Cottoni interacts with, just a general acceptance that it suppresses estrogenic breast cancer in the same way as tamoxifen, and therefore must behave like a SERM in some way. And even furthermore, Letrone caused such ridiculously massive LH surges in some beta testers that I'm inclined to believe it has another mechanism of action apart from merely reducing E2 which causes the HPTA to up-regulate - in which case none of this matters and my restart protocol of Rebirth and Letrone combined at a full dose will kick ass regardless.
Just wondering if anyone has any scientific insights before I take the plunge. Unless I hear advice to the contrary, I'll be taking my first dose of both Rebirth and Letrone tomorrow morning after breakfast, when I'll have my baseline bloods in my hand and an appointment booked for day 28 or 29 of my log for the follow up blood work
I'm having a very hard time finding any definitive answers to this question, but I feel it's an important one before I finally commit to taking both of these products at the same time as opposed to consecutively. What I'm trying to find out is, do we know which estrogen receptor - alpha or beta - is responsible for telling the hypothalamus to stop producing GnRH or the pituitary to stop producing LH, when E2 gets too high?
The reason I ask is because one of the compounds in Rebirth, ellagic acid, is known to completely antagonise (block) ER beta, but slightly agonise (activate) ER alpha (the scientific studies cite it as "a small but significant estrogenic effect"). This is perfect for preventing gyno and other estrogen related sides, which is well documented, but what about the HPTA feedback loop? My concern is the possibility that the slight agonistic effect of Ellagic Acid on ER alpha will lessen the effects of the massive estradiol reduction expected with Letrone, if - and only if - it's the alpha receptor which controls the HPTA rather than the beta receptor.
Frustratingly, I've spent the last several days looking for medical studies on this and all I can find are papers which contradict eachother. So in other words, nobody seems to know for sure which receptor tells the HPTA when to shut itself down, . And I'm inclined to trust Rebirth on this because we've seen other logs of Rebirth during PCT in which LH and FSH had significant rises over the period, even after extraordinary heavy androgen cycles, so my instinct is to just go with it and stop asking questions
But obviously if there's a chance that Ellagic Acid's agonistic effect on the alpha receptor will lessen the effect of Letrone, that's something I should take into account.Obviously aside from all this, there's E.Cottoni which could well be an antagonist of both receptors and therefore neutralise this issue altogether - there doesn't seem to be any research examining specifically which receptors E.Cottoni interacts with, just a general acceptance that it suppresses estrogenic breast cancer in the same way as tamoxifen, and therefore must behave like a SERM in some way. And even furthermore, Letrone caused such ridiculously massive LH surges in some beta testers that I'm inclined to believe it has another mechanism of action apart from merely reducing E2 which causes the HPTA to up-regulate - in which case none of this matters and my restart protocol of Rebirth and Letrone combined at a full dose will kick ass regardless.
Just wondering if anyone has any scientific insights before I take the plunge. Unless I hear advice to the contrary, I'll be taking my first dose of both Rebirth and Letrone tomorrow morning after breakfast, when I'll have my baseline bloods in my hand and an appointment booked for day 28 or 29 of my log for the follow up blood work
