Dear all,
I have been trying to understand the mechanism of action of Ecdyterones to hypothetically assess the possible side effects of such supplement.
I far as I can understand , here are two main types of estrogen receptors:
ERα is present mainly in mammary gland, uterus, ovary (thecal cells), bone, male reproductive organs (testes and epididymis), prostate (stroma), liver, and adipose tissue.
By contrast, ERβ is found mainly in the prostate (epithelium), bladder, ovary (granulosa cells), colon, adipose tissue, and immune system.
Beta-ecdysterones are ERβ agonists.
With that been said, it appears that pure beta-ecdysterones should not cause gynecomastia. There appears to be particular promise for the use of ERβ-selective agonists to increase the "beneficial effects of estrogen" (in quotes since it appears that according to this forum there are no such beneficial effects).
As far as I can tell from the literature, ERβ agonism is mostly related with cardiovascular, improvements in metabolism and obesity and neuroprotective benefits.
I would like to know what is exactly the ERβ-RBA and ERβ-RBA of ecdysterone since that could change the picture. Additionally, my intuition is telling me that in case that ecdysterone were purely ERβ agonists, that should block ERβ receptors making endogenous estrogens more prone to ERα, right? (Since estradial ERβ-RBA=ERβ-RBA=50%).
As you can tell I do not know much but I would really like to understand how do these "promising substances" work (in the hormonal contex).
Best regards,
I have been trying to understand the mechanism of action of Ecdyterones to hypothetically assess the possible side effects of such supplement.
I far as I can understand , here are two main types of estrogen receptors:
ERα is present mainly in mammary gland, uterus, ovary (thecal cells), bone, male reproductive organs (testes and epididymis), prostate (stroma), liver, and adipose tissue.
By contrast, ERβ is found mainly in the prostate (epithelium), bladder, ovary (granulosa cells), colon, adipose tissue, and immune system.
Beta-ecdysterones are ERβ agonists.
With that been said, it appears that pure beta-ecdysterones should not cause gynecomastia. There appears to be particular promise for the use of ERβ-selective agonists to increase the "beneficial effects of estrogen" (in quotes since it appears that according to this forum there are no such beneficial effects).
As far as I can tell from the literature, ERβ agonism is mostly related with cardiovascular, improvements in metabolism and obesity and neuroprotective benefits.
I would like to know what is exactly the ERβ-RBA and ERβ-RBA of ecdysterone since that could change the picture. Additionally, my intuition is telling me that in case that ecdysterone were purely ERβ agonists, that should block ERβ receptors making endogenous estrogens more prone to ERα, right? (Since estradial ERβ-RBA=ERβ-RBA=50%).
As you can tell I do not know much but I would really like to understand how do these "promising substances" work (in the hormonal contex).
Best regards,
