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HCG converting to estrogen more so than T ???
- Thread starter dyna5
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I think what you are asking is how is it that hCG causes an increase in E2 production since T is converted to E2. hCG itself is not converted to E2. IIRC, the mechanism is due to hCG-stimulated CYP19A1 (aromatase) expression. In fact, E2 is a marker for hCG effect.
In addition the testes produce some amount of estrogen when stimulated.
foreveryoung
New Member
I believe the adrenals and/or pituitary can produce estrogens as well
in my body, hcg is an evil thing, maybe some people's systems have luck with it, but it has been nothing but a bad thing for me in decades of experimenting
The PRIMARY sources for "estrogens" include:
Testis; < 5%
Peripheral (prostate, adipose tissue, glandular breast tissue) conversion via aromatase; ~ 80%
Adrenals; ~ 20%
LH and HCG are not selective for testicular testosterone production. Either the secretion of LH or the supplementation of HCG increase gonadal aromatase activity which increases estrogen production.
jim
Testis; < 5%
Peripheral (prostate, adipose tissue, glandular breast tissue) conversion via aromatase; ~ 80%
Adrenals; ~ 20%
LH and HCG are not selective for testicular testosterone production. Either the secretion of LH or the supplementation of HCG increase gonadal aromatase activity which increases estrogen production.
jim
foreveryoung
New Member
I wasn't thinking when I typed pituitary there
is there any type of direct effect of LH or hcg on adrenals?
is there any type of direct effect of LH or hcg on adrenals?
Excellent Question ...
Nishii M, Nomura M, Sekine Y, et al. Luteinizing Hormone (LH)–Releasing Hormone Agonist Reduces Serum Adrenal Androgen Levels in Prostate Cancer Patients: Implications for the Effect of LH on the Adrenal Glands. Journal of Andrology 2012;33(6):1233-8. Luteinizing Hormone (LH)–Releasing Hormone Agonist Reduces Serum Adrenal Androgen Levels in Prostate Cancer Patients: Implications for the Effect of LH on the Adrenal Glands - Nishii - 2013 - Journal of Andrology - Wiley Online Library
Recently, adrenal androgens have been targeted as key hormones for the development of castration-resistant prostate cancer therapeutics. Although circulating adrenal androgens originate mainly from the adrenal glands, the testes also supply about 10%.
Although widely used in androgen deprivation medical castration therapy, the effect of luteinizing hormone–releasing hormone (LH-RH) agonist on adrenal androgens has not been fully studied.
In this study, changes in testicular and adrenal androgen levels were measured and compared to adrenocorticotropic hormone levels. To assess the possible role of LH in the adrenal glands, immunohistochemical studies of the LH receptor in normal adrenal glands were performed. Forty-seven patients with localized or locally progressive prostate cancer were treated with LH-RH agonist with radiotherapy.
Six months after initiation of treatment, testosterone, dihydrotestosterone, and estradiol levels were decreased by 90%–95%, and dehydroepiandrosterone-sulfate, dehydroepiandrosterone, and androstenedione levels were significantly decreased by 26%–40%. The suppressive effect of LH-RH agonist at 12 months was maintained.
Adrenocorticotropic hormone levels showed an increasing trend at 6 months and a significant increase at 12 months. LH receptors were positively stained in the cortex cells of the reticular layer of the adrenal glands.
The long-term LH-RH agonist treatment reduced adrenal-originated adrenal androgens. LH receptors in the adrenal cortex cells of the reticular layer might account for the underlying mechanism of reduced adrenal androgens.
Nice query FY and FU post DOC!
It's my understanding the influence of LH on the adrenals is much more dependent upon ACTH than LH levels.
That is if cortisol is low, such as in the early AM hours the influence of ACTH would supersede elevated LH levels which also occur during this period.
Consequently the adrenals primary effect is to increase estrogen rather than testosterone.
Another reason AIs are an important part of effective PCT, IMO.
Jim
It's my understanding the influence of LH on the adrenals is much more dependent upon ACTH than LH levels.
That is if cortisol is low, such as in the early AM hours the influence of ACTH would supersede elevated LH levels which also occur during this period.
Consequently the adrenals primary effect is to increase estrogen rather than testosterone.
Another reason AIs are an important part of effective PCT, IMO.
Jim
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