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The pituitary

BBing4972

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Get Shredded!
I know it doesn't work this way but not sure why. Wouldn't that be nice if it did.

So if serms work by blocking the estrogen receptors in the pituitary, thereby tricking it into thinking the body needs more estrogen, therefore triggering an LH response so the body makes more testosterone to be converted to estrogen,.. How come when estrogen levels are normal, even during a high testoerone cycle, does the pituitary not produce a normal amount of LH?
 
HPTA stands for Hypothalamic-Pituitary-Testicular Axis. A link between 3 glands/clusters that results in testosterone and sperm production.

Hypothalamic:
This refers to the Hypothalamus. This is a small cluster in the brain that links your central nervous system to the endocrine system. This is where it all begins.
Hypothalamus sends a signal out to the Pituitary gland. This signal is called Gonadotropin Releasing Hormone (GnRH). Gonadotropins are your Luteinizing Hormone (LH) and Follicle Stimulating Hormones (FSH). These are explained in the next step.

Pituitary:
This refers to the Pituitary gland in your head, just under the brain, and releases LH, FSH, and more (because it received the signal from the hypothalamus). To stay on topic, we'll just discuss LH and FSH. LH is a hormone that is sent over to the testes for the purpose of stimulating Leydig Cells to produce testosterone. FSH is another hormone sent to the testes for the purpose of sperm production, which is accomplished by joining testosterone in the stimulation of Sertoli Cells. Both LH and FSH are required as they work in synergy for the betterment of production by the testes.

Testicular (also known as Gonadal; ie HPGA):
This refers to the testes. This is where your Leydig Cells and Sertoli Cells (mentioned above) reside. These are cells that produce testosterone and sperm when stimulated by LH and FSH (which arrived because the pituitary sent them). This event completes the chain reaction that started at the Hypothalamus, and now we have testosterone and sperm production.

So now you see the link between glands and clusters in your body that result in testosterone and sperm production. The descriptions above are very "dumbed down", so you can see how complex this system can be. All these glands are for your state of health and stability. Disruption in any of your HPTA glands could cause problems. It's a chain reaction and it's as strong as the weakest link. For example, if your Hypothalamus is sending GnRH, and your pituitary does not respond properly, then it won't send LH/FSH to the testes, rendering GnRH useless as you will not produce testosterone effectively, or none at all. This is why men with Low testosterone begin testosterone therapy .

LowT

****not my words, copied from one of our many respected Vets
 
I know it doesn't work this way but not sure why. Wouldn't that be nice if it did.

So if serms work by blocking the estrogen receptors in the pituitary, thereby tricking it into thinking the body needs more estrogen, therefore triggering an LH response so the body makes more testosterone to be converted to estrogen,.. How come when estrogen levels are normal, even during a high testoerone cycle, does the pituitary not produce a normal amount of LH?
this might be what you're looking for. http://www.evolutionary.org/how-testosterone-supplementation-shuts-down-hpta/
 
galois that looks like as close of an answer as I will get. thank you for that

it's just interesting that tricking the HPTA into thinking there isn't enough estrogen (with SERMS), makes it secrete more LH and FSH. so you'd think that at a normal estrogen level, even while on cycle with increased exogenous testosterone levels, the HPTA would signal for normal LH and FSH secretion.
 
galois that looks like as close of an answer as I will get. thank you for that

it's just interesting that tricking the HPTA into thinking there isn't enough estrogen (with SERMS), makes it secrete more LH and FSH. so you'd think that at a normal estrogen level, even while on cycle with increased exogenous testosterone levels, the HPTA would signal for normal LH and FSH secretion.

I agree with you.

If the HPTA were as simple as we're led to believe, reducing E2 to below natty levels ought to force the pituitary to pump out huge amounts of LH & FSH in response, and therefore produce a natty T level in addition to any exogenous hormones.

Obviously it's just not that simple since bloodwork shows on-cycle people being shutdown regardless of AI dose and crashed E2... maybe the high levels of test are able to out-compete the AI to get at the aromatase in situ and create more E2. Or maybe there are actually *some* testosterone receptors there as well that haven't been seen (or noted) by the literature. Dunno, but there's definitely a problem.
 
I agree with you.

If the HPTA were as simple as we're led to believe, reducing E2 to below natty levels ought to force the pituitary to pump out huge amounts of LH & FSH in response, and therefore produce a natty T level in addition to any exogenous hormones.

Obviously it's just not that simple since bloodwork shows on-cycle people being shutdown regardless of AI dose and crashed E2... maybe the high levels of test are able to out-compete the AI to get at the aromatase in situ and create more E2. Or maybe there are actually *some* testosterone receptors there as well that haven't been seen (or noted) by the literature. Dunno, but there's definitely a problem.

exactly what i was thinking. glad you're picking up what im putting down!
 
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