Hypothalamus....

[Flier]

So....the Hypothalamus is getting signals from a number of external and internal sources and sends "Neurohormones" to the Pituitary(amongst other organs), which again sends LH/FSH to the testicles(if we are discussing testosterone production)

So....unless we have a healthy Hypothalamus, it does not matter if we have a healthy Pituitary, because without the Neurohormones to stimulate the Pituitary, we will not produce LH.

When we finish a cycle, we take SERMS to stimulate the Pituitary. Is that because the Hypothalamus is not sending it´s Neurohormones?

When we do a cycle, we "shut down" the Pituitary, do we also "shut down" the Hypothalamus?

We take SERMS to stimulate the Pituitary to start producing LH quicker, but what does that help if we have ignored the Hypothalamus, and when we end PCT with the Hypothalamus "shut down", our LH will go right back down to 0?

As a PCT, why don´t we instead stimulate the Hypothalamus to send stronger Neurohormones to the Pituitary?
How would we do this?

I have low LH/FSH (4/4).
Maybe this is because my Hypothalamus is sending weak Neurohormones to my Pituitary.
Can I test for Hypothalamus function?
The Hypothalamus is also responsible for Dopamine and Seratonin release, so very important for overall well being and mood, along with a healthy amount of Test and T3.

[Lemonada8]

SERMS also modulate the feedback on the hypothalamus. They hypothalamus is the homeostatic center of the brain, it has an 'operator' part in regulation by initiating release of hormones. When you are on a 'cycle', it is uncertain if the hypothalamus is 'shut down', like you are mentioning it but there is definately some down-activation due to exogenous hormones and feedback loops.
If ur hypothalamus isnt working, wont get any pituitary activation even with SERMS. Nolva increases the response to LHRH and amplitude of LH spikes initiated. Clomid increases the initial release of LH but continued high doses can lead to LHRH insensitivity, it also increases the pulse frequency by the hypothalamus.

There is a new area of studies using kisspeptin-10, which seem to 'reset' the hypothalamic clock of gonadotropins therefore putting our brains back in 'puberty' production mode. Its a rather interesting field and we are still finding out new things.


As for your case, there can be many different issues that result in low LH and FSH. To test this would be very extensive and you would have to basically get yourself in a research setting, i dont know of much in-depth testing that is a common occurance. You could get pituitary responsiveness tested with synthetic GnRH, but thats still pretty involved.

The anterior pituitary produces many hormones, which can be out of balance because even though they dont regulate each other directly there still is some cross regulation.
ie - how tren can have prolactin/thyroid issues (its a very strong AR binding compound)

[gearbox]

Great read

[Flier]

SERMS also modulate the feedback on the hypothalamus. They hypothalamus is the homeostatic center of the brain, it has an 'operator' part in regulation by initiating release of hormones. When you are on a 'cycle', it is uncertain if the hypothalamus is 'shut down', like you are mentioning it but there is definately some down-activation due to exogenous hormones and feedback loops.
If ur hypothalamus isnt working, wont get any pituitary activation even with SERMS. Nolva increases the response to LHRH and amplitude of LH spikes initiated. Clomid increases the initial release of LH but continued high doses can lead to LHRH insensitivity, it also increases the pulse frequency by the hypothalamus.

There is a new area of studies using kisspeptin-10, which seem to 'reset' the hypothalamic clock of gonadotropins therefore putting our brains back in 'puberty' production mode. Its a rather interesting field and we are still finding out new things.


As for your case, there can be many different issues that result in low LH and FSH. To test this would be very extensive and you would have to basically get yourself in a research setting, i dont know of much in-depth testing that is a common occurance. You could get pituitary responsiveness tested with synthetic GnRH, but thats still pretty involved.

The anterior pituitary produces many hormones, which can be out of balance because even though they dont regulate each other directly there still is some cross regulation.
ie - how tren can have prolactin/thyroid issues (its a very strong AR binding compound)

I was planning a 3 month 60mg ED Toremifene cycle starting January as a blind effort to stimulate the Pituitary.
From what you are saying, by doing this I will also stimulate the Hypothalamus pulse frequency, but do you think this is too long and risking desensitivity of the Pituitary?
I read a study on 60mg ED, 3 months Tore cycle on select men who greatly increased their LH, Test, Sperm count, and some men who were previously infertile made their partner pregnant in the following months

[Lemonada8]

you will also increase SHBG due to the estrogen-agonism in the liver.

Are you having fertility issues? or just with the LH, FSH values?

25mg clomid have had greater success than tamox in fertility studies, but each have their own benefits.

[Flier]

you will also increase SHBG due to the estrogen-agonism in the liver.

Are you having fertility issues? or just with the LH, FSH values?

25mg clomid have had greater success than tamox in fertility studies, but each have their own benefits.

No reason to believe I have fertility issues. I´m getting my Test values up to normal....hopefully, after being shut down for 1.5 years due to playing around with AAS.
I did my last AAS shot 8 months ago, and my value is today 12 (8-34), and rising.
Note....I´m doing Tore, not Tamox.