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  1. #1
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    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)

  2. #2
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    Quote Originally Posted by Lemonada8 View Post
    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

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