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Thread: HGH and gyno

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    jg42058p's Avatar
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    HGH and gyno

    I've heard that in some rare cases, HGH can cause gyno problems.
    Is this rumor true or is it just a myth?

    If it is true, then is it caused by progesterone or estrogen?

    thanks

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    Deep_Fried is offline Junior Member
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    Quote Originally Posted by jg42058p View Post
    I've heard that in some rare cases, HGH can cause gyno problems.
    Is this rumor true or is it just a myth?

    If it is true, then is it caused by progesterone or estrogen?

    thanks
    Neither.

    The HGH molecule itself, more specifically, the 22Kda isoform of HGH (predominant isoform used in synthetic GH) has a certain degree of binding affinity for the extracellular prolactin receptor. Some people are affected significantly, and some not at all. It certainly depends on the individual, sensitivity and degree of PRL receptor expression in susceptible tissues.
    Last edited by Deep_Fried; 12-28-2008 at 01:49 AM.

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    so are you saying that the rumor is true and it can cause gyno?

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    Deep_Fried is offline Junior Member
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    Quote Originally Posted by jg42058p View Post
    so are you saying that the rumor is true and it can cause gyno?
    I am stating a fact of edocrinology related to HGH having a quite strong binding affinity for the Prolactin receptor, although not quite as strong as prolactin itself.

    SO, YES. HGH CAN act like Prolactin and can agonize the PRL receptor, causing the same downstream signaling events that would be mitigated by the binding of Prolactin itself.

    I would say this is quit a bit more substantial than rumor, no?

    Keep in mind, though, that the kind of gyno that is mitigated through the PRL receptor, greatly depends on whether you have preexisting mammary tissues and the degree of expression of the PRL receptor. This means that a person with a very small % of existing gyno (due to Estrogen), may not have much target tissue to be affected greatly via this pathway (PRL).

    But, if you have had a bad case of Gyno, Pubertal or AAS derived, you may find that you do not need much PRL stimulation to cause this existing tissue to be susceptible to the lactogenic effects of Prolactin, or HGH for that matter.

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    Quote Originally Posted by Deep_Fried;43****8
    I am stating a fact of edocrinology related to HGH having a quite strong binding affinity for the Prolactin receptor, although not quite as strong as prolactin itself.

    SO, YES. HGH CAN act like Prolactin and can agonize the PRL receptor, causing the same downstream signaling events that would be mitigated by the binding of Prolactin itself.

    I would say this is quit a bit more substantial than rumor, no?

    Keep in mind, though, that the kind of gyno that is mitigated through the PRL receptor, greatly depends on whether you have preexisting mammary tissues and the degree of expression of the PRL receptor. This means that a person with a very small % of existing gyno (due to Estrogen), may not have much target tissue to be affected greatly via this pathway (PRL).

    But, if you have had a bad case of Gyno, Pubertal or AAS derived, you may find that you do not need much PRL stimulation to cause this existing tissue to be susceptible to the lactogenic effects of Prolactin, or HGH for that matter.
    that makes sense. But - Do you think letrozole (femara) or some other aromitase inhibitor would prevent this type of gyno effect?

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    Deep_Fried is offline Junior Member
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    Quote Originally Posted by jg42058p View Post
    that makes sense. But - Do you think letrozole (femara) or some other aromitase inhibitor would prevent this type of gyno effect?
    No, since this has nothing to do with Estrogen or its receptor. Like I stated already, it has to do with HGH binding to the prolactin receptor (PRL-R).

    AI will lower E which will not change the fact that HGH is still able to bind to a PRL-R.

    Cabergoline, on the other hand, will lower Prolactin due to its dompmine agonist action, BUT still this compound will not keep HGH from binding to the PRL-R.
    It MAY however, lower existing Prolactin and keep additional prolactin from agonizing the PRL-R in addition to the added HGH agonism of this receptor. This could possibly shift the balance, lowering the cumulitive effect of both Prolactin and HGH on the PRL-Rto a minimum, which could possibly provide some benefit.

    Still it is important to realize that even if you theoretically KILL prolactin to zero (hypothetical), there will still be HGH able to provide possble prolactinistic action throught this receptor.

    Does this make sense?

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    thanks for the input. good info.

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