Secondary hypogonadism occurs when the cause of the testosterone deficiency lies in the pituitary gland, rather than the testes. This seems to be the case with most finasteride users, it seems - low LH and FSH, in addition to low T.
In Shippen’s book, he discusses his use of chorionic gonadotrophin in treating secondary hypogonadism. CG stimulates Leydig cells into producing more testosterone, thus exercising the bodies own testosterone-producing machinery. But this part in particular stands to me:
“CG works nicely with other natural boosters and, in early stages of the male menopause, is often only needed to give an initial cycling boost to the endocrine system. The pituitary continues on after this shove in the normal direction activates control panel receptors.”
So, does this then mean that one series of hCG injections can actually permanently resolve the problem by activating “control panel receptors”? If so, can anyone maybe elaborate on the mechanism underlying this?
I believe the proper term would be “increase basal expression.”
Can the “basal expression” of relevant gonadotrophins (LH, FSH) ever be increased? Or is the body’s production of these hormones always constant, only to be altered, ephemerally, by drug therapy?
Can someone with secondary hypogonadism who is using hCG increase their basal expression of the hormone, perhaps by “activating control panel receptors.” When they ceased using hCG, basal expression would have increased, and they would have permanently elevated levels of gonadotrophics, thus effectively curing their ailment.
I couldn’t give you a definitive answer, as I’m not an expert on HTPA-restarting drug use since I have yet to try any such treatments myself (trying to find a doctor willing to believe and work with you on Fin-related problems is the first challenge). Hypo-is-Here would likely have some more detailed thoughts on this topic.
From what I understand, LH/FSH are controlled by negative feedback loops between testes and the Pituitary (ie the HTPA). The Pituitary releases GnRH which then stimulates release of LH or FSH, depending on the blood levels of Testosterone, Progesterone or Estradiol (for LH) or inhibin and activin (for FSH) – ie, if if levels are high, it inhibits LH/FSH release.
So to answer your question… I believe these levels can obviously change depending on what else is going on with the other hormones in your body. For example, if you had high E2 and were able to bring it it down to optimal levels, which may also improve the T/E ratio, you might find LH is no longer inhibited by the high E2 and thus LH and Testosterone may increase.
… is regarding use of Clomid to “reset” the HTPA/boost T production in a young man after anabolic steroid shutdown, it might shed some insight into your thoughts as to wether it is possible to obtain permanently altered levels of gonadotrophs after such therapy (ie, if one were using hCG instead).
From what I understand, some things to watch out for with hCG (since it mimics the effects of LH in the body) are high doses (ie 5000iu/day) and wether one uses it intermittently vs continually. High doses/continued use can possibly desensitize the leydig cells and thus lead to decreased Testosterone production. I’ll have to dig up more research to investigate this area but those are some things I have come across with a brief Google.
