Quote Originally Posted by cucu View Post
First, LH and FSH do not inhibit themselves, is that right? The classic negative feedback loop involves T, like T inhibits GnRH which leads to LH/FSH reduction, and T inhibits LH/FSH. Therefor, providing exogenous LH/FSH or analogs wouldn't inhibit their production.

Second, that was not the point of my question. It was whether we would be able to rescue/protect testicular function by providing FSH. The link Java Man provides some unecdotal evidence that refer to " better feeling", "recovery a breeze" which only point to testosterone secretion restoration, but not sperm quality. Does any one have any view on that?

On another note. Wouldn't it make more sense hijacking/replacing the entire spectrum of gonadal hormones (GnRH, LH and FSH in their physiological doses and T in supraphysiological) and then jump-start your GnRH? Which might not be needed as hypothalamus seems to be pretty resilient.
To your first point... If you administer hCG to mimic LH (even without exogenous testosterone), you are still suppressing your natural LH production.

Back on topic... The demand for hCG on cycle is intended to maintain your Leydig cells, which is what LH analogue stimulates into testosterone production. Testosterone, coupled with FSH will stimulate Sertoli cells into spermatozoa. There isn't any evidence in humans that lead us to believe that tentative FSH suppression could result in desensitized sertoli cells. Even in most extreme cases and clinical trials where FSH was severely depleted, forcing secretion via clomiphene or HMG lead to generous performance by sertoli cells.

Would it hurt to use HMG on cycle? No. But it's not exactly as readily available as hCG and frankly, I haven't see anything that would trigger the need.

By the way, the length of time suppression occurs should be observed and considered far more than supra-physiological levels with respect to recovery.