Clomid works by blocking estrogen receptors at the hypothalamus and also stimulates it to release gonadtropin, aka GnRH. GnRH goes back to the pituitary to stimulate the release of LH (Luteinizing Hormone) and FSH (Follicle Stimulating Hhormone). LH, in turn, stimulates the testes to produce and secrete testosterone and perform spermatogenesis.
There is something called the Hypothalamic Pituitary Testicular Axis (HPTA) which encompasses this entire process. This sort of chain reaction sounds good until you get in to the androgenic effects of steroids.
Exogenous androgenic substances (such as injected testosterone) reduce your hypothalamus' ability to release GnRH. This in turn effects your levels of LH and FSH, all of which are necessary to tell your body to produce testosterone. If androgens suppress the release of these hormones, and clomid does such wonderful things to increase the release of these hormones, shouldn't we reach a sort of homeostasis in the middle?
Another underlying problem is that artifical androgens, regardless of external supplementation with other pharmaceuticals, cause our bodies to become desensitized to LH, which is probably the most important hormone in restoring the testes' ability to produce testosterone. Llewellen's research shows almost immediately after the cessation of testosterone supplementation, LH levels start to rise, but testosterone production took much longer to start.
The only hormone shown to have significant impact on maintaining some degree of testosterone production while on cycle is HCG. HCG works by mimicking our own body's natural LH, which we are equally as desensitized to at this point after supplementing with exogenous testosterone. The reason it works though is that we are bombarding our endocrine system with far greater levels of LH than our body is used to seeing. The effect off this is not apparent while on cycle, as our testes are still desensitized to the LH, but upon cessation of exogenous testosterone, the bombardment of LH in our system serves to reduce the time it takes our testes to "wake up" and start producing endogenous testosterone.
An anti-estrogen is needed in compliment the HCG because, post cycle, we still have increased levels of estrogen in our systems. Testosterone and estrogen both have negative and positive feedback signals that our body uses for various purposes. Without the testosterone in our system post cycle to provide its negative and positive feedback singals, we're left with only the ones coming from estrogen. An anti-estrogen, like Nolvadex, serves to block our estrogen receptors so our bodies can longer receive these signals, thus negating the effects of increased estrogen levels without testosterone.
I went a little overboard, moving in to PCT a bit more, but that should give you a pretty decent understanding of just a few of the basics of how testosterone and our endocrine system works in regard to the cessation and restarting of endogenous testosterone production.
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