Wow. That was really helpful, thanks. I did not know that.
Ok. Cool. Next question: How important would you say HCG is? What if I could find an aromataze inhibitor and clomid, but still no HCG?
When it comes to pharmacology, more is not necessarily better.
As for hCG, I don't understand why anyone would want to create another level of suppression in their HPTA? There is really no use for hCG, it desensitizes leydig cells in your testes to Leutinizing hormone so that when you eventually cease using hCG it takes a while for your testes to become sensitive to your own body's natural LH, thus prolonging your recovery. The use of hCG in males is limited to increasing fertility in HRT such that guys have enough viable sperm for their partners to conceive. When you are "shut down" your testes actually become more sensitive to LH due to receptor up-regulation. All that hCG will do is prolong your recovery.
I'd rather taper off and for this reason I wouldn't bother with SERMS as aromatase inhibitors like anastrazole are a better accompaniment to this protocol. Adding more PCT drugs into the mix just means more poly-pharmacy and more side effects.
With regard to hCG, receptor down regulation is just a reality for receptor mediated drug therapy. While the literature on this particular topic is scarce I have seen one showing the effects in humans as well as rats, albeit the human study was with large dosages greater than 1000iu. Regardless, while you may be able to safely administer therapeutic doses of hCG without inducing primary hypogonadism, why would you? LH is not the problem when it comes to coming off cycle, LH concentrations rise simultaneously with a fall in serum androgen levels and it is a myth that all exogenous testosterone must clear your system before your HPTA restarts. Your body cannot tell the difference between endogenous and exogenous testosterone.
So if hCG mimics LH yet serum LH rises with falling androgen concentrations anyway, whats the point in administering it? Having said that it is important to note that when I say androgens I mean testosterone. Other AAS which have different binding affinities for the androgen receptor may still be suppressing LH production in spite of negligible levels of circulating testosterone. For this reason I have seen it been recommended that a low dose test bridge (100mg/ week) be used before the taper in order to allow time for other AAS to clear your system. The bridge should be equal to at least 4x the longest half life of any co-administered androgens/anabolics.
GnRH is released from the hypothalamus which also senses sex hormone levels. GnRH acts to stimulate the release of FSH and LH from the pituitary.
There is no reason why a taper would not work and actually takes no longer than a conventional PCT in the protocol I've previously outlined. Further to this, because leydig cells are not permanently damaged, not keeping them stimulated while on cycle isn't really going to affect you so long as you taper off. The taper gives your testes time to resume normal response to LH as you are not all of a sudden dropping testosterone cold turkey. You have enough exogenous testosterone in your system to maintain sexual function and hold onto gains but not enough to suppress your natural LH production and compromise testicular function.
You have to stand back a bit and look at the big picture, ultimately a PCT is about recovering as quickly as possible and with the least side effects as possible. A test taper allows you to do this. Sure you can take hCG here and there and then SERMs to offset leydig cell desensitization and then time hCG to mimic LH secretion as best you can, then deal with the added sides from nolva clomid, hCG etc. But you wan't your body to achieve homeostasis, I don't see how throwing more drugs into the mix all the while lining your dealer's pockets is going to be the easiest way of doing this. I guess its up to the individual and what they feel is the best option for them.
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