and another 1...........
I advise my AAS patients to use small amounts of HCG (250IU to 500IU) every third day, right from the beginning of the cycle. This serves to maintain testicular form and function. This is infinitely better than waiting until they have seriously atrophied. It makes more sense to me to keep the horse in the barn, so to speak, then to have to chase it across three counties later on. I am also a big fan of maintaining estrogen within physiological ranges. Both therapies have been shown to hasten recovery.
Any more than 500IU of HCG per day causes too much aromatase activity. This drives up estrogen levels, unopposed by increased testosterone production. Some feel aromatase is actually toxic to the Leydig cells of the testes. You are then inducing primary hypogonadism (which is permanent) while treating steroid-induced secondary (hypogonadotrophic) hypogonadism (which is temporary--hopefully).
If 250IU or 500IU on two days each week isn’t enough to stave off testicular atrophy, then I recommend using it more days each week (as opposed to taking larger doses). In fact, I wouldn’t mind having a guy use 250IU per day ALL THROUGH the cycle. Those that have tell me they thus avoid that edgy, burned-out feeling they usually get. They also say they simply feel better each day. Subjective reports, to be sure, but they are hard not to appreciate. Especially when HCG is so inexpensive.
The testes are then ready, willing and able to again produce testosterone at the end of the cycle. They have been shown to represent the rate-limiting step in HPTA recovery (usually). LH levels rise fairly rapidly, but endogenous testosterone production is limited by lack of testicular stimulation by same. I also want to make sure a SERM, such as Clomid or Nolvadex, is at effective serum dosage (around 50mg QD for Clomid, 20mg QD for Nolvadex) when serum androgen levels drop to a concentration roughly equal to 200mg of testosterone per week. That is when androgenic inhibition at the HP no longer dominates over estrogenic antagonism with respect to inducing LH production. Of course, if the fellow has been doing Clomid or Nolvadex all along the way (and I now prefer Nolvadex over Clomid, due to the possibility of negative sides from the Clomid), he is all set to simply continue it at the end (no need to switch from one to the other). BTW, I see no evidence of any benefit in using BOTH SERM’s (Selective Estrogen Receptor Modulator—the class of drugs Nolvadex and Clomid belong to) at the same time. I used to think a couple of weeks of the SERM was enough; now I like to see an entire month after the last shot of AAS (and migration of long to short esters as the cycle matures), BEFORE beginning to taper down the SERM. Tapering the SERM is a must at the end, dropping the dose in half every five days until you are taking only 12.5mg of Clomid, or 5mg of Nolvadex, before stopping.
I want my patients to stop taking HCG a week or so after the end of the cycle. Exactly how long you take it depends upon the half-life of the AAS used, and their dosing. Otherwise, the testosterone production HCG induces will further inhibit recovery, as will using Androgel, or any other testosterone preparation, while in recovery. There is no escaping this, as there is no such thing as a “bridge”. Just because you are not inhibiting the HPTA for the entire 24 hours does not mean you are not suppressing it at all. IOW, you can’t “fool” the body—it is smarter than you are.
I like Arimidex during the cycle (in fact, consider use of an AI while taking aromatizable steroids is a necessity) but it ABSOLUTELY should not be used post cycle (even though it has been shown to increase LH production) because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile, is too great (this also drives libido back into the ground—and we don’t want that, do we?).
All this is meant to get my guys through recovery as fast as possible (the real goal, yes?). So far, all of them who have tried it have reported they are recovering faster than when they have tried other protocols.
Copyright 2004 John Crisler, DO. This article may, in its entirety or in part, be reprinted and republished without permission, provided that credit be given to its author, with copyright notice and
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