It is called the “post cycle crash”, and is one of the more unwelcome aspects of steroid use. As the saying goes, there is a price to be paid for everything, and in the case of steroids, one of those prices (a temporary one anyway) is your natural hormone production. What happens is quite simple; when you take steroids your body stops making them. Once you stop taking steroids, you can be left with a gap until your body starts making its own again. Here, you can be faced with low levels of androgens and normal levels of corticosteroids. Your body will (should) eventually recognize and fix the imbalance, but i can take weeks or even months. This gap is a bad place to be physiologically, as without normal androgen levels to balance the catabolic effects of corticosteroids, a good deal of your new muscle mass may be lost. To help your body maintain its size, you will want to restore endogenous testosterone production quickly. The methods for doing this seem to be different everywhere you look: “Take HCG, don’t take HCG, use an aromatase inhibitor, just take clomid, forget Clomid and take Nolvadex.” What option is really best? Without an understanding of exactly what is going on in your body, and why certain compounds help to correct the situation, choosing the right Post-Cycle Therapy (PCT) program can be quite confusing. In, this section the roles of anti-estrogens and HCG during this delicate window of time are discussed, while detailing an effective strategy for their use.

The HPTA Axis

The hypothalamic-Pituitary-Testicular Axis, or HPTA for short, is the thermostat for your body’s natural production of testosterone. Too much testosterone, and the furnace will shut off. Not enough, and the heat is turned up (to put it simply). For the purposes of our discussion, we can look at this regulating process as having three levels. At the top is the hypothalamic region of the brain, which releases the hormone GnRH (Gonadotropin-Releasing Hormone) when it senses a need for more testosterone. GnRH sends a signal to the second level of the axis, the pituitary, which releases Luteinizing Hormone in response. LH for short, this hormone stimulates the testes (level three) to secrete testosterone. The same sex steroids (testosterone, estrogen) that are produced serve to counterbalance things, by providing negative feedback signals (primarily to the hypothalamus and pituitary) to lower the secretion of testosterone. Synthetic steroids send the same negative feedback. This quick background of the testosterone-regulating axis is necessary to furthering our discussion, as we need to first look at the underlying mechanisms involved before we can understand why natural recovery of the HPTA post-cycle is a slow process. Only then can we implement an ancillary drug program to effectively deal with it.

Testicular Desensitization

Although steroids suppress testosterone production primarily by lowering the level of gonadotropic hormones, the big roadblock to a restored HPTA after we come of the drugs is surprisingly not LH. This problem was made clearly evident in a study published in 1975. Here, blood parameters, including testosterone and LH levels, were monitored in male subjects who were given testosterone enanthate injections of 250mg weekly for 21 weeks. Subjects remained under investigation for an additional 18 weeks after the drug was discontinued. At the start of the study, LH levels became suppressed in direct relation to the rise in testosterone, which was to be expected. Things looked very different, however, once the steroids had been withdrawn. LH levels went on the rise quickly (by the third week), while testosterone barely budged for quite some time. In fact, on average it was more than 10 weeks before any noticeable movement in testosterone production started at all. This lack of correlation makes clear that the problem in getting androgen levels restored is not necessarily the level of LH, but more so testicular atrophy and desensitization to LH. After a period of inactivation, the testes have lost mass (atrophied), making them unable to perform the required workload. The protracted post-cycle window can, likewise, no longer be looked at as one of low testosterone and low LH. Much of it actually involves low testosterone and normal (even high) LH.

The Role of Anti-Estrogens

It is important to understand that anti-estrogens alone are inadequate to restore normal endogenous testosterone production after a cycle. These agents ordinarily increase LH levels by blocking the negative feedback of estrogens. But LH rebounds quickly on its own post-cycle, without help. Plus, there is not an elevated level of estrogen for anti-estrogens to block during this window, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels are actually lower here, not higher. Any estrogen rebound that occurs post-cycle, likewise, happens with a rebound in testosterone levels, not prior to it (there is an imbalance in the ration of androgens to estrogens post cycle, but this is another topic altogether). On their own, we are seeing no mechanism in which anti-estrogenic drugs can effectively help here. I can, however, see why this fact would be easy to overlook. The medical literature filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels in men, and in normal situations they indeed perform this function fairly well. Combine this with the fact that just as many studies can be found to show that steroid use lowers LH when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that we need to focus on LH. We would miss the true problem, testicular desensitization, unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in the focusing solely on anti-estrogenic drugs.

The Role of HCG

With anti-estrogens alone proving to be ineffective, we are left to focus on a very different level of the HPTA in order to hasten recovery: the testes. For this we will need the injectable drug HCG. If you are not familiar, HCG, or Human Chorionic Gonadotropin, is a prescription fertility agent that mimics the body’s natural LH. Although the testes are equally desensitized to this drug as they are to LH (they work through the same receptor), we are administering it as a measured drug and are, therefore, not constrained by the limits of our own LH production. In other words, we can give ourselves a good close dose of drug (as much LH as we need, really), shocking the testes with unnaturally high levels of stimulation. We want it to reach a level above what our bodies, even when supported by anti-estrogens, could do on its own. The result should be a more rapid restoration of original testicular mass, which would allow normal levels of testosterone to be output much sooner than without such an ancillary program in place. What we are looking at now is HCG actually being the pivotal post-cycle drug, which anti-estrogens playing more of a supportive role.