This is an extract from the power pct program, you can look up the studies online.
When you take AAS, your body stops making natural hormones (i.e., test). Once you stop taking steroids, you can be left with a gap until your body starts making its own again, which can take months. Here, you can be faced with low levels of androgens and normal levels of corticosteroids. Corticosteroids have a pronounced catabolic (muscle-depleting) state on our bodies, and without the androgens 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 (natural) 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 just take Nolvadex." What option is reall best? Without an understanding of what is really happeningin your body, and why certain compounds help to correct the situation, choosing he correct PCT program can be quite confusing.
The HPTA Axis
The Hypothalamic-Pituitary-Testicular Axis (HPTA) 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 very simply). For the purpose of our discussion, we can look at this regulating process as having three levels. At the top is te 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 mechanism 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.
Although steroids supress testosterone production primarily by lowering the level of gonadotropic hormones, the big roadblock to a restored HPTA after we come off steroids is surprisingly not LH. This problem was made clearly evident in a study published back 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, a low dose for even a beginner's cycle. 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 3rd 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 subtrate used for the synthesis of estrogen 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 ratio 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 is 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 very 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 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 dose of the drug (as much LH as we really need), 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, with anti-estrogens playing more of a supportive role.
The PoWeR PCT Program
The PCT program outlined below represents what I consider to be an ideal and effective PCT program. It was developed by the doctors at the Program for Wellness Restoration (PoWeR), who have a formidable history helping patients recover from abnormal hormonal functioning following steroid therapy. One of the key doctors on this program, Dr. Michael Scally, claims to have successfully treated more than 100 cases of hypogonadism/hypogonadotropic hypogonadism, and is very well known in the field of androgen replacement therapy. PoWeR published this program as part of a recent clinical study, which involved 19 healthy male subject who were taking supraphysiological (highly suppressive) doses of testosterone cypionate and nandrolone decanoate for 12 weeks. Their HPGA Normalization Protocol focuses on the combined use of hCG, Nolvadex, and Clomid, and is perhaps the only clinical documented post-cycle therapy program to be found in the medical literature (it is amazing how little attention has been paid to hormone normalization in clinical medicine). The most notable variation from a classic PCT stack, such that I have been a longtime supporter of, is the combined use of two anti-estrogens. In this case I cannot say there is a disadvantage to such us; perhaps it is indeed the better option.
NOLVADEX: ran for 45 days from day 1
CLOMID: ran for 30 days from day 1
hCG: ran for 16 days from day 1
Examining the program closely, we note that the testes are hit hard with hCG at the onset of therapy. Its intake, however, is limited to only 16 days. The doctors undoubtedly recognize that when hCG is taken for too long or at too high a dosage it can desensitize the LH receptor. This would only further exacerbate the post-cycle program, not help it. Anti-estrogens are used during and after hCG, with a dosage of 10mg of Nolvadex and 100mg of Clomid per day, rounding out this compliment of drugs. Clomid is used for a shorter period of time than Nolvadex, likely because of the desensitizing effect it too can have (on the pituitary gland) with continued use. Among other things, these two anti-estrogens will continue to foster LH release as testosterone levels start to go back up, as well as combat any potential estrogenic side effects that may be caused by hCG's up-regulation of testicular aromatase activity. Although the first couple of weeks the anti-estrogens probably do very little, they should be much more helpful toward the middle and end of the program. During this clinical investigation, normal hormonal function was restored in all subjects within 45 days of drug cessation. This is a definite success, far more favorable than the protracted recovery window noted in studies without PCT, such as the 250mg/week testosterone enanthate investigation. Such a detailed recovery program should follow any serious steroid cycle. It is the best way to maintain your gains at their maximum, and that is, after all, what we are after.