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PCT Basics
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PCT Basics - 08-23-2011, 09:26 PM

PCT Basics

The biggest fear of steroid users is that they will lose their own testosterone production, lose their testicle size, and worst of all, lose all the muscle they gained. To minimize the possibility of this happening, athletes resort to a practice called PCT. Post-cycle therapy (or PCT) refers to the combination of drugs and/or supplements that one takes after a cycle of anabolic steroids (or prohormones), in the attempt to restart the hypothalamic pituitary testicular axis (HPTA), as well as minimize muscle mass loss.

PCT alone, however, is not enough. In addition to deciding what substances you administer during the post-cycle period, you must also consider what you do during your cycle to best prepare your body for an efficient and speedy recovery when your cycle is over.

The steroid(s) You Choose Means Everything

The first thing to consider is the hormones you take. As you may already know, some hormones are more suppressive than others. The DHT derivatives are generally the least suppressive. These include (in approximate order of increasing suppressive potential) mesterolone, methenolone, oxandrolone, stanozolol, furazabol, and mestanolone. The reason that these are less suppressive than other steroids is that they do not aromatize to estrogens, nor are they appreciably progestational. Remember, your hypothalamus responds to androgens, estrogens, and progetagens. So by sticking to DHT derivatives you will only stimulate negative feedback on one of the sex hormone pathways (androgenic pathway).

DHT derivatives also give very high-quality gains with minimum water retention. Exceptions to the rule with DHT derivatives include 1-testosterone, methasterone (also known as superdrol), and methyl-1-testosterone. These steroids are particularly potent, so even though they possess minimal estrogenic and progestational activity, they will cause substantial suppression through the androgenic pathway.

The next class of anabolic steroids is the testosterone derivatives. These include testosterone and its esters, methyltestosterone, boldenone and its esters, methandrostenolone, bolasterone, 4-androstenediol and 4-androstenedione. These are generally strong androgens that have— to varying extents— the ability to aromatize to estrogens. However, they do not possess enough progestational activity to be of concern in that arena. However, due to the dual influence on hypothalamic estrogen receptors and androgen receptors, these will generally cause more suppression per active dose than the aforementioned classical DHT derivatives.

A subclass of testosterone derivatives includes some halogenated and hydroxylated testosterone analogs. These include clostebol, 4-hydroxytestosterone, turinabol, and fluoxymesterone, and ‘halodrol.’ Due to the unique chemical substitutions on these molecules, they are unable to aromatize, so these are less suppressive than traditional testosterone derivatives (with the possible exception of fluoxymesterone).

The next class of hormones is the 19-nor derivatives. There are two major types of 19-nors that possess markedly differing levels of suppression— 17alpha-alkylated and non-17alpha alkylated. The non-17alpha alkylated steroids include nandrolone, norandrostenedione, norandrostenediol, and trenbolone. The first three are steroids that can aromatize and have moderate progestational potential— therefore they are substantially suppressive. Trenbolone cannot aromatize, but it is very androgenic and does have a small amount of progestational activity so it too is quite suppressive.

As far as the second class of 19-nors goes— the 17alpha-alkylated ones— they are wickedly suppressive. These include norethandrolone, norbolethone, tetrahydrogestrinone (THG), normethandrone, and mibolerone, and metribolone. THG, metribolone, and mibolerone cannot aromatize, but the others can. Nonetheless, all of these have very high agonist activity at both hypothalamic androgen and progesterone receptors, so they produce major shutdown. These drugs do have their positives though; they can produce major, rapid, and dramatic gains in muscle mass and bodyweight. They are heavy-duty anabolics.

Preventing On-Cycle Testicular Atrophy

So now you understand that your choice of anabolic steroid determines the potential for HPTA suppression. The next step is to address the issue of on-cycle testicular atrophy that may occur. Testicular atrophy is the actual shrinking of the testosterone and sperm-producing cells of the testicles, due to the reduction of gonadotropin (LH and FSH) signals from the pituitary. Often this atrophy can actually be felt and seen. Short-term mild testicular atrophy usually will resolve itself; however, more severe and long-term atrophy is quite problematic. When the tissues of the testes shrink too much or over a long period of time, it can be difficult to get them to recover back to full size and functionality— even in the presence of adequate gonadotropin signaling.

The solution to minimizing on-cycle testicular atrophy is the use of exogenous gonadotropins. Human chorionic gonadotropin (HCG) and human menopausal gonadotropin (HMG) are the two options. What these injectable preparations do is provide your body with artificial gonadotropins, which will stimulate your testicles to produce testosterone and sperm. While these products are good at maintaining testicular size and functionality, they do nothing to address the problem of diminished LH and FSH production in the brain. Furthermore, prolonged use (of HCG) can cause desensitization of LH receptors at testicular leydig cells. So it is best to use these products as infrequently as possible during a cycle. Usually once every three weeks or so during a cycle, a few shots should be taken (spaced out every other day) and this should suffice.

After the Cycle

When your cycle is done, your LH and FSH levels will be suppressed. If you choose the right drugs and/or incorporate gonadotropin therapy during your cycle, you should have minimal testicular atrophy. It’s time for PCT.

As I mentioned before, PCT goes beyond just regaining full hypothalamic pituitary testicular axis function. It also should involve the use of special anti-catabolic compounds that will suppress the loss of muscle protein that may occur during the sensitive period between after the cycle and before full recovery. I will address the HPTA issues first and then the muscle loss issue.

Priming the Pump Again

It is my belief (and there are many opinions on this) that one should start their PCT with a selective estrogen receptor modulator (or SERM). These are also referred to as estrogen receptor antagonists. The most popular two of these are tamoxifen and clomiphene, but recently the drugs raloxifene, toremifine and enclomiphene (the active isomer of racemic clomiphene) have fallen into favor as well. These drugs work by binding to the estrogen receptor and occupying it; however, unlike classical estrogens, they fail to cause a full estrogenic biological response in tissues. When the tissue in question is the hypothalamus, SERM binding will result in an apparent ‘estrogen signaling deficit.’ This deficit causes the hypothalamus to release gonadotropin-releasing hormone (GnRH) which then travels to the pituitary where it further stimulates the production of gonadotropins (LH and FSH). The gonadotropins of course then proceed on to the testes, where they stimulate testosterone production and spermatogenesis.

The biggest problem with SERMs, however, is the fact that they not only raise testosterone levels— they also raise estrogen levels. While the SERM is still in the system, this is not a big problem because the SERM is keeping estrogenic biological activity in check. However, upon discontinuation of a SERM, there is a strong potential for testosterone/estrogen imbalance, and this imbalance can lead to a quick reversal of the HPTA recovery as well as estrogenic side effects such as gynecomastia.

The solution here is to switch to an aromatase inhibitor when the SERM is discontinued. Aromatase inhibitors work to actually reduce estrogen production, and in doing so, they continue to stimulate LH and FSH, while at the same time normalizing the testosterone estrogen ratio. Commonly used aromatase inhibitors are arimidex, fadrozole, exemestane, and the over-the-counter options 6-oxo and ATD. Aromatase inhibitors should be taken the last week of the SERM cycle (both drugs are overlapped for a week or so) and then continued until testosterone levels are normalized (blood tests are crucial here).


Last but not least you have to get your body into an anti-catabolic environment after your cycle, so your muscle mass does not dwindle away during this sensitive period. You start with the basics of course and that is to maintain a high-protein intake and proper pre- and post-workout nutrition. Beyond that, one of the best anti-catabolics out there is good old growth hormone. Just ask any football player who juices in the off-season and they will tell you that GH is a savior to them. In addition to GH, there is the drug called Trental (pentoxyfilline), which blocks many of the pathways related to muscle atrophy and can really help maintain mass during catabolic conditions. Other supplements of mention are the 7-oxygenated DHEA derivatives, which are known to antagonize many of the negative effects of cortisol in the body, as well as suppress catabolic inflammatory cytokines.

Plan Well and Grow

The bottom line is that you really can have your cake and eat it, too. Well, sort of. In other words, with a properly planned anabolic regimen, you can gain substantial muscle mass, keep most of it, and come out of it with ‘big jimmy and the twins’ as happy as ever.
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