Understanding Post-Cycle Therapy

Post-Cycle Therapy, or PCT for short, refers to the practice of using certain medications to assistant in the discontinuance of anabolic steroids. While steroids are not addictive drugs in a classical sense, they do suppress your own hormone production, at least temporarily. This is an issue that should be addressed at the conclusion of use. If the steroids are discontinued abruptly without addressing internal hormone production, the result could be a prolonged state of hypogonadism (low androgen levels) characterized by a substantial loss of muscle mass, reduced energy levels, depression, and impaired libido/sexual functioning. Steroid-using bodybuilders refer to this as the “post cycle crash”. In this section, we will examine the natural control of hormone production as it relates to this crash. We will also discuss certain medications that are commonly used during the postcycle window to help stimulate natural testosterone production and correct the hormonal imbalance.

The HPTA Axis

In the human body, the Hypothalamic-Pituitary-Testicular Axis (HPTA) controls testosterone biosynthesis. The HPTA is a tightly regulated system of checks and balances that works to assure the correct level of testosterone is maintained. We can look at this regulating process as having three levels. At the top is the hypothalamic region of the brain, which releases 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, to produce Luteinizing Hormone (LH). LH in turn sends a message to the Leydig’s cells in the testes (level three) to secrete testosterone. Given this role, LH is regarded as the primary direct messenger controlling testosterone synthesis. Testosterone and other sex steroids that are produced as a result of this LH stimulation serve as a counterbalance. They provide negative feedback to lower the secretion of LH and testosterone, preventing overproduction. Synthetic anabolic steroids, of course, send the same negative feedback. The serum level of testosterone is, therefore, a reflection of both positive and negative stimulation fighting each other for hormonal control.

The Hypothalamic-Pituitary-Testicular Axis: The hypothalamus releases Gonadotropin Releasing Hormone (GnRH), which stimulates the pituitary to release luteinizing hormone (LH) and follicle stimulating hormone (FSH). This (primarily LH) promotes the release of testosterone from the testes. Androgens, as well as estrogens and progestins, in turn cause negative feedback inhibition at the hypothalamus and pituitary, lowering the output of gonadotropins and testosterone when too much hormone is present.

 

Unaided HPTA Recovery

The suppression of natural testosterone synthesis by steroid use is typically a temporary phenomenon. Even if you do nothing, your body’s normal androgen synthesis will usually return a few to several months after the cycle is concluded. The problem is, this can be a very long time when you are relying on testosterone for so many things, including the maintenance of muscle tissue. In fact, much of the muscle mass achieved during AAS administration can be lost in the weeks and months to follow if low androgen levels are left unchecked. Post-Cycle Therapy is widely used by bodybuilders and athletes to stimulate the HPTA, so normal hormone production levels may come back more quickly. In order to accomplish this effectively, however, we need to first understand what HTPA recovery normally looks like without assistance. Only then can we identify the levels of the HPTA that are most open to manipulation with support medications.

Studies on the post-cessation aspect of anabolic steroid use, especially in AAS abusers, are lacking. In most cases we must refer to single-agent studies, usually of hormone replacement patients. One of the most detailed views of what a post-cycle crash probably looks like comes from an investigation into testosterone enanthate.354 It involves a group of men that were given weekly injections (250 mg) for 21 weeks, a dose that admittedly does go beyond normal HRT use. Various hormones were measured each week during the study, and for more than 4 months after the medication was discontinued. A review of the data shows that at the start of the study, LH levels were suppressed in direct relation to the rise in testosterone (see Figure I). Once the steroid was withdrawn, however, there was a delay between the return towards normal LH production (which began to correct by the 3rd week) and testosterone (which took more than 10 weeks before noticeable correction).

The above study suggests that one of the first things to happen after steroid cessation is that the brain recognizes testosterone levels are low again. This will cause GnRH and LH levels begin correcting fairly quickly. The substantial delay between this and an increase in testosterone levels is caused largely by testicular unresponsiveness to luteinizing hormone. After months of receiving extremely weak stimulation, they will have lost a substantial amount of mass (atrophied). This is a well-documented side effect of anabolic steroid use, even if a size difference may not be immediately visible in all cases. When LH levels begin surging back, the testes will initially be unable to handle the workload. This is expected to correct itself in time, but it may take many weeks for the testes to slowly restore to their original mass. With a good portion of the post-cycle recovery period actually being characterized by normal (even high) levels of LH, we must address recovery broadly if we expect it to be effective.

 

Figure I. LH and Testosterone measurements starting 1 week after the last injection of 250mg of testosterone enanthate (pretreated measures were 5 mU/ml and 4.5 ng/ml respectively).Note that between weeks 1 and 5, as testosterone levels are declining due to the cessation of exogenous androgen administration, LH levels are beginning to correct. From weeks 5 to 10, testosterone levels remain at or very near baseline, although LH is increasing by this point.No notable correction in testosterone occurs until after the 10-week mark.

hCG in Post-Cycle Therapy

Human Chorionic Gonadotropin (hCG) is a fertility drug that mimics the actions of luteinizing hormone. It is commonly used during the post-cycle period to address testicular atrophy, which as we have seen is one of the fundamental roadblocks to hormonal recovery. The hCG is typically taken at a substantial dosage for a period of 2-3 weeks. Testicular atrophy is caused by a lack of LH stimulation, and likewise recovery is function of increased LH. The objective with hCG is to maximize stimulation of the testes so their original mass is recovered more quickly than if we relied solely on physiological LH production. It is important that hCG not be overused. Testicular sensitization to this hormone is a delicately regulated mechanism. When hCG is taken for too long or at too high a dosage, the LH receptor can become desensitized.355 This can actually interfere with recovery of hypothalamic-pituitary-testicular axis. A detailed program utilizing hCG is outlined later in this section. For additional information, please refer to the Human Chorionic Gonadotropin drug profile in this book.

Anti-Estrogens in PCT

The anti-estrogenic drugs Clomid (clomiphene citrate) and Nolvadex (tamoxifen citrate) are also commonly used during the post-cycle period. These drugs are used to block the negative feedback inhibition of estrogen, which occurs primarily at the hypothalamus.356 This may foster the heightened release of GnRH, and subsequently LH and testosterone. While estrogen levels are not especially high in men, it is still a very strong inhibitor of testosterone release.357 Since it is also formed from the aromatization of testosterone in peripheral tissues, its role in the regulation of androgen biosynthesis is regarded as a fairly direct one. The purpose of using anti-estrogens is to both trigger correction in LH levels more quickly, and to augment total LH. They may also be necessary to combat gynecomastia in some individuals, which can occur even with low estrogen levels (it is partly a function of the androgen to estrogen balance in the breast).

It is important to note that the use of anti-estrogens alone is generally not regarded as an effectively strategy for addressing hormone recovery at the conclusion of a steroid cycle. This is because these drugs only work by fostering the heightened release of luteinizing hormone. We expect that the post-cycle window is already partly characterized by normal/high LH levels. Thus, while anti-estrogens may have an additive effect in this regard, they do not effectively and directly address the main roadblock to hormonal recovery after steroid use, namely testicular atrophy. Because of this, it is also generally advised to directly target the testes with hCG. This usually means the initiation of a traditional PCT program after every formidable period of AAS use, which utilizes all three of the medications discussed in this section. There are some exceptions when an abbreviated PCT program may be desirable, which we will discuss later on.

Traditional PCT Program

The following post-cycle therapy program was developed by Dr. Michael Scally, one of the most well known and accomplished individuals in the field of anabolic steroids and male hormone replacement medicine. Scally has been a particularly strong force lobbying the medical community and government to recognize the hormonal imbalance that follows steroid use, something he has dubbed anabolic steroid induced hypogonadism (ASIH). He has also treated and done blood work on hundreds of patients, and while doing so developed the following PCT program. A slightly modified form of this program was outlined in a clinical report involving 19 healthy male subjects taking supraphysiological (highly suppressive) doses of testosterone cypionate and nandrolone decanoate for 12 weeks. Scally’s “HPGA Normalization Protocol” focuses on the combined use of hCG, Nolvadex, and Clomid, and is perhaps the most trusted and clinically supported post-cycle therapy program presently available.

This post-cycle therapy program begins with a substantial dose of hCG (2000 IU every other day for 20 days). Anti-estrogens are also used during this period. This is potentially important because hCG may up-regulate testicular aromatase activity.358 Thus, their use can minimize both estrogenic side effects and reduce negative feedback inhibition of testosterone release. The anti-estrogens taken are tamoxifen citrate (20 mg twice per day) and clomiphene citrate (50 mg twice per day). Clomid is used for a shorter period of time, in a stepping down of the program’s medications. While in the first couple of weeks the anti- estrogens may not be highly effective, they should prove more critical towards the middle and end of the program. In the published version of Scally’s program (which is slightly modified from the above), normal hormonal function returned in all subjects within 45 days. This is a definite success, far more favorable than the protracted recovery window reported in the study with 250 mg/week of testosterone enanthate.

Protocols: Human chorionic gonadotropin (hCG) is taken at 2000IU every other day for 20 days. Clomiphene citrate 50 mg is taken twice per day for 30 days.Tamoxifen citrate is taken 20 mg twice per day for 45 days.

The timing for a Post-Cycle Therapy program can be as important as its composition. If it is initiated too late, valuable days of normal hormone levels (and also some muscle mass) may be lost. If you start the program too early, you may miss the optimal window of effectiveness. The 20-day period of time in which hCG is used is the most critical, and thus we time the PCT program around this medication. In particular, we want to make sure that hCG is being applied right around the time that exogenous steroids are dropping below the threshold of physiological androgen stimulation. In the case of testosterone (the easiest drug to understand and explain), this would be right before blood levels drop below the normal level (350 ng/dL). There should be a small overlap with the on-cycle period, so that hCG has a little time to work before AAS levels are completely diminished.

The exact timing for PCT program is determined by the elimination half-life of the drug(s) used. We will use testosterone cypionate/enanthate as an example. We know each injection has an elimination half-life of approximately 8 days. A dose of 200 mg/week should produce blood levels of around 2000-2400 ng/dL after several weeks of use. It would take about 3 half lives (24 days) for testosterone levels to drop to approximately 250-300 ng/dL at that dose. Thus, the PCT program would be initiated a few days to one week after the last testosterone injection. The program would be delayed with higher doses. For example, at 500 mg per week of TC/TE it should take approximately 4 half lives (32 days) for testosterone to drop below the normal range. In this case, PCT would be initiated about two weeks after the last testosterone injection. With an orals-only cycle (with no extended half-life due to an injection site reservoir), PCT is initiated 7-10 days before the last steroid pills are taken.

 

Timing The Start of PCT

Type of AAS used : PCT Initiation


Cypionate/Enanthate : 3-7 days after last injection (200 mg/week)

Cypionate/Enanthate : 10-14 days (500 mg/week)

Decanoate : 10-14 daysn (200 mg/week)

Decanoate : 18-21 days (500 mg/week)

 

References:

354. Effect of long-term testosterone oenanthate administration on male reproductive function: Clinical evaluation, serum FSH, LH, Testosterone and seminal fluid analysis in normal men.J. Mauss, G. Borsch et al. Acta Endocrinol 78 (1975) 373-84
355. Desensitization to gonadotropins in cultured Leydig tumor cells involves loss of gonadotropin receptors and decreased capacity for steroidogenesis. Freeman DA, Ascoli M Proc Natl Acad Sci U S A 1981 Oct;78(10):6309-13
356. Inhibition of luteinizing hormone secretion by testosterone in men requires aromatization for its pituitary but not its hypothalamic effects: evidence from the tandem study of normal and gonadotropin-releasing hormone-deficient men. Pitteloud N, Dwyer AA, DeCruz S, Lee H, Boepple PA, Crowley WF Jr, Hayes FJ. J Clin Endocrinol Metab. 2008 Mar;93(3):784-91. Epub 2007 Dec 11.
357. The effect of aromatase inhibition on sex steroids, gonadotropins, and markers of bone turnover in older men. Taxel P, Kennedy DG et al. J Clin Endocrinol Metab. 2001 Jun;86(6):2869-74.
358. Acute stimulation of aromatization in Leydig Cells by Human Chorionic Gonadotropin In-vitro. Proc Natl Acad Sci USA 76:4460-3,1079

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