PCT - 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. Steroidusing 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. 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.

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.
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.

References

Wlliam Llewellyn (2011) - Anabolics

Your experience with PCT - Post-Cycle Therapy

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