by Mike Arnold
As the greatest development in the area of adjunctive performance enhancement in the last 20 years, post-cycle therapy offers undeniable benefits to the cycling steroid user. The ability to maintain long-term endogenous testosterone production, preserve muscle mass between cycles, reduce off time from AAS, and protect fertility are usually the most appreciated. With so much confusion on the subject, let’s take a few minutes to discuss the various PCT drugs and their role in maintaining our hormonal landscape. Although differences in financial status, goals, and degree of suppression prevent a single program from meeting the needs of all, there are some basic guidelines that any effective PCT program should adhere to.
Normally, PCT is referred to as the time period during which natural testosterone production is restored through the use of recovery drugs and is initiated after a cycle has been completed. However, it is not necessarily limited to this singular objective. Being a general term, PCT can apply to the post-cycle normalization of any/all bodily systems adversely affected by AAS. In this article we will be focusing specifically on testosterone and sperm production—the synthesis of which is governed directly by the HPTA. Technically speaking, PCT falls under the umbrella of HPTA Maintenance; a more comprehensive term which encompasses both pre and post-cycle care, but before we can properly understand how PCT works, we must first understand the HPTA and its role in regulating our hormonal environment.
The HPTA, short for hypothalamic-pituitary-gonadal-axis, is a negative feedback system designed to monitor and control both testosterone levels and sperm production. Its primary agenda is to make sure that testosterone levels do not rise too high or too low, thereby maintaining homeostasis. Homeostasis is defined as a relatively stable state of equilibrium or a tendency toward such a state between the different but interdependent physiological processes of an organism. In laymen’s terms, homeostasis is a state of balance. The HPTA achieves this balance when the hormones testosterone, estrogen, LH, and FSH all line up, resulting in ideal levels of testosterone and sperm.
In reality, the pursuit of homeostasis is a never-ending process of checks & balances, in which each of the above mentioned hormones is constantly counter-balancing the other in an attempt to normalize the production of testosterone & sperm. This system of checks & balances is known as the negative feedback loop and involves the hypothalamus (the part of the brain which controls various endocrine functions), the pituitary gland, and the testes. From this we get the first three letters of abbreviated term “H.P.T.A”.
There are multiple negative feedback systems in the body, all of which are comprised of a sensor, a control center, and an effector. Their job is to assess and respond to a particular stimulus. In the case of the HPTA, testosterone is the stimulus, while the hypothalamus acts as both the sensor and the control center and the pituitary is the effector. Here’s how it works. When a factor being regulated changes (stimulus), the sensor picks up on that change and relays the information to the control center. The control center then sends out a message to the effector, which takes action to normalize the factor.
In the case of the HPTA, testosterone is the factor being regulated. When testosterone levels fall below the body’s ideal set-point (stimulus), the hypothalamus (which acts as both the sensor and control center) reads this change and then signals the pituitary (the effector) to secrete LH and FSH (LH is the hormone responsible for testosterone production and FSH for sperm production). This process will continue until testosterone levels have been normalized. As another example, let’s look at the typical home heating system. In this case, the temperature is the factor being regulated. When the temperature falls below the set-point (stimulus), the thermometer (sensor & control center) recognizes the change and subsequently signals the heater (the effector) to kick on until the temperature reaches the proper setting. This is exactly how the HPTA regulates testosterone and sperm production. See below.
When we use steroids the body reacts to them in the same way it reacts to its naturally produced testosterone. Therefore, when blood androgen levels rise into the supraphysiological range (as they always do when using steroids), the hypothalamus interprets this as testosterone excess. The hypothalamus responds to this elevation by telling the pituitary to stop secreting LH and FSH. Using BB’ing terminology, this is what we refer to as a state of “suppression”—when the pituitary is no longer releasing the hormones necessary for maintaining testosterone and sperm production.
Now, it makes sense why the hypothalamus would tell the pituitary to stop releasing LH, but why FSH? The answer is simple. Although it requires two separate hormones (LH & FSH) to produce testosterone and sperm, the release of these hormones is regulated by the same factor—testosterone levels. So, if the production of both testosterone and sperm are dependent on testosterone levels, anytime blood levels of testosterone rise outside of the normal range, it will adversely affect the production of both testosterone and sperm.
However, testosterone levels aren’t the only thing capable of impacting our testosterone-sperm production. The HPTA also uses estrogen as a means of regulating these hormones. Unlike women, whose ovaries produce estrogen directly, men rely on aromatization (conversion of testosterone into estrogen) in order to supply their body with estrogen. Under normal circumstances (e.g. drug-free) this is not a problem, as estrogen levels are usually balanced with testosterone at a set ratio, providing a fairly reliable indicator of testosterone output. Because of this, when estrogen levels climb out of a normal range, the body thinks that testosterone levels are also elevated. It attempts to deal with this by reducing LH & FSH output, effectively lowering testosterone and sperm levels. In the same way, when estrogen levels get too low, the body increases testosterone production in order to make up for the deficit via increased aromatization.
It is important to understand that when we use steroids, the HPTA experiences suppression at both the pituitary (decreased LH production) and the testes (decreased test & sperm production leading to atrophy). Both of these issues must be addressed if we wish to experience the most rapid recovery possible. Enter HCG. Many people misunderstand the role of HCG in a BB’rs recovery plan, assuming that its use will assist in recovery of the HPTA. This couldn’t be further from the truth. In reality, HCG is a suppressive compound, leading to a decrease in LH production. At this point you may be asking “If HCG is suppressive, then why do so many people use it to increase/maintain testosterone production?” Glad you asked.
HCG has only one purpose in a BBr’s program—to maintain functioning of the testes. Basically, HCG is recognized by the testicles as LH, which allows it to bypass both the hypothalamus and the pituitary (the 1st and 2nd links in the chain) and stimulate testosterone production directly at the testes (the 3rd link in the chain). So, while HCG will increase testosterone production, it does so by fooling the body into thinking that adequate LH is present. Because of this, natural LH production will remain suppressed. This makes HCG a suppressive substance at the level of the hypothalamus and pituitary. None the less, there are definite benefits to using HCG, but only when used at the proper time.
When PCT is initiated, two things need to happen in order to experience a full recovery. One, the pituitary needs to begin secreting adequate amounts of LH & FSH and two, the testes need to re-grow to their previous size, as atrophied testes are not able to produce testosterone or sperm at 100% capacity. By using HCG only while under the suppressive influence of AAS (i.e. steroids are still in the system), we are able to maintain testosterone production throughout the entire cycle. This prevents the testes from shrinking, enabling them to take full advantage of the natural surge in LH & FSH that occurs when we begin using recovery drugs during PCT. By limiting the use of HCG only to the on-cycle period, its suppressive effect becomes is irrelevant, as LH & FSH production will already be suppressed by the AAS.
HCG therapy should be initiated at the onset of one’s cycle, not a few weeks into the cycle and certainly not afterward. The reasoning is simple. It is easier to maintain function than it is to restore it. Why allow the testes to atrophy, only to turn around a few weeks later and fight to reverse it? Common sense dictates a more practical approach. When it comes to any aspect of the HPTA, the less disruption, the better. HCG should continue to be administered until 2 days before the last steroid exits the system, due to the drug’s 33 hour half-life.
Unfortunately, HCG has only a moderate effect on maintaining sperm production when under the influence of AAS—sustaining about 20% of one’s normal production according to one study. Certainly, this is better than nothing, but not ideal. If maintaining sperm count while on-cycle is important to you, then HMG (a combination of FSH & LH) or straight FSH are far more potent options, as these drugs directly promote increased sperm production. However, unless one is actively trying to impregnate their spouse, then it is probably in their best interest to forego this option, as HMG is somewhat expensive and sperm count is fairly easily restored with conventional PCT. Unlike testosterone production, which can be permanently inhibited to varying degrees through steroid use, sperm count is much more easily restored, especially when employing the appropriate fertility meds. Rarely do former steroid users lose the ability to have children. Also, keep in mind that sperm count is of little relevance when one isn’t trying to conceive, unlike testosterone deficiency, which can adversely affect several different aspects of one’s everyday life and health. For these reasons, focusing directly on sperm count usually isn’t necessary.
There have been many different recommendations over the years for post-cycle therapy. Traditionally, PCT has consisted of either one or two SERM’s, such as Clomid and/or Nolvadex, run for a period of 4-6 weeks. Both of these drugs work similarly to HCG in that they increase testosterone & sperm production, but the main difference is in “how” they do so. While HCG acts directly at the testes, bypassing the hypothalamus and pituitary, SERM’s work at the level of the hypothalamus by blocking estrogen. Remember how I said earlier that estrogen is suppressive of LH & FSH production? Well, by preventing estrogen from reaching the hypothalamus, it thinks that estrogen levels are still too low. As a result, the hypothalamus signals the pituitary to secrete more LH & FSH, which then travels to the testes, kicking testosterone and sperm production into high gear.
By stimulating the pituitary to secrete LH & FSH instead of suppressing it like HCG does, SERM’s assist in the recovery of the entire HPTA system. This way, by the time PCT is finished, everything is working properly and testosterone production continues uninhibited. However, their ability to initiate testosterone production at the hypothalamus is also their Achilles’ heel when it comes to on-cycle test production. Quite frankly, SERM’s are completely ineffective at turning on testosterone-sperm production when blood levels of AAS are still elevated. Although the SERM’s can still block estrogen at the hypothalamus when using steroids, the supraphysiological androgen blood levels associated with AAS use will completely suppress LH release regardless of whether estrogen is blocked or not.
This makes HCG the ideal on-cycle agent for maintaining testicular function and SERM’s the superior off-cycle drug for HPTA recovery. When both are used at the proper time, recovery is accelerated beyond what would occur when using either one alone.
In recent years, more and more BB’rs have begun turning to AI’s for both on-cycle use and during PCT. There is good reason for this. In terms of on-cycle use, its cuts down on the incidence of estrogen-relates side effects, but it also prepares the BB’ for a quicker recovery by minimizing estrogen levels at the start of PCT. Remember, estrogen is highly suppressive of natural testosterone & sperm production, so by normalizing estrogen levels during one’s cycle, there is less of a hurdle to overcome after beginning PCT.
Being excellent recovery drugs in their own right, AI’s have been extensively studied in the area of testosterone-sperm production, with repeated studies demonstrating an increase in both total & free T levels comparable to those achieved with SERM administration. SERM’s and AI’s work through the same basic mechanism—by eliminating/minimizing the suppressive influence of estrogen at the hypothalamus. However, while SERM’s “block” estrogen from reaching the hypothalamus, AI’s actually reduce estrogen synthesis. Either way, the end result is the same—less estrogen comes in contact with the hypothalamus, leading to an increase in LH release.
While clinical studies comparing the effects of a 2 SERM combo to a 1 SERM, 1 AI combo are lacking, real-world evidence suggest that the SERM-AI combo is superior. This is probably because SERMs all work through the same pathway, which limits their ability to reduce estrogen exposure at the hypothalamus, while SERM’s and AI’s work through similar, yet different pathways, minimizing exposure as much as possible. This type of synergistic effect is common in many other areas of performance enhancement, so it would not be unusual to see it happen here.
There is some debate as to whether the use of 2 SERM’s (usually Clomid & Nolvadex), combined with an AI, is any more beneficial than the standard 1 SERM, 1 AI combination. Still, some are convinced that it provides superior results. I have not taken a stance on the issue yet, but it certainly wouldn’t hurt, so if you want to try both methods, I suggest getting bloodwork after each and comparing the results.
When deciding which AI you are going to use for PCT, I suggest choosing a Class I aromatase inhibitor, also known as a suicide inhibitor, as this type of AI permanently deactivates any estrogen it comes in contact with. This will eliminate the possibility of encountering estrogen rebound after completion of PCT. Estrogen rebound can be a real problem for some people, so you may as well be safe rather than sorry. Perhaps even more importantly, some of the Class I AI’s (ex. Aromasin) do not have negative effects of cholesterol levels, unlike AI’s such as Letrozole and Arimidex.
Although there is a lot to learn regarding the underlying complexities of HPTA maintenance, applying what you’ve learned here is relatively simple. When done correctly, recovery is greatly enhanced, providing all the benefits mentioned in the beginning of the article. Aside from the HPTA, the time you take off during PCT also provides the body with an opportunity to normalize some of its other health markers, which will certainly get out of range when using AAS for an extended period of time. All in all, HPTA maintenance is a beneficial and healthy practice for all those who cycle their AAS. To neglect it would be either foolish or a demonstration of ignorance. Until next time…