Post Cycle Therapy

Post cycle therapy (PCT) is perhaps the most important aspect of anabolic steroid use.

In the 1950s, 1960s, and 1970s, the mechanisms by which anabolic steroids affect the body were not fully understood, so the concept of PCT did not exist before the late 1980s and early 1990s.

This was a time when doctors, scientists, and anabolic steroid users were just beginning to learn about the mechanics of anabolic steroids and their effects on the endocrine system.

From the earliest days of anabolic steroid use, it was understood that exogenous administration of anabolic steroids triggered a negative feedback loop in the body's hypothalamic-pituitary-testicular axis (HPTA), resulting in the suppression or shutdown of endogenous testosterone production.

Unfortunately, in the early days of anabolic steroid use (between the 1950s and 1990s), there were limited compounds or knowledge on how to effectively mitigate these effects.

It's a very different story today, where the scientific and medical understanding of anabolic steroid use has grown exponentially since the "golden age" of anabolic steroid use by bodybuilders and athletes.

The development of a myriad of beneficial compounds aimed at hormonal recovery after anabolic steroid use and the increase in scientific and medical knowledge has made anabolic steroid use and associated endocrine disorders much safer than in the past.

With the proper knowledge of how to properly and efficiently restore the body's HPTA and hormonal system through post cycle therapy (PCT), an individual can not only come off an anabolic steroid cycle while retaining almost all of their muscle gains, but also increase their chances of coming off with a fully functioning endocrine system and healthy HPTA to over 90%.

After using exogenous anabolic steroids, most users will experience what is referred to as a "hormonal crash" or "post cycle crash", a condition in the body where key hormones essential to maintaining newly created muscle mass are suppressed or shut down.

The key hormones in question are LH (luteinizing hormone), FSH (follicle stimulating hormone), and most importantly, testosterone.

LH and FSH are known as gonadotropins, which are hormones that signal the gonads (testes) to start or increase the production and secretion of testosterone.

Low levels of these hormones can throw your overall hormonal balance out of whack, resulting in low testosterone levels and, in most cases (depending on many factors), high estrogen levels and normal levels of cortisol (a steroid hormone that destroys muscle tissue).

When testosterone levels are low and cortisol levels are in the normal (or high) range, cortisol poses a threat to newly built muscle from a recent anabolic steroid cycle (testosterone adequately inhibits and offsets cortisol's catabolic effects on muscle tissue).

Also of concern is SHBG (sex hormone binding globulin), a protein that binds to sex hormones (testosterone) and renders them inactive, "handcuffing" them so that they cannot exert their effects.

In addition, due to the supraphysiologic levels of androgens from a recent anabolic steroid cycle, SHBG is typically elevated for several weeks after a cycle.

While the body typically corrects this hormonal imbalance and restores endogenous testosterone levels on its own over time without assistance, studies have shown that this occurs over a period of 1-4 months without the intervention of testosterone stimulants.

This is enough time for the hormonal imbalance to wreak havoc on your body and cause you to lose most or all of your newly gained muscle during this time.

Therefore, every anabolic steroid user should be concerned with the fastest possible hormonal recovery, which should be aided and enhanced by the proper use of testosterone stimulating compounds.

Furthermore, if the body is left to recover on its own, it is very likely that long-term endocrine damage will occur to HPTA over time, which can lead to anabolic steroid-induced hypogonadism (the inability to produce adequate levels of testosterone for life).

Therefore, it is of utmost importance to not only restore HPTA function to normal levels as quickly as possible, but also to prevent permanent damage by using a proper post-cycle regimen that includes several restorative compounds, which should be prioritized over maintaining recently gained muscle mass.

Which post-cycle treatment protocol should I use?

There are many different types of PCT protocols that have been developed over the years, and at first glance, any individual would be extremely confused as to how many different opinions exist in the anabolic steroid-using community, and how many different established PCT protocols exist.

In this post, we will present the best and most efficient post cycle therapy protocol possible, backed by valid scientific data and logical reasoning.

This article will also dispel a number of myths surrounding PCT and outline PCT protocols that should not be followed due to recent advances and better scientific and medical understanding of how a proper post cycle therapy protocol should work.

At this point in time, there are some very outdated and consequently ineffective PCT protocols that are still used by many anabolic steroid users, and this poses a serious risk not only to the individual who is unknowingly using an outdated post cycle therapy program, but also to anyone who may be observing, learning from, and gathering ideas from that individual.

A lack of understanding of what specifically is going on in the endocrine system during this critical time and a lack of understanding of what compounds to use, what each compound does, and how to use them appropriately can lead to serious problems.

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HPTA: How it works

The HPTA is the hypothalamic-pituitary-testicular axis, an interconnected axis of the body's endocrine glands that processes and regulates testosterone production.

Shown above is a diagram of the HPTA.

The HPTA regulates how much testosterone is produced and circulated in the body at any given time.

Every individual has a maximum amount of testosterone production programmed into them by their genetics (DNA), and this is the most important determinant.

There are other factors that determine how much testosterone an individual produces, including age, diet, body composition, lifestyle, and physical activity.

All of these factors affect an individual's overall testosterone production.

HPTA functions in what is known as a negative feedback loop, in which the body reduces the production and secretion of testosterone when it senses too much testosterone circulating in the body, and adjusts accordingly when it senses too little.

This sensing and adjustment, known as a negative feedback loop, is essentially controlled by the hypothalamus, which is considered the "master" gland for all endocrine and hormonal functions in the body.

Negative feedback loops are ultimately the body's attempt to maintain hormonal homeostasis, which means regulating a system (in this case, the body's internal systems) to maintain a stable and consistently favorable state.

All endocrine glands operate in some way and to varying degrees through negative feedback loops.

In the case of post cycle therapy, it is primarily the negative feedback loop of HPTA that is at issue.

In HPTA, the concern during PCT is the restoration of homeostasis and regulation of the following five hormones:

- GnRH (gonadotropin-releasing hormone)

- LH (luteinizing hormone)

- FSH (follicle stimulating hormone)

- Testosterone

HPTA starts at the first axis point, the hypothalamus, which senses the body's need to produce more testosterone and releases varying amounts of GnRH.

GnRH is the hormone that signals the next axis point, the pituitary gland, to begin manufacturing and releasing two important gonadotropins (LH and FSH).

LH and FSH are the two hormones responsible for signaling the third axis point, the testes, to begin the production and release of testosterone.

This is the final step in the production of testosterone in the HPTA.

There are two main hormonal factors that act to inhibit, reduce, suppress, or stop testosterone production in the HPTA

- Excess testosterone

- Excess estrogen

There are other hormones, such as progestins and prolactin, that also play a role in inhibiting and suppressing HPTA function, but these are the main conditional hormones of concern.

When the hypothalamus senses excessive levels of testosterone and/or estrogen in the body (either through the use of exogenous androgens in an anabolic steroid cycle or otherwise), it attempts to restore balance by essentially doing the opposite of what we described earlier.

The hypothalamus reduces or stops the production of GnRH, which in turn stops the production of LH and FSH, and ultimately reduces or stops the production of testosterone.

Production of the various signaling hormones within the HPTA will not begin until the ideal hormonal environment in the hypothalamus is restored, and it often takes months for the body to accomplish this process on its own without the intervention of testosterone stimulants.

It should be very clear why the recovery of HPTA takes so long naturally, due to the actions of HPTA described.

A basic understanding of the mechanism of HPTA and the negative feedback loop described above is essential to understanding how and why a proper post cycle therapy (PCT) program should be developed and utilized after an anabolic steroid cycle.

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Determine what makes HPTA recovery difficult

When using anabolic steroids, there are a number of key determinants of how difficult it will be for an individual to regain HPTA and endogenous testosterone function during PCT.

These factors include, in no particular order of importance, the following

1. individual response

2. type of anabolic steroid used

3. cycle length (testicular desensitization)

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1. Individual Reactions

Each individual reacts in a different way to every chemical, compound, anabolic steroid, food, or drug in existence.

Some people may experience no HPTA suppression or disruption at all, while others may experience severe HPTA suppression and disruption to the point where they need much more time than most to fully recover.

As with everything else, there are 'lucky' individuals on one end of the spectrum who recover very quickly and easily, and 'unlucky' individuals on the other end who have an extremely difficult time recovering after treatment.

In between the two extremes is the mean.

Again, this is due to the individual's genetic programming of how the HPTA responds and tries to maintain homeostasis.

2. Types of anabolic steroids used

All anabolic steroids inhibit or block HPTA through the mechanism of a negative feedback loop, there are no exceptions.

Various anabolic steroids are known to inhibit it mildly, while others are known to inhibit it strongly.

It all depends on a number of different reasons, most of which we won't go into here.

In any case, regardless of how mildly or severely anabolic steroids inhibit HPTA, if all anabolic steroids are used for a typical cycle of several weeks at a time, they will eventually shut down HPTA, or at the very least severely inhibit the hormonal signaling process.

3. Cycle length (degree of testicular desensitization)

This is probably the most important and most influential factor.

The longer the duration of anabolic steroid use, the more the majority of Leydig cells in the testes remain dormant and inactive, and the longer the period of time these interstitial cells remain dormant and inactive, the inherently more difficult it is to get these cells to respond again to the stimulation of LH and FSH.

Research has shown that the problem with recovery of Leydig cells after anabolic steroid use is not due to a lack of LH, but rather because the Leydig cells have become desensitized to LH [1].

In one study in which male subjects were given exogenous testosterone for 21 weeks, LH levels were suppressed shortly after the start of treatment.

However, at the end of the 21-week period and within three weeks after exogenous testosterone administration was stopped, LH levels were observed to rise, but in most subjects, testosterone levels did not rise until several weeks later.

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Three Key Testosterone Stimulants for HPTA Recovery During PCT

Before diving into the details of the three types of testosterone stimulating compounds for hormonal recovery during post cycle therapy, it is very important for individuals to understand that using any single compound except one or two is inadequate for hormonal recovery during PCT.

Ideally, any post cycle therapy program should be a multi-component PCT program that includes several different compounds that work together to provide the most effective and fastest HPTA recovery after an anabolic steroid cycle.

The three categories of compounds are

1. selective estrogen receptor modulators (SERMs)

2. aromatase inhibitors

3. HCG (human chorionic gonadotropin)

SERMs

Medications in the SERM category include Nolvadex (tamoxifen citrate), Clomid (clomiphene citrate), raloxifene, and Fareston (toremifene citrate). The nature of SERMs is that they exert a mixture of estrogen agonist and estrogen antagonist effects on the body.

This means that SERMs can block the effects of estrogen at the cellular level in certain tissues, but they can enhance the effects of estrogen in other parts of the body.

This can be a positive or negative effect.

For example, Nolvadex has an estrogenic effect in the liver, which for all intents and purposes is a positive effect because its effects in the liver lead to positive changes in the cholesterol profile (which is what many people want).

To varying degrees, all SERMs act as estrogen antagonists at this site, mitigating the effects of estrogen on breast tissue and reducing or blocking the side effects of gynecomastia.

In terms of the effect of SERMs on endogenous testosterone stimulation, they act as estrogen antagonists in the pituitary gland, which in turn triggers the release of LH and FSH.

Elevated estrogen levels in men can, and do, suppress the secretion of endogenous testosterone through a negative feedback loop, leading to hypogonadism [2].

SERMs for this purpose should absolutely be added to any PCT protocol and should not be excluded under any circumstances.

However, regardless of this, the focus should not be solely on SERMs.

Aromatase inhibitors

These include compounds such as aromasin (Exemestane), Arimidex (Anastrozole), and Letrozole (Femara).

Aromatase inhibitors (AIs) work to lower total circulating estrogen levels in the body by inhibiting the aromatase enzyme, the enzyme that converts androgens to estrogen, rather than blocking the activity of estrogen at the cellular level in other tissues.

When androgens are converted to estrogen, estrogen levels become excessive, and as discussed earlier in this article, a negative feedback loop is initiated, resulting in suppressed testosterone production.

By lowering total circulating plasma estrogen levels, the negative feedback loop works in a positive way, causing LH and FSH to be released to produce and secrete more testosterone.

This is essentially because the hypothalamus recognizes that circulating estrogen levels are too low and attempts to increase circulating testosterone levels so that some of the secreted testosterone can be redirected into estrogen to restore hormonal balance.

Another importance of aromatase inhibitors is that they can mitigate the estrogenic effects of HCG, which we'll discuss shortly.

However, it is important to note that most aromatase inhibitors do not work well with SERMs like Nolvadex, and you will need to be very specific about which aromatase inhibitor you choose to use during PCT.

Human chorionic gonadotropin (HCG)

Human chorionic gonadotropin is mostly synthetic LH.

It is a protein hormone that is manufactured in large quantities in pregnant women and contains 100% of the same protein subunits as LH, so when administered to men, it mimics the actions of LH in target tissues such as the testes.

The result is increased testosterone production through stimulation of Leydig cells by HCG.

HCG should not be used alone because its very nature as a gonadotropin causes a negative feedback loop: when HCG is used, the pituitary gland stops secreting LH until the HCG is stopped.

Therefore, HCG must be used in conjunction with a SERM, specifically an aromatase inhibitor, as it has been proven to increase aromatase activity in the testes, leading to elevated estrogen levels [3].

Synthesizing

You may be wondering which compounds to choose from the three categories listed and how to use them appropriately.

The answer lies in understanding the properties of each compound and how to use them efficiently and appropriately.

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HCG

The first item we'll look at is HCG.

From the 1960s to the mid-1980s, most anabolic steroid users didn't use any compounds for hormone recovery, and the term PCT didn't even exist back then.

When the use of HCG became increasingly popular (around 1980), it was the only compound used.

Since then, the medical and scientific understanding of it has grown exponentially, and there is no reason for an informed and properly trained person to not utilize HCG alone for PCT.

When utilized in conjunction with one of the other two categories of compounds (AIs and SERMs), the dynamics are quite different.

We've already mentioned that the difficulty in recovering HPTA after an anabolic steroid cycle is a result of Leydig cell desensitization.

HCG is essentially an analog of LH, and testes that have been through a prolonged anabolic steroid cycle will be equally desensitized to HCG as they are to LH.

However, the human body produces its own LH in amounts that are far too inefficient for adequate and rapid testosterone production. As the aforementioned studies show, the body's natural LH and FSH increase following an anabolic steroid cycle is not a sharp peak, but rather a very slow and steady slope, with studies showing that LH levels did not begin to reach normal physiologic measurements until three weeks after exogenous testosterone was discontinued.

Thus, the body's own natural LH production does not provide sufficient capacity for stimulation, nor does it provide the immediate stimulation to the testes needed for the initial increase in testosterone that is required in the weeks following cycle therapy.

HCG, used in a specific manner during the first 1-2 weeks of PCT at a dose of 100-1,500 IU every 2 days, provides a high dose to the testes to provide a "shock" effect on the testes and to maintain this shock effect on the Leydig cells in the testes for the first 1-2 weeks of post cycle therapy.

Indeed, the remarkable effectiveness of HCG for this purpose has been demonstrated, and it has even been proposed clinically to utilize HCG for the treatment of anabolic steroid-induced hypogonadism [4].

In line with this idea, the other two compounds (SERM and AI) will be utilized as adjunctive compounds to the use of HCG during this 1-2 week period, and after HCG is discontinued early in the PCT, only the SERM will be used to drive the hormonal recovery process.

Despite the good news that HCG is helping hormone recovery, there are still two issues that need to be addressed

- The fact that HCG increases aromatase production, which increases estrogen levels.

- When HCG administration is stopped, there is little endogenous LH and FSH production left due to exogenous administration.

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Aromatase inhibitor: Aromasin (Exemestane)

The first of the two remaining issues that need to be addressed is the fact that HCG increases testicular aromatase expression and causes an increase in estrogen in the body.

It is also important to note that it can increase testicular progesterone levels.

As we have already explained that estrogen suppresses endogenous testosterone production, elevated estrogen is of course undesirable during PCT, and there is no doubt that individuals do not want to experience estrogenic side effects during PCT.

So the option here is to include an aromatase inhibitor.

However, there is a big problem with the other two of the big three aromatase inhibitors (Arimidex and Letrozole).

The problem is that in a PCT program that includes the use of SERMs like Nolvadex and Clomid, which are known to be absolutely essential components of a PCT program, Arimidex and Letrozole have a direct negative interaction with Nolvadex.

The problem here is that Arimidex (or letrozole) and Nolvadex directly cancel each other out.

One study showed that when Arimidex is used in combination with Nolvadex, Nolvadex decreases the plasma concentration of Arimidex (and Letrozole, another commonly used aromatase inhibitor) [5].

The bottom line is that using Nolvadex with Arimidex or Letrozole is a very bad idea and can be counterproductive when used together in a PCT protocol.

Aromasin, unlike the other two aromatase inhibitors mentioned above, has been proven to have no interaction with Nolvadex at all, so this issue can be avoided completely.

In one study, aromasin did not show any decreased effects or decreased plasma levels when used in combination with Nolvadex [6].

Another advantage of choosing aromasin over all other AIs is the fact that several studies have demonstrated that aromasin negatively affects cholesterol profiles in a much lesser way than other aromatase inhibitors, and in one particular study of cancer patients, 24 weeks of aromasin (Exemestane) administration did not affect cholesterol profiles [7].

Some other studies have also shown no effect on cholesterol levels from aromasin use [8].

While some studies have demonstrated negative effects on cholesterol profiles from aromasin use, they have also shown that aromasin's effects on cholesterol are not as significant or as negative as other aromatase inhibitors [9].

Finally, in addition to these benefits, several studies have demonstrated that aromasin has the ability to increase testosterone levels in men.

For example, in one particularly notable study, 12 healthy young male subjects were randomized to receive 25 mg and 50 mg of aromasin for 10 days, and it was observed that not only was estrogen suppressed by a significant amount (38%), but the subjects' testosterone levels increased by 60% [10].

Given these details, aromasin would be the best aromatase inhibitor of choice to counteract the HCG-induced increase in aromatase activity.

Therefore, aromasin should only be used at the full dose of 25 mg per day while using HCG.

Once HCG is discontinued, aromasin should also be discontinued.

Now the only next issue to address is stimulating and maintaining adequate endogenous LH release to continue recovery until the body is able to become self-sufficient again.

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SERMs: Nolvadex and Clomid

This is a question we often hear from first time anabolic steroid users.

Clomid or Nolvadex, which one do I use?

First of all, the best addition to HCG in a PCT protocol is Nolvadex (tamoxifen citrate).

Studies have shown that using HCG and nolvadex together has shown remarkable synergy in terms of stimulating endogenous testosterone production, and nolvadex has actually been proven to be effective in blocking the desensitizing effect on Leydig cells in the testes caused by high doses of HCG [11].

This is very important because just as too little LH secretion over a long period of time can cause desensitization to gonadotropins, too much gonadotropin stimulation (HCG or other forms) can likewise cause desensitizing effects.

Second, Nolvadex is not only much more effective than Clomid in stimulating endogenous testosterone production, but it is also a more cost-effective choice than Clomid itself.

Studies have shown that a daily dose of 150 mg of Clomid (clomiphene citrate) increased endogenous testosterone levels in 10 healthy men by approximately 150%, and incidentally, a daily dose of 20 mg of Nolvadex (tamoxifen citrate) increased endogenous testosterone levels by the same amount [12].

It is very clear here that clomid is very effective for this purpose, but Nolvadex seems to be the cost-effective choice in that it is cheaper than clomid when comparing mg vs. mg.

The benefits of Nolvadex over Clomid don't end there.

Clomid, like Nolvadex, has an estrogen antagonist effect on the pituitary gland, but it actually has an estrogen agonist effect on the pituitary gland as well [13].

What this means is that clomid actually acts as an estrogen in the pituitary gland to varying degrees, triggering a negative feedback loop and reducing the output of testosterone-stimulating gonadotropins (LH and FSH).

This is a very serious problem during the post cycle therapy period, which is the period when HPTA is no longer functioning and trying to recover.

Ideally, you would want a SERM that has almost 100% estrogen antagonistic effects on the pituitary gland, and Nolvadex is the perfect choice for this.

In terms of Nolvadex dosage, the standard dose to stimulate PCT and the release of GnRH (gonadotropin releasing hormone), LH, FSH, and ultimately testosterone is a simple Nolvadex dosage of 20-40mg daily.

All studies involving Nolvadex doses used to stimulate endogenous testosterone production have used only 20 to 40 mg of Nolvadex daily, and in fact, doubling the dose to 40 mg or more has been shown to have no significant difference in endogenous testosterone secretion.

The only reason many people use 40mg of Nolvadex daily for the first week or two of a PCT program is to reach optimal peak plasma levels more quickly so that HPTA can be restored more quickly.

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Conclusion

An ideal post-cycle treatment protocol should look like this