PCT: Post-Cycle Therapy

 

It is called the “post cycle crash” and is one of the more unwelcome aspects of steroid use. As the saying goes, there is a price to be paid for everything, and in the case of steroids, one of those prices (a temporary one anyway) is your natural hormone production.What happens is quite simple; when you take steroids your body stops making them.Once you stop taking steroids, you can be left with a gap until your body starts making its own again. Here, you can be faced with low levels of androgens and normal levels of corticosteroids. Your body will (should) eventually recognize and fix the imbalance, but it can take weeks or even months.This gap is a bad place to be physiologically, as without normal androgen levels to balance the catabolic effects of corticosteroids, a good deal of your new muscle mass may be lost.To help your body maintain its size, you will want to restore endogenous testosterone production quickly.The methods for doing this seem to be different everywhere you look:”Take HCG, don’t take HCG, use an aromatase inhibitor, just take Clomid, forget Clomid and just take Nolvadex.”What option is really best? Without an understanding of exactly what is going on in your body, and why certain compounds help to correct the situation, choosing the right Post-Cycle Therapy (PCT) program can be quite confusing. In this section, the roles of anti-estrogens and HCG during this delicate window of time are discussed, while detailing an effective strategy for their use.

The HPTA Axis

axis

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 promotes the release of testosterone from the testes. Testosterone, as well as estrogens and progestins, in turn cause negative feedback inhibition at the hypothalamus (and to some extent the pituitary), lowering the output of gonadotropins and testosterone when too much hormone is present.

The Hypothalamic-Pituitary-Testicular Axis, or HPTA for short, is the thermostat for your body’s natural production of testosterone.Too much testosterone, and the furnace will shut off. Not enough, and the heat is turned up (to put it very simply). For the purposes of our discussion, we can look at this regulating process as having three levels. At the top is the hypothalamic region of the brain, which releases the hormone 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, which releases Luteinizing Hormone in response. LH for short, this hormone stimulates the testes (level three) to secrete testosterone.The same sex steroids (testosterone, estrogen) that are produced serve to counterbalance things, by providing negative feedback signals (primarily to the hypothalamus and pituitary) to lower the secretion of testosterone. Synthetic steroids send the same negative feedback.This quick background of the testosterone-regulating axis is necessary to furthering our discussion, as we need to first look at the underlying mechanisms involved before we can understand why natural recovery of the HPTA post-cycle is a slow process. Only then can we implement an ancillary drug program to effectively deal with it.

 

Testicular Desensitization

post_cycle_LH_levels

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 already rebounding. From weeks 5 to 10, testosterone levels remain at or very near baseline, despite the substantial increases in LH by this point. No notable rebound in testosterone is noted until after the 10-week mark.

Although steroids suppress testosterone production primarily by lowering the level of gonadotropic hormones, the big roadblock to a restored HPTA after we come off the drugs is surprisingly not LH.This problem was made clearly evident in a study published back in 1975. Here, blood parameters, including testosterone and LH levels, were monitored in male subjects who were given testosterone enanthate injections of 250mg weekly for 21 weeks. Subjects remained under investigation for an additional 18 weeks after the drug was discontinued. At the start of the study, LH levels became suppressed in direct relation to the rise in testosterone, which was to be expected.Things looked very different, however, once the steroids had been withdrawn (see Figure I). LH levels went on the rise quickly (by the 3rd week), while testosterone barely budged for quite some time. In fact, on average it was more than 10 weeks before any noticeable movement in testosterone production started at all. This lack of correlation makes clear that the problem in getting androgen levels restored is not necessarily the level of LH, but more so testicular atrophy and desensitization to LH. After a period of inactivation,the testes have lost mass (atrophied), making them unable to perform the required workload.The protracted post-cycle window can, likewise, no longer be looked at as one of low testosterone and low LH. Much of it actually involves low testosterone and normal (even high) LH.

 

The Role of Anti-Estrogens

It is important to understand that anti-estrogens alone are inadequate to restore normal endogenous testosterone production after a cycle.These agents ordinarily increase LH levels by blocking the negative feedback of estrogens. But LH rebounds quickly on its own post-cycle, without help. Plus, there is not an elevated level of estrogen for anti-estrogens to block during this window, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels are actually lower here, not higher. Any estrogen rebound that occurs post-cycle, likewise, happens with a rebound in testosterone levels, not prior to it (there is an imbalance in the ratio of androgens to estrogens post cycle, but this is another topic altogether). On their own, we are seeing no mechanism in which anti-estrogenic drugs can effectively help here. I can, however, see why this fact would be easy to overlook. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels in men, and in normal situations they indeed perform this function fairly well. Combine this with the fact that just as many studies can be found to show that steroid use lowers LH when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that we need to focus on LH. We would miss the true problem, testicular desensitization, unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in focusing solely on anti-estrogenic drugs.

The Role of HCG

With anti-estrogens alone proving to be ineffective, we are left to focus on a very different level of the HPTA in order to hasten recovery: the testes. For this we will need the injectable drug HCG. If you are not familiar, HCG, or Human Chorionic Gonadotropin, is a prescription fertility agent that mimics the body’s natural LH. Although the testes are equally desensitized to this drug as they are to LH (they work through the same receptor), we are administering it as a measured drug and are, therefore, not constrained by the limits of our own LH production. In other words, we can give ourselves a good dose of drug (as much LH as we need, really), shocking the testes with unnaturally high levels of stimulation. We want it to reach a level above what our bodies, even when supported by anti-estrogens, could do on its own.The result should be a more rapid restoration of original testicular mass, which would allow normal levels of testosterone to be output much sooner than without such an ancillary program in place. What we are looking at now is HCG actually being the pivotal post- cycle drug, with anti-estrogens playing more of a supportive role.

The PoWeR PCT Program

The PCT program outlined below represents what I consider to be an ideal and effective post-cycle program. It was developed by the doctors at the Program for Wellness Restoration (PoWeR), who have a formidable history helping patients recover normal hormonal functioning following steroid therapy.One of the key doctors on this program, Dr. Michael Scally, claims to have successfully treated more than 100 cases of hypogonadism/hypogonadotrophic hypogonadism, and is very well known in the field of androgen replacement therapy. PoWeR published this program as part of a recent clinical study, which involved 19 healthy male subjects who were taking supraphysiological (highly suppressive) doses of testosterone cypionate and nandrolone decanoate for 12 weeks.Their HPGA Normalization Protocol focuses on the combined use of HCG, Nolvadex, and Clomid, and is perhaps the only clinically documented post-cycle therapy program to be found in the medical literature (it is amazing how little attention has been paid to hormone normalization in clinical medicine).The most notable variation from a classic PCT stack, such that I have been a longtime supporter of, is the combined use of two anti-estrogens. In this case I cannot say that there is a disadvantage to such use; perhaps it is indeed the better option.

hpga

 

Examining the program closely, we note that the testes are hit hard with HCG at the onset of therapy. Its intake, however, is limited to only 16 days.The doctors undoubtedly recognize that when HCG is taken for too long or at too high a dosage, it can desensitize the LH receptor78.This would only further exacerbate the post-cycle problem, not help it. Anti-estrogens are used during and after HCG, with a dosage of 10mg of Nolvadex and lOOmg of Clomid per day rounding out this compliment of drugs. Clomid is used for a shorter period of time than Nolvadex, likely because of the desensitizing effect it too can have (on the pituitary gland) with continued use. Among other things, these two anti-estrogens will continue to foster LH release as testosterone levels start to go back up, as well as combat any potential estrogenic side effects that may be caused by HCG’s up-regulation of testicular aromatase activity79. Although in the first couple of weeks the anti- estrogens probably do very little, they should be much more helpful towards the middle and end of the program. During this clinical investigation, normal hormonal function was restored in all subjects within 45 days of drug cessation.This is a definite success,far more favorable than the protracted recovery window noted in studies without post-cycle therapy, such as the 250mg/week testosterone enanthate investigation highlighted in Figure I. For me, I believe such a detailed recovery program should follow any serious steroid cycle. It is the best way to maintain your gains at their maximum, and that is, after all, what we are after.

 

Giving the Injection

All anabolic/androgenic steroid solutions were designed for deep intramuscular injection. The most common sites of injection are the upper outer quadrant of gluteus (buttock) and the outer side of the mid to upper thigh.This provides an ample area of thick muscle, facilitating the goal of a deep (typically 1 to 1 1/2 inch) deposit of the steroid solution into muscle tissue. Occasionally these solutions are also injected into smaller muscles such as the deltoid, biceps, or triceps.

The chosen site is not crucial, although there are some things to consider in deciding. For starters, the gluteus and thigh muscles are the best for larger injection volumes.They are sufficiently large in size that a 3ml deposit will not be extremely irritating. When using the shoulders and other small muscles, 1-1 1/2 mL is the typical limit for comfort. Administering more may result in a deep soreness and possibly swelling to the muscle. The upper outer gluteus also has the lowest pain sensitivity to needle penetration, and is likewise an easy site to start with.The thickness and level of blood circulation given to a site also affect the rate of steroid release, although this does not amount to a great deal of variation. Technically a steroid deposit will remain in the gluteus muscle for the longest period of time, and release slightly faster in the thigh or shoulder (most rapid). Over the course of a cycle the difference would probably not be noticeable to the athlete.

Syringe/Needle Size

The gauge represents the size (diameter) of a needle. The larger the number, the finer the needle is in thickness. This measurement bears no relation to the size (capacity) of the syringe, which in many cases is sold separately from the needle. The type of needle used for steroid injections varies depending on the type/viscosity of solution (water/oil) and site of injection, ranging from the standard deep intramuscular oil needles of 21-22 gauge to a fine insulin needle of 27-28 gauge. Below are a few stock needle/syringe combinations and their corresponding use with anabolic/androgenic steroids.

3mL syringe, 22-gauge needle, 11/2 inch in length

3mL syringe, 23-gauge needle, 1 inch in length

Above are the standard needle sizes used for the injection of oil-based compounds in the gluteus or thigh. Here you should limit injection volume to 3ml. Occasionally this size needle is also used for water-based compounds that contain steroid in the form of unusually large particles. For example, Winstrol-V and some Australian veterinary testosterone suspensions will jam in a needle any smaller. Having to use such a large size makes repeated injections extremely uncomfortable.

3mL syringe, 25-gauge needle, 5/8 inch in length

Often referred to as a vitamin needle, this is a standard sized needle used for the thigh or deltoid injection of oil-based compounds. Water-based steroids are also commonly injected at the same sites with this needle, but solutions with finely ground steroid (Stanazolic and Winstrol from Zambon in Spain, for example) are more comfortably given with an insulin needle.

ImL syringe, 27-gauge needle, 1/2 inch in length

ImL syringe, 28-gauge needle, 1/2 inch in length

ImL syringe,29-gauge needle, 1/2 inch in length

These are standard insulin needles used by athletes for the injection of water-based steroids, HCG, insulin, and growth hormone into smaller muscles such as the deltoid, biceps, or triceps.These are also the only sized needles comfortable to use for the subcutaneous injection of insulin and growth hormone. In desperate situations insulin needles are sometimes also used for the injection of oil-based compounds in the deltoid. While extremely tedious, there is no immediate danger with such a practice provided normal protocol were followed.

Injection Protocol

  1. Sanitize the intended area of injection with an alcohol swab, and wash hands thoroughly.

  2. If using a multiple-dose vial, clean the stopper with alcohol also.

  3. Remove the syringe’s packaging, and fill with an equal amount of air in comparison to the intended dose. Inject the air into the vial, a practice that keeps a balance of internal/external pressure (making future withdrawal easier).

  4. Draw solution into the syringe, and remove needle from the vial.

  5. Holding it needle side upright, tap the side of the syringe, and expel any extra air bubbles (tiny bubbles are not a danger to health, but this is still correct practice).

  6. Stretch the skin over the site of injection with the thumb and forefinger of your free hand, and penetrate the muscle with the needle.

  7. Pull back on the stopper to make sure the syringe does not fill with blood. Should blood be present, the needle should be removed, and reinserted into another area (to avoid injecting into a blood vessel).

  8. Press the stopper down firmly and steadily until all of the oil has been injected.

  9. Remove the needle, and press down on the injection site with an alcohol swab.

  10. Repackage and dispose of the needle. If it must be reused, it can be stored in the freezer to minimize contamination.

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