Everything That’s Wrong With Your PCT ?

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What do you think about this article?
How doe you guys end the cycle?
And do you shoot HCG during cycling, to prevent your balls from shrinking?

Everything That’s Wrong With Your PCT

Discussion of pharmaceutical agents below is presented for information only. Nothing here is meant to take the place of advice from a licensed health care practitioner. Consult a physician before taking any medication.

In the world of steroid users, it has become mandatory to follow post cycle therapy (PCT) upon cessation of steroid use. Many great PCT protocols have been outlined over the years, and many individuals have had great success with following such protocols. Nevertheless, what works can always work better. This is especially the case for those that have had a lack of success following popular advice. In this article I will address the major problems with popular PCT protocols and clarify exactly how we should use the items at our disposal for optimum recovery from AAS. Three main topics will be covered in this article –

hCG on cycle -- I will show you the best way to use HCG, which will protect your "testicular real-estate", and prime your HPTA for the fastest and most complete recovery possible.
SERMs. -- Drugs such as Clomid and Nolvadex are some of the most toxic drugs in a steroid-users cabinet. I will present the evidence of this toxicity and provide alternatives.
Peptides for PCT -- Peptides such as Growth Hormone and IGF-1 have much more of a role in PCT than most people realize. Besides preserving muscle gains, these hormones can actually help restore testicular function after a cycle.
HCG unraveled

Human Chorionic Gonadotropin (hCG) is a peptide hormone that is used in place of LH to stimulate hormone production from the gonads.1 LH is the primary signal sent from the pituitary to the testes, which stimulates the leydig cells within the testes to produce testosterone. When steroids are administered, LH levels rapidly decline. The absence of an LH signal from the pituitary causes the rapid onset of testicular degeneration. The testicular degeneration begins with a reduction of leydig cell volume, and is then followed by rapid reductions in intra-testicular testosterone (ITT), peroxisomes, and Insulin-like factor 3 (INSL3) – All important bio-markers and factors for proper testicular function and testosterone production.2-6,19 However, this degeneration can be prevented by a small maintenance dose of hCG ran throughout the cycle. Unfortunately, most steroid users have been engrained to believe that hCG should be used after a cycle. Though, we will learn that a faster and more complete recovery is possible if hCG is ran during a cycle.

Firstly, we must understand the clinical history of hCG to understand the most efficient way to use it. Many popular "steroid profiles" advocate an hCG dose of 2500-5000iu once or twice a week. These were the kind of dosages used in the historical hCG studies for hypogonadal men who had reduced testicular sensitivity due to prolonged LH deficiency.85,86 That is, testes desensitize when not presented with a sufficient LH signal. In men with normal LH levels and testicular sensitivity, the maximum increase of testosterone is seen from a dose of only ~250iu, with minimal increases obtained from 500iu or even 5000iu.2,11 (It appears the testes maximum secretion of testosterone is about 140% above base line.12-18) So, if you have allowed your testes to desensitize over the length of a typical steroid cycle, (8-16 weeks) then you would require a higher dose to elicit a response in an attempt to restore normal testicular size and function – but there is cost to this, and a high probability that you won’t regain full testicular function.

To get an idea of how quickly testicular degeneration occurs from your average multi-AAS cycle, consider this: LH levels are rapidly decreased by the 2nd day of steroid administration.2,9,10 By shutting down the LH signal and allowing the testis to be non-functional over a 12-16 week period, leydig cell volume decreases 90%, ITT decreases 94%, INSL3 decreases 95%, while the capacity to secrete testosterone decreases as much as 98%.2-6 It should be mentioned that visually analyzing testes size is a poor method of judging your actual testicular function, since testicular size is not directly related to the ability to secrete testosterone.4 This is because the leydig cells, which are the primary sites of testosterone secretion, only make up about 10% of the total testicular volume. Therefore, testicular size may appear normal on a cycle, but the testes ability to secrete testosterone upon LH or hCG stimulation can actually be significantly diminished.3-5



The decreased testosterone secretion capacity was well demonstrated in a study on power athletes who used steroids for 16 weeks, and were then administered 4500iu hCG post cycle. It was found that the steroid users were about 20 times less responsive to hCG, when compared to normal men who did not use steroids.8 In other words, their testosterone secretion capacity was dramatically reduced because they did not receive an LH signal for 16 weeks. The testes essentially became desensitized and crippled. Case studies with steroid using patients show that aggressive long-term treatment with hCG at dosages as high as 10,000iu E3D for 12 weeks were unable to return full testicular size.7 Other studies with men using low dose steroid implants for 6 weeks showed unsuccessful return of Insulin-like factor-3 (INSL3) concentration in the testes upon 5000iu/wk of HCG treatment for 12 weeks.6

These studies show that postponing hCG usage until the end of a cycle, increases your need for a higher dose of hCG, and decreases your odds of a full recovery. As a consequence to using a higher dose of hCG, estrogen will be increased disproportionately, which then causes further HPTA suppression while increasing the risk of gyno.11 For example, high doses of hCG are known to raise estradiol 165%, while only raising testosterone 140%.11 Higher doses of hCG are also known to reduce LH receptor concentration and degrade the enzymes responsible for testosterone synthesis within the testes12,13,19 (the last thing someone wants during recovery). While these negative effects of hCG can be partly mitigated by the use of a drug such as tamoxifen, it will create further problems associated with using a toxic SERM. (covered in the next section)

In light of the above evidence, it becomes obvious that we must take preventative measures to avoid this testicular degeneration. Besides, with hCG being so readily available, and such a painless shot, it makes you wonder why anyone wouldn’t use it on cycle. Based on studies with normal men using steroids, ~100iu HCG administered everyday was enough to preserve full testicular function and ITT levels, without causing desensitization typically associated with higher doses of hCG.2 It is important that low-dose hCG is started before testicular degeneration occurs, which appears to rapidly manifest within the first 2-3 weeks of steroid use.

Recap – For optimal preservation of testicular function during cycle, use 100iu hCG ED starting 3 days after your first AAS dose. Drop the hCG a week before the AAS clear the system. For example, you would drop hCG a week after your last Testosterone Enanthate shot. Or, if you are ending the cycle with orals, you would drop the hCG a week before your last oral dose. This will allow for a sudden and even drop in hormone levels, while initiating LH and FSH production from the pituitary, making for a seamless recovery.

A more convenient alternative to the above recommendation would be a weekly shot of 500iu hCG, throughout the entire cycle. Beyond this dose, one could calculate a rough estimate for their required hCG dosage by multiplying 40iu x days of LH absence. (40iu x 60 days = 2400iu HCG dose)

As an alternative to the on cycle hCG protocol, you could follow a plan based on modulation of the gonadotropin pulse generator. (seen here)

Note: If following any of these protocols, hCG should NOT be used after the cycle.

Clomid & Nolva; A closer look

The use of Clomid and Nolvadex, as Selective Estrogen Receptor Modulators (SERMs), has gradually become well established in the steroid using community. The popular push of these drugs has almost made them mandatory. They have essentially become hormonal vitamins – vitamins that can do no wrong and provide seemingly endless benefits of testosterone support, bloat reduction, gynecomastia prevention and cholesterol health. It seems that we are all well educated about the benefits of Clomid and Nolvadex, so in this segment, I will present the risks and consequences from the short and long term use of Clomid and Nolvadex.

Upon examination of the research available for Clomid (clomiphene) and Nolvadex (tamoxifen) we find that the research is quite extensive, and contradicting.21 We see many early studies with tamoxifen done on breast cancer patients, which show an acceptable "safety profile", with an apparent lack of adverse effects.22 On the other hand, many of the early in vivo animal studies showed severely toxic effects, with the development of cancer in the liver, uterus, or testes upon tamoxifen administration.30-34,41 However, this evidence was largely disregarded by ex vivo (test tube) research on human cell-lines which appeared to show a lack of toxic effects.21

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For example, tamoxifen was generally accepted as being non-toxic to human liver upon the conclusion that tamoxifen did not cause noticeable DNA adducts (damage) during short-term ex vivo studies with human liver cells.35,36 This was in contrast to the in vivo animal studies showing dramatic carcinogenic effects on the liver.30-34,41 As scientists learned that the toxic effects from tamoxifen are from the metabolism and buildup of the a-hydroxytamoxifen, 4-hydroxytamoxifen and N-desmethyltamoxifen metabolites. It became apparent that ex vivo research was largely flawed due to low-rate metabolism.21 The carcinogenic effects of tamoxifen proved to be even more unusual and elusive, when it was hypothesized that tamoxifen had both genomic and non-genomic toxicity, which affecting different animals, in different organs.21 This created an obvious clinical challenge for measuring genotoxicity in a test tube. Eventually, it was established that tamoxifen was a bona-fide carcinogen in all species, at least in one way or another.21,37-39 Recent human studies have shown tamoxifen treated women to have 3x the risk of developing fatty liver disease, which appeared as soon as 3 months into therapy at only 20mg/day.24-26 In some cases, the disease lasted up to 3 years, despite cessation from tamoxifen therapy. Five and ten year follow-ups with patients on long term tamoxifen therapy showed cases of deadly hepatocellular carcinoma.27-29 In a 2000 case study involving tamoxifen induced liver disease, D.F Moffat et al made a profound statement –

"In addition, hepatocellular carcinoma in tamoxifen treated patients may be under-reported since there may be reluctance to biopsy liver tumours which are assumed to be secondary carcinoma of the breast."

In other words, it appears that the liver carcinoma from a large number of breast cancer patients on tamoxifen therapy has been misdiagnosed as a metastasis infection from the breast cancer itself.28 Upon closer examination it was found that the cancerous lesions in the livers of the long-term tamoxifen therapy case studies were identical to those seen in the early animal studies showing tamoxifen to be a potent hepatotoxin.28-34 Although the effects took much longer to manifest, it became obvious that tamoxifen was toxic to the human liver.

Another well known risk of tamoxifen therapy is the increased risk of developing endometrial cancer (uterine cancer).23,42 This is due to tamoxifen actually acting as an estrogen agonist in the uterus, presumable from the 4-hydroxytamoxifen metabolite.33,40 This estrogenic metabolite triggers abnormal growth of the uterus and the formation of cancer causing DNA adducts.33 As male bodybuilders we assume this presents no risk. On the contrary, the implications are quite scary when we realize the male equivalent to the uterus is the prostate -- differentiating from the same embryonic cell line and sharing the same oncogene, Bcl-2, and high concentration of the estrogen receptor. It is likely that tamoxifen has the same estrogenic action, and DNA damaging effects within the prostate.60-62 It is no wonder that tamoxifen failed as a treatment for prostate carcinoma.43

Aside from restoring testosterone levels post cycle, tamoxifen is often used to combat gyno during cycle when "flare ups" occur. While tamoxifen may provide immediate inhibition of growth, and serve as valuable tool, it also has the ability to up-regulate the progesterone receptor.54-56 This is a true contradiction, which dramatically increases your chances of bringing upon gyno in future cycles when utilizing Nandrolone (Deca) or Trenbolone, both of which act upon the progesterone receptor. It is interesting to speculate: is tamoxifen use directly related to the increased gyno occurrences seen with modern day steroid users?

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When we bring our attention to Clomid, we find less research is available on long term human toxicity, probably because of the relatively short term (3-4 week) clinical application for ovarian stimulation,59 although long term follow ups with patients who received Clomid for ovulation induction have shown an increased risk of developing uterine cancer.74 This is to be expected, since many of the same carcinogenic tendencies found with tamoxifen are the same effects seen with clomiphene.44,45,57,58 Upon analysis of anecdotal reports from Clomid and nolva users, we see the typical short term side effects of low libido, erectile dysfunction, and emotional instability – despite many men showing normalized testosterone and estrogen levels during the use of these SERM’s. Research on male breast cancer patients also shows frequent reports of low libido, thrombosis (arterial blockage), and hot flashes with tamoxifen use.47 Another common side effect associated with both SERMs, but more common with Clomid, is the loss of visual accuracy and development of visual "tracers", due to the ocular toxicity.46

It’s a common practice these days for experienced bodybuilders to implement some dosage of IGF-1 either during or after a cycle to "pick up" a lagging body part, or to preserve gains in muscle. Growth Hormone (GH) is also a versatile drugd for cutting or bulking, with increasing popularity as it becomes more affordable. The value of IGF-1 and GH becomes so much more significant when we realize there integral role in testicular function. In fact, it seems that these hormones are more effective at building testes, than muscles.
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As the medical community became more aware of the side-effects associated with clomiphene and tamoxifen treatment, newer and safer SERMs, such as toremifene and raloxifene hit the developmental fast track. Toremifene appears to be less liver toxic, but it is an analog of tamoxifen, so it also carries many of the related genotoxic effects.48,49 Raloxifene appears to be even safer by being the least liver toxic, and not having any potential issue with the uterus or prostate.50-52 Unfortunately, raloxifene has been associated with a higher incidence of thromboembolism52 (arterial blockage), and also has very low oral absorption, making it an expensive alternative at a typical 120mg/day dose.53 Still, raloxifene could presumably be equally effective as Clomid or Nolvadex at restoring HPTA function, while imparting less side effects.53 Newer SERMs are already being evaluated such as bazedoxifene, arzoxifene, and lasofoxifene, in hopes of reducing risk even further.

Another SERM that may be useful for post cycle therapy is resveratrol.87,88 Resveratrol is a natural polyphenol extracted from grape skin, that has recently been under heavy research for its cancer fighting effects in the breast, prostate and liver.63-69 Contrary to Nolva or Clomid, resveratrol appears to actually have beneficial effects on the liver,70 as well as having multiple benefits on cardiovascular health by limiting LDL oxidation and improving endothelial function.71-73 Improved blood vessel function may be a mechanism by which resveratrol improves erectile function in many men. Research also suggests that resveratrol may actually extend life, by reducing oxidative stress on organs such as the heart,77 and preventing the metabolic syndrome by fighting insulin resistence.79,80 It’s becoming well known that insulin resistance is a leading cause of low testosterone.82 More specifically, improving insulin sensitivity will increase your leydig cell sensitivity, and therefore increase the testes response to LH.81

It should be pointed out that resveratrol may not be the best choice to combating emergency gyno, due to its lower binding affinity to the human ER of about 90x less than tamoxifen, and about 30x less than clomiphene.75,76 However, considering that resveratrol is a pure estrogen antagonist at the pituitary,89 while Clomid has mixed agonist/antagonistic effects,90-94 resveratrol could be a suitable substitute for PCT. Aside from acting as a SERM, resveratrol can also help control estrogen by actually limiting aromatase enzyme production.82 Based on the research, it appears that at least 100mg/day would needed to increase LH, FSH and testosterone production.84 This is comparable dose of resveratrol found in an advanced topical based product, Dermacrine Sustain (found here - http://www.primordialperformance.com).

Admittedly, no steroid users are dropping dead from a 4 week protocol of Nolva or Clomid, and many will say "the consequences far outweigh the benefits" -- but why deal with the potential consequences when alternatives are available?

Peptides for testicular recovery

Research has shown GH to be vitally important in testicular function, 95-97 but it is generally accepted that the beneficial effects are directly mediated by hGH’s conversion to IGF-1.98 As many of you know, IGF-1 is created in the liver by GH, upon interacting with insulin. So, we will be focusing on the usage and benefits of IGF-1, rather than GH, as it seems more cost effective and directly related to our purpose of optimizing recovery.

In short, IGF-1 increases steroidogenic acute regulatory protein (sTAR),98 and cholesterol side chain cleaving enzyme (CYP 11A)99. These are both rate-limiting steps and are critical factors for converting cholesterol into hormones, such as testosterone. IGF-1 also has the ability to increase the concentration of steroidogenic enzymes in the testes, such as 3b HSD.100 IGF-1 can also increase the testes sensitivity to LH and hCG by increasing the number of LH receptors.99-102

These positive effects on testicular function make IGF-1 an ideal drug for PCT. A dose of IGF-1 Lr3 at 80mcg/day, split two times per day, would likely be the most cost effective dose.

In conclusion, we have learned that utilizing hCG during a steroid cycle will significantly prevent testicular degeneration. This helps create a seamless transition from "on cycle" to "off cycle". Then, by avoiding the deleterious SERMs such Clomid and Nolvadex and opting for safer alternatives, you can seemingly avoid any sort of post cycle crash, while maintaining a strong libido and uncompromised emotional health.