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PCT for Prop, Primo, Mast cycle...


Welcome to the EliteFitness.com Bodybuilding Site! Please join this discussion about PCT for Prop, Primo, Mast cycle... within the Anabolic Steroids category.

Excerpt: I ran a 14 week cycle with... 1-14 Primo 450mg/week 1-14 Prop 225mg/week 1-6 Anavar 50mg/day 7-14 Mast 300mg/week 3-14 HCG 500iu/week 13-14 HMG 75iu/week I just started my PCT with Sustain Alpha, Aromasin, Unleashed and Post Cycle... Do you think the PCT will be enough? I have Adex, Nolva and Clomid on hand as well. Also have more HMG, should institute this into the PCT as well? Any informed opinions?

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  1. #1
    Amateur Bodybuilder Barch's Avatar
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    PCT for Prop, Primo, Mast cycle...

    I ran a 14 week cycle with...

    1-14 Primo 450mg/week
    1-14 Prop 225mg/week
    1-6 Anavar 50mg/day
    7-14 Mast 300mg/week
    3-14 HCG 500iu/week
    13-14 HMG 75iu/week

    I just started my PCT with Sustain Alpha, Aromasin, Unleashed and Post Cycle... Do you think the PCT will be enough? I have Adex, Nolva and Clomid on hand as well. Also have more HMG, should institute this into the PCT as well? Any informed opinions?

  2. #2
    Mad Scientist chefbone's Avatar
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    Re: PCT for Prop, Primo, Mast cycle...

    I would never solely rely on OTC products for PCT. Always base PCT on Nolva/Clomid and if you want to add the OTC stuff to go right ahead.




  3. #3
    Amateur Bodybuilder genetics's Avatar
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    Re: PCT for Prop, Primo, Mast cycle...

    Quote Quote posted by chefbone View Post
    I would never solely rely on OTC products for PCT. Always base PCT on Nolva/Clomid and if you want to add the OTC stuff to go right ahead.

    +1

    I'm about to start my pct after finishing a 20 weeker and am' running the trs along with nolva 40/40/20/20

  4. #4

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    Re: PCT for Prop, Primo, Mast cycle...

    He's got more than OTC products... HMG and Aromasin aren't OTC and very effective for PCT.

    I'd definitely use the HMG. I'd also add forged post cycle, as I really think that is a great product.

    If you notice you are having problems, which you shouldn't with that stack... Then you could add the nolvadex

  5. #5
    Amateur Bodybuilder Barch's Avatar
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    Re: PCT for Prop, Primo, Mast cycle...

    Quote Quote posted by sonicwaste View Post
    He's got more than OTC products... HMG and Aromasin aren't OTC and very effective for PCT.

    I'd definitely use the HMG. I'd also add forged post cycle, as I really think that is a great product.

    If you notice you are having problems, which you shouldn't with that stack... Then you could add the nolvadex
    Yeah, I've been debating whether to just use the Nolva and Clomid, or to with the PCT that I'm running. I used just the TRS, Unleashed and Post Cycle for my most recent PCT and it went really well. However, my last cycle was quite a bit shorter, as well...

  6. #6
    Da Pope
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    Re: PCT for Prop, Primo, Mast cycle...

    Quote Quote posted by chefbone View Post
    I would never solely rely on OTC products for PCT. Always base PCT on Nolva/Clomid and if you want to add the OTC stuff to go right ahead.

    Bullshit and a pile of crap...... You are still living in the stone age man. The otc products work. Not all of them but the ones he is talking about doo.

  7. #7
    Da Pope
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    Re: PCT for Prop, Primo, Mast cycle...

    Preface - Over the past 15 years, the use of Clomid and Nolvadex, as Selective Estrogen Receptor Modulators (SERMs) has become a staple in the HRT and bodybuilding communities.

    The popularity of these drugs stems from the popular advice to use these drugs for everything from testosterone recovery, bloat reduction, to gyno prevention. In many communities SERMs have become akin to vitamins -- vitamins that can do no wrong and provide seemingly endless benefits.

    This article is not intended to examine the proper use or possible applications of Clomid or Nolvadex. Instead, we will be exploring the historical development of these drugs, the short-term side-effects and long-term consequences.

    As I will illustrate, these drugs are true danger to men’s health.

    Synthetic estrogens, the beginning -

    It was the 1930’s and there was a new age of hormone-dependant pathologies on the rise. Scientists were eager to determine the structural requirements of estrogen for new drug design.Diphenylethane

    In 1937 Sir Charles Dodd of the Middlesex Hospital of London found estrogenic activity in a molecule with two benzene rings linked together via a short carbon chain (eg, diphenylethane). (1) Soon thereafter, a synthetic, non-steroidal estrogen known as diethylstilboestrol (DES) was created from this basic molecular backbone. (1) By 1941, DES was an FDA approved drug, and by the 1950’s, DES gained widespread popularity as the drug of choice for menopausal symptoms, cancer treatment, and prevention of miscarriages. (2)Diethylstilboestrol

    DES sparked the interest of ambitious drug manufactures that saw this synthetic molecule as a potential “molecular backbone” which could be tailored for estrogenic activity, and patented for maximum profit.

    Within months, a research group from the University of Edinburgh found that the addition of a benzene ring to the original diphenylethane structure created an somewhat of an anti-estrogen known as triphenylethylene. (1) Although it had very weak estrogenic activity, it was called an anti-estrogen because it competed with the body’s more powerful estradiol for the ER receptors.

    Although the complex estrogenic action of triphenylethylene was not fully understood, it was considered the perfect molecular platform for future drug development because of its high oral bioavailability and extended half-Triphenylethylenelife due to its lipophilicity (fat solubility). As it was later discovered, the estrogenic action could be manipulated with structural modifications for more specific agonist/antagonist actions. (3) Despite the lack of understanding for its full physiological effects, triphenylethylene would become the molecular backbone for generations of SERM’s to come.

    By the early 1940’s, the world’s largest chemical manufacturers, including Imperial Chemical Industries (ICI), got word of the triphenylethylene development, and seized the opportunity to expand this new class of compounds. By the 1950’s, the synthesis of new triphenylethylene based molecules had began picking up momentum, as the first FDA approved SERM’s started appearing on the market.

    One of the first was Triparanol, which was sold as a cholesterol lowering SERM, until it was eventually pulled from the market in the 1950’s for causing cataracts in patients. (7) Later, Ethamoxytriphetol (MER-25) was discovered and found to be a reliable contraceptive and anti-cancer agent in rats, but failed in humans due to the drug’s severe toxicity and stimulation of “acute psychotic episodes”. (6)

    Despite these early warning signs, development continued.

    Among one of the newer SERM’s to appear in the late 1950’s, was a mixture of two stereoisomers -- zuclomiphene and enclomiphene -- both having unique estrogenic and anti-estrogen actions. This mixture was collectively called clomiphene, and later marketed as Clomid.

    Enclomiphene Zuclomiphene

    Then, in 1962, ICI synthesized ICI-46474, another mixture of a trans and cis isomers with mixed estrogenic and anti-estrogenic activity. (7) Ultimately, the trans isomer was found to be the predominate anti-estrogen, which was isolated and eventually named tamoxifen, and later marketed as Nolvadex.

    Originally, ICI pushed these new SERM’s to market as a “morning after” contraceptives, which were eventually approved by the FDA. (4) Yet again, the profit hungry and presumptuous drug manufacturer based its findings on rat studies, which would prove to be a mistake upon subsequent human research that showed the SERM’s induced, rather than inhibited ovulation. (4) Needless to say, tamoxifien was withdrawn as a contraceptive.

    And remember DES, the original synthetic estrogen developed back in the 1930’s? As it turned out, DES was found to increase the risk of breast cancer by 50%. Further research linked DES to millions of vaginal and testicular cancers among the children of mothers who took DES during pregnancy. (2,5)

    The light on synthetic anti-estrogens was dim, and by the late 1960’s, there was little enthusiasm to continue R&D with triphenylethylene based SERM’s, especially considering their inherently toxic effects (7, 10)

    It wasn’t until 1971, that tamoxifen would be dug up from the dead and considered as a candidate for cancer treatment.

    Treating cancer with a carcinogen –

    When research is done on anti-cancer drugs (such as SERMs), the aim is to find a drug that prolongs life, with the least amount of acute side-effects. In other words, the goal isn’t so much about finding a cure, as it is finding something that can alleviate the symptoms and/or prolong life. Tamoxifen

    For an estrogen dependant cancer, the idea was simple – Block the proliferative action of estrogen with an anti-estrogen and slow the cancer growth. What could be more appropriate than an already available, orally active, patentable synthetic estrogen such as tamoxifen? It was a practical shoo-in.

    Therefore, in 1971, when drug researchers decided to examine all of the historical anti-cancer SERM data, they found that all of the SERM’s showed anti-proliferative activity on estrogen dependant cancer, and all of them demonstrated some extent of toxicity. (10, 37-39) However, the SERM that happened to show the least amount of toxicity was tamoxifen. (clomiphene missed the mark by showing a high rate of cataract formation)

    At the time, Pierre Blais, a well known drug researcher, commented on the finding (5) -

    “Tamoxifen is a garbage drug that made it to the top of the scrap heap. It is a DES in the making."

    In spite of the criticism from a number of researchers, the FDA approved tamoxifen as a cancer treatment in 1977, and in 1985 ICI was awarded a US patent for tamoxifen in the treatment of breast cancer. (5) Soon, tamoxifen would become the most popularity prescribed cancer drug.

    “Its FDA approved for cancer treatment. It must be safe!”

    It’s wrong to assume that an “FDA approved” drug has a proven safety profile. The FDA has continually issued stronger health warnings for tamoxifen over the years. For instance, in 1994 the FDA demanded that the tamoxifen manufacturer Zeneca (an ICI sub-division), issue warning letters to health care practitioners about the increased risk of endometrial and gastro-intestinal cancers with tamoxifen use. Zeneca also reported adverse effects similar to those seen with DES, such as reproductive abnormalities in the animals whose mothers received tamoxifen. (remember, DES was the original synthetic estrogen, and also an analog to tamoxifen)

    A number of cancer researchers have pointed out the health risks too, such as Elwood et al (6) -

    “[Tamoxifen], therefore, is not appropriate for use in the general population because of the known increased risk of endometrial cancer”

    “So why is tamoxifen the most popularly prescribed cancer drug, if it’s so toxic?”

    The answer is simple. Tamoxifen is the lesser of two evils.

    Tamoxifen remains the most popularly prescribed drug because it is one of the few drugs that has shown a “statistically significant” improvement of the survival rate of breast cancer patients.* (Not to mention, tremendous financial motives and intraworking’s from its patent holder Zeneca)

    Remember, the goal in cancer treatment is to prolong life -- even if it means committing to therapy that is potentially cancerous or injurious to future health (as confirmed in long-term follow up’s and close examinations of tamoxifen patients).

    So, perhaps the risks are worthy for the cancer patient, but are they worthy for the health conscious male?

    * Most research has shown tamoxifen to improve the survival rate by 4-14%. For instance, over a 5 year period, 74% of the women survived who used tamoxifen, compared to 70% of the women on placebo. Depending on the type of cancer, this may translate into an extra 2-3 years of life for a cancer patient. (9) Continuing tamoxifen therapy for more than 5 years, results in increased tumor recurrences and serious side effects. (8)

    Translating the science, for men’s health -

    Fast forward 30 years, through hundreds of human and animal trials and we find that the research is quite extensive, and contradicting. (21)

    The damaging evidence from many early rat studies showed severely toxic effects, including the development of cancer in the liver, uterus, or testes upon tamoxifen administration. (30-34,41) However, this evidence was largely disregarded by further test tube studies on human cell-lines which appeared to show a lack of toxic effects. (21)

    This misleading test tube data gave the green flag to perform large scale human studies with tamoxifen in the 80’s and 90’s. Even more misleading, was the majority of the human research described tamoxifen as having a “low incidence of troublesome side effects” and that the “side effects where usually trivial”. (22)

    As science would uncover, the lack of human toxicity reported in original tamoxifen research was a result of insufficient study duration, inability to detect low level DNA damage with insensitive methodologies, and/or misdiagnosis of collateral cancers as metastasis infections from the breast cancer itself. (15, 21, 28-34)

    A word on clomiphene (Clomid) –

    Clomiphene (Clomid) consists of two stereoisomers which possess radically different pharmacodynamics. Zuclomiphene has predominantly estrogenic effects and slow clearance while the enclomiphene isomer has predominately anti-estrogenic effects and quick clearance. (9) This creates a dichotomy between estrogen blockage and estrogen stimulation and an acute imbalance once Clomid administration is discontinued. Bodybuilders will often complain of “estrogenic rebound” after stopping Clomid, which could be attributed to the lingering estrogenic isomer zuclomiphene as the anti-estrogenic enclomiphene has long cleared the system. (Recently, enclomiphene has been isolated by the pharmaceutical company Repros, for use in Androxal™.)

    For all intents and purposes, tamoxifen is a superior SERM, simply for the fact that tamoxifen provides a purely anti-estrogenic isomer, whereas Clomid provides a mix of anti and pro estrogenic effects.

    In regards to the health consequences about to be listed, it can be safely assumed that Clomid will share similar detrimental effects as tamoxifen, since it shares the same triphenylethylene backbone and carcinogenic tendencies. (44,45,57,58)

    Liver cancer -

    Originally, tamoxifen was accepted as being non-toxic to human liver upon finding that tamoxifen did not cause noticeable liver damage (DNA adducts) during short-term test tube studies with human liver cells. (35,36)

    However, it became apparent that test tuberesearch was largely flawed due to the low rate of metabolism in such a superficial environment. (21) It was soon discovered that the hepatotoxic effects from tamoxifen are from the metabolism and buildup of the a-hydroxytamoxifen and N-desmethyltamoxifen metabolites, which would only appear in an in vivo environment. (15) Surely enough, the results from the original rat studies showing dramatic carcinogenic effects on the liver, 30-34,41 soon correlated with human data when researchers found the same type of liver DNA adducts in tamoxifen patients. (15, 28-34)

    More recent human research has reported tamoxifen treated women to have 3x the risk of developing fatty liver disease, which occurs as soon as 3 months into therapy at only 20mg/day. (24-26) In some cases, the disease lasts up to 3 years, despite cessation from tamoxifen therapy. Five and ten year follow-ups with patients on long term tamoxifen therapy shows cases of deadly hepatocellular carcinoma. (27-29)

    In 2002, a bizarre study examined the use of tamoxifen for hepatocellular carcinoma treatment in humans. It was assumed that since tamoxifen could inhibit proliferation of breast cancer, it could offer the same benefit for liver cancer. The devastating results could not have been further indicative of tamoxifen’s hepatotoxic nature, as the tamoxifen treatment significantly increased the rate of death, compared to the group not receiving tamoxifen. (14)

    Finally, in a case study reviewing tamoxifen induced liver disease; D.F Moffat et al made a profound statement –

    “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 an infection from the breast cancer itself. (28)

    Although tamoxifen induced liver cancer may take years to manifest in a healthy male, its damaging effects could easily be exaggerated by other popular hepatotoxic drugs, such as 17aa oral steroids. (15)

    Prostate cancer -

    In 1996, the International Agency for Research on Cancer (IARC) concluded that tamoxifen clearly promotes uterine cancer in humans – at a standard 20mg/day dose. (16,23,42) This is due to tamoxifen acting as an estrogen agonist in the uterus, presumably from the 4-hydroxytamoxifen metabolite, which triggers abnormal growth of the uterus and the formation of cancer causing DNA adducts. (33, 40)

    Contrary to popular thought, these implications are quite scary for a male when we realize the male equivalent to the uterus is the prostate – which differentiates from the same embryonic cell line, shares the same oncogene, Bcl-2, and high concentration of estrogen receptors. In fact, there is no reason to assume that tamoxifen would not initiate the same cancerous growth in the prostate. (60-62) It is no wonder that tamoxifen failed as a treatment for prostate carcinoma. (43)

    Note: This same risk would be applicable to Clomid, which has also been linked to uterine cancer and ovarian hyper-stimulation. (18, 19, 57, 59)

    Libido reduction & erectile dysfunction -

    Erectile dysfunction, low libido, and general impotence are typical complaints from men recently discontinuing steroids or HRT therapy, which is often combated by Clomid or Nolvadex, paradoxically so.

    Regardless of any positive effects on fertility or testosterone levels, Clomid and Nolvadex use is highly correlated with erectile dysfunction, libido suppression, and even emotional disorders. (10,47)

    Research with male breast cancer patients has also reported decreased libido, and thrombosis associated with tamoxifen use. (47) The thrombotic effect (blood vessel clogging) could explain the mechanism by which SERM’s may inhibit erectile function, by reducing circulation to erectile tissue. (47, 52)

    Increased susceptibility to gyno -

    Tamoxifen is often used to combat gyno during cycle when “flare ups” occur. While tamoxifen may provide immediate inhibition of proliferation, and serve as valuable tool, it can actually increase future susceptibility to gyno.

    This is caused by tamoxifen’s ability to up-regulate the progesterone receptor. (54-56) This can dramatically increase the chances of developming gyno in future cycles when utilizing progestin based anabolics such as Nandrolone (Deca) or Trenbolone (or any pro-hormone acting 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?

    Ocular toxicity –

    Another possible side effect associated with SERMs is visual cloudiness, loss of vision and even cataract formation. Although this tends to be a more common side effect from high dosed SERM therapy, standard 20mg/day tamoxifen regimes have been reported to cause these symptoms of ocular toxicity. (17, 46)

    Newer SERM’s -

    As the medical community became more aware of the side-effects associated with 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 a closely related analog of tamoxifen, so it also carries many of the related genotoxic effects. (48,49) Raloxifene

    Raloxifene is a newer SERM based off a benzothiophene structure, which appears to make it less toxic in the liver, uterus or prostate. (50-52) Unfortunately, Raloxifene has been associated with a higher incidence of thromboembolism (52), and also has very low oral absorption, making it an expensive alternative at a typical dose (120mg/day). (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. (further enumerating the evidence of toxicity with the tamoxifen generation of SERM’s)



    What to do now?

    Firstly, it should become a priority to create awareness about the possible side effects of SERMs. Once educated, users will be able to start reducing their requirements of these drugs, and begin adopting healthier, more responsible alternatives.

    Carefully planned cycles, and the proper use of aromatase inhibitors (AIs) must pursue over haphazard combinations of excessively dosed aromatizing AAS’s -- which require high doses of SERM’s to reduce possible side-effects. Whereas avoiding SERM’s in HRT will involve the natural clearance and management of endogenous estrogens.

    It will be important to maintain testicular function during cycle for a quick and efficient recovery of natural testosterone production for PCT – negating the need for high dose 2-3 month SERM based PCT’s. (For more information on the proper use of hCG during cycle, visit here)

    Thus, abolishing the bad habit of SERMing will involve community wide enlightenment with careful, comprehensive planning of worthy alternatives.

  8. #8
    Da Pope
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    Re: PCT for Prop, Primo, Mast cycle...

    Human Chorionic Gonadotropin (hCG) is a peptide hormone that mimics the action of luteinizing hormone (LH). LH is the hormone that stimulates the testes to produce testosterone. (1) More specifically 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 testes to stop producing testosterone, which causes 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, during PCT. Upon reviewing the science and basic endocrinology you will see 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 its purpose and its most efficient application. Many popular “steroid profiles” advocate using hCG at a dose of 2500-5000iu once or twice a week. These were the kind of dosages used in the historical (1960’s) hCG studies for hypogonadal men who had reduced testicular sensitivity due to prolonged LH deficiency. (21,22) A prolonged LH deficiency causes the testes to desensitize, requiring a higher hCG dose for ample stimulation. In men with normal LH levels and normal 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 their normal capacity.) (12-18) 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.

    One term that is critical to understand is testosterone secretion capacity which is synonymous to testicular sensitivity. This is the amount of testosterone your testes can produce from any given LH or hCG stimulation. Therefore, if you have reduced testosterone secretion capacity (reduced testicular sensitivity), it will take more LH or hCG stimulation to produce the same result as if you had normal testosterone secretion capacity. If you reduce your testosterone secretion capacity too much, then no amount of LH or hCG stimulation will trigger normal testosterone production – and this leads to permanently reduced testosterone production.

    To get an idea of how quickly you can reduce your testosterone secretion capacity from your average steroid 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)

    Note: 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, when the testes may only appear 5-10% smaller, the testes ability to secrete testosterone upon LH or hCG stimulation can actually be significantly reduced to 98% of their normal production. (3-5) The point here is to not judge testosterone secretion capacity by testicular size.

    The decreased testosterone secretion capacity caused by steroid use 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) Another study with men using low dose steroids 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) (INSL3 is an important biomarker for testosterone production potential and sperm production. 20)

    These studies show that postponing hCG usage until the end of a steroid 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 at the end of a cycle, estrogen will be increased disproportionately to testosterone, which then causes further HPTA suppression (from high estrogen) while increasing the risk of gyno. (11) For example, high doses of hCG have been found to raise estradiol up to 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 testes (12,13,19 ) -- the last thing someone wants during recovery. While these negative effects of hCG can be partly mitigated by the use of a SERM such as tamoxifen, it will create further problems associated with using a toxic SERM (covered in another article).

    In light of the above evidence, it becomes obvious that we must take preventative measures to avoid this testicular degeneration. We must protect our testicular sensitivity. 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 sensitivity is reduced, which appears to rapidly manifest within the first 2-3 weeks of steroid use. Also, it’s important to discontinue the hCG before you start PCT so your leydig cells are given a chance to re-sensitize to your body’s own LH production. (To help further enhance testicular sensitivity, the dietary supplement Toco-8 may be used)

    A more convenient alternative to the above recommendation would be a twice a week shot of 200iu hCG, or possibly a once a week shot of 500iu. However, it is most desirable to adhere to a lower more frequent dose of hCG to mimic the body’s natural LH release and minimize estrogen conversion. If you are starting hCG late in the cycle, one could calculate a rough estimate for their required hCG ‘kick starting’ dosage by multiplying 40iu x days of LH absence, since the testes will be desensitized, thus requiring a higher dose. (ie. 40iu x 60 days = 2400iu HCG dose)

    Note: If following the on cycle hCG protocol, hCG should NOT be used for PCT.

    Recap –

    For preservation of testicular sensitivity, use 100iu hCG ED starting 7 days after your first AAS dose. At the end of the cycle, drop the hCG two weeks before the AAS clear the system. For example, you would drop hCG about the same time as your last Testosterone Enanthate shot. Or, if you are ending the cycle with orals, you would drop the hCG about 10 days before your last oral dose. This will allow for a sudden and even clearance in hormone levels, while initiating LH and FSH production from the pituitary, to begin stimulating your testes to produce testosterone. Remember, recovery doesn’t begin until you are off hCG since your body will not release its own LH until the hCG has cleared the system.

    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” thus avoiding the post cycle crash.

  9. #9

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