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Thread: Tips On PCT

  1. #21
    Join Date
    Apr 2010
    Where women glow and men chunder



    I believe that sex is one of the most beautiful, natural, wholesome things that money can buy

  2. #22
    Hazcat Guest


    Danno remind us of your stats brother, it's been a while.

  3. #23
    Join Date
    Feb 2010
    In the Florida Woods, USA


    Quote Originally Posted by hazcat View Post
    Danno remind us of your stats brother, it's been a while.
    Danno is the manno and a world traveler. He's been to bars where guys squirt milk out of their breasts. Just kidding, but he really has.
    He's my man whore hero.
    The information given is for entertainment purposes only. I do not use steroids nor condone their use. I am not a trained health professional and therefore any answer given is strictly an intellectual exercise, not advice on how to use steroids.
    Muscle Forged In Pain!

  4. #24
    Hazcat Guest


    Clomid & Nolvadex – The Dark Side
    Posted on October 11, 2009 by Eric Potratz
    Preface – Over the past 15 years, the use of Clomid and Nolvadex, as Selective Estrogen Receptor Modulators (SERMs) has become a staple in the Hormone Replacement Therapy (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 truly dangerous to men’s health.

    Synthetic estrogens, the beginning -

    It was the 1930s 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.

    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 (e.g., 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 1950s, DES gained widespread popularity as the drug of choice for menopausal symptoms, cancer treatment, and prevention of miscarriages. (2)

    DES sparked the interest of ambitious drug manufactures who 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 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-life 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 of its many physiological effects, triphenylethylene would become the molecular backbone for generations of SERMs to come.

  5. #25
    Hazcat Guest


    By the early 1940s, 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 1950s, the synthesis of new triphenylethylene based molecules had begun picking up momentum, as the first FDA approved SERMs 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 1950s 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 SERMs to appear in the late 1950s, 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.

    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 SERMs 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 SERMs induced, rather than inhibited ovulation. (4) Needless to say, tamoxifen was withdrawn as a contraceptive.

    And remember DES, the original synthetic estrogen developed back in the 1930s? As it turned out, DES was found to increase the risk of breast cancer by 50%. Further research linked DES to millions of ******* 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 1960s, there was little enthusiasm to continue R&D with triphenylethylene based SERMs, 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.

    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 SERMs 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)

  6. #26
    Hazcat Guest


    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 popularly 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 for 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 ups 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 80s and 90s. Even more misleading, 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 metastases 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 divergent effects 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)

  7. #27


    Thanks guys for all the great information. I got some great gains out of that cycle. Got to 185lbs and still holding strong. Well its been about 3 months now and Im going for another round, but a little different this time. Im gonna run:

    Test E 250 twice a week
    Deca 250 once a week
    D-Bol 40mg a day for the first 6 weeks

    Im also taking milk thistle, cranberry extract and drinking lots of water. Im hoping to get to 200 or more pounds.

  8. #28


    Quote Originally Posted by diggs1870 View Post
    Newbie to the site and gotta say, I love it Im 35, 5' 10" 160LBS and been training for about 10 years. This is my first cycle. Im doing:

    Anavar 10mg 4 times a day for 3 weeks
    Test-E 250 Once a week for 10 weeks
    Deca 300 Once a week for 10 weeks

    Im looking for some info on what kind of Post Cycle I should run. Any help would be greatly appreciated
    PCT 4 weeks mg/day
    25mg ED

    You can blast HCG prior to PCT, I don't use HCG.

  9. #29

  10. #30


    Quote Originally Posted by MattyIce View Post
    PCT 4 weeks mg/day
    25mg ED

    You can blast HCG prior to PCT, I don't use HCG.
    Im gonna run nolva, clomid and arimidex. Think that will do the trick?

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