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Old 09-23-2010, 01:15 PM
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16 Ways to Fight Gynecomastia

Gynecomastia = Gyno - Most people think the only way to combat gyno is to use Nolvadex or Clomid. Considering the undesirable side-effects of these drugs, I generally don’t prefer these as the first line of defense. I have expressed my concerns about SERM’s in my article – Clomid & Nolvadex – The Dark Side.

In this article I summarize alternative methods for combating the occurrence of gyno. The advice given in this article is the result of over 10 years experience in counseling individuals with AAS induced gyno.

If you have gyno as a result of an endocrine disorder, I advise consulting your doctor before making changes to your prescribed medical regimen.



You Do Not Have Gyno!


During mammary tissue growth (the onset of gyno), you may notice the following symptoms -

Puffy or swollen nipples
Overly sensitive nipples
Itchiness around the nipples
Editorial note: I promise -- that is the last time I will ever say nipples.

Now, just because you may have these symptoms does not mean you HAVE GYNO. It simply means that you HAVE GYNO SYMPTOMS. Remember, it is normal to have a small flat pea sized lump under the nipple. This is NOT gyno.

Now, if you allow these above symptoms to progress for several weeks then you may develop gyno. So if you are experiencing any of the above symptoms then you are smart to take action before it’s too late – But please stop emailing me saying you “have gyno” after 3 days on a cycle – this is physiologically impossible.

The good news is that even if you do have a slight case of gyno that you developed from a cycle, it’s probably 100% reversible. Read on…

Nipples.



Gyno Hysteria


No level of gyno is “permanent”. Any level of gyno can be reversed by dietary, supplemental and/or hormonal intervention. Mammary tissue (gyno) can be catabolized like any other tissue in the body. It’s just a matter of creating the right physiological environment within your body. Therefore, as far as I’m concerned, all gyno is temporary or semi-permanent at worse.

Here are the basic levels of gyno -

Level 1 – A dime sized glandular lump – which can emerge as soon as 2-3 weeks after “gyno symptoms” appear. This type of gyno can transform into a more serious level 2 gyno if left untreated for more than 4-6 weeks. In most cases, this initial level 1 gyno disappears once the hormonal environment improves, which is generally 2-3 weeks after the inflicting steroids clear the system.

Level 2 – A quarter sized glandular lump. This type of gyno does not completely disappear on its own, but may gradually shrink to “Level 1” size after discontinuing the inflicting steroids. Completely reversing level 2 gyno requires aggressive dietary and supplemental intervention in conjunction with prescription grade drugs.

Generally, the levels of gyno can be referred to in the following way –

level 1 = temporary

level 2 = semi-permanent

Be warned, if gyno is allowed to grow large enough, the cost of surgery may be more cost efficient than trying to battle the gyno through drug and lifestyle changes – which could otherwise take months or years of intervention.

Following the 16 points below will help you prevent and reverse level 1 & 2 gyno -



The 16 Points


Consider all the following points. Remember, there are many factors that can contribute to gyno and performing just a handful of the points below may be the key to avoiding gyno all together.

1. Your naturally occurring 5a-reduced metabolites are your friends in preventing and reversing gyno. 5a-reduced metabolites include androsterone, androstanedione, androstanediol and dihydrotestosterone (DHT) as the most powerful 5a-reduced hormone. These hormones help prevent gyno by lowering estrogen and blocking the effect of estrogen at the hormone receptor. (1-8) Unless you have serious androgen related hair loss you want to keep your 5a-reduced metabolites relatively high to avoid gyno.

Methods for increasing 5a-reduced metabolites (DHT) are listed in preferred order –

Topical testosterone applied to the scrotum will rapidly increase DHT levels with minimal estrogen conversion. (for more information on topical steroids, read this article)
Use a DHT pro-hormone such as androsterone, found in AndroHard. This will raise DHT with zero risk of estrogen conversion.
Injectable testosterone along with an AI to prevent excessive estrogen conversion.
High dose oral 4-DHEA or DHEA along with an AI to prevent excessive estrogen conversion.

2. If you are concerned about gyno, avoid finesteride at all costs. It lowers all 5a-reduced metabolites to undesirable levels and has an extremely long half-life which continues to suppress DHT levels long after discontinuing the drug. (9) Progesterone would be a better anti-DHT alternative if you are concerned with hair loss. Plus, progesterone can clear the system within 24hrs making a mistake in dosing much less risky.

3. Almost all sources of gyno can be linked back to having insufficient levels of 5a-reduced metabolites in the body. In theory, any amount of estrogen/progesterone can be blocked by sufficient DHT. (10-14) Also, high DHT and enlargement of the prostate is a myth, however high estrogen and high DHT can lead to an inflamed prostate, so you want to at least make an effort to keep estrogen in a normal range. (14)

4. Trenbolone, TREN, Nandrolone can cause gyno because they lack a potent 5a-reduced metabolite (dihydronandrolone is weaker than dihydrotestosterone). (15) If you are worried about gyno from progestational steroids you should consider boosting your 5a-reduced metabolites during the cycle (mentioned above). This can avoid most if not all of the gyno problems associated with progestational hormones. I should mention here that aromatase inhibitors alone (AI’s) will not help prevent gyno from progestational compounds. It is the antagonistic action of 5a-reduced hormones that is required.

5. Nothing is going to antagonize estrogen at the estrogen receptor (ER) better than actual DHT. While DHT derivatives or analogs such as Anavar, Winstrol, Masteron, Epistane, Superdrone, ect may be 5a-reduced, they cannot convert to actual DHT and thus cannot directly inhibit gyno at the receptor level (since they lack the ultra-high binding affinity for the AR that true DHT possesses). (16)

6. Natural anti-estrogens (resveratrol, chrysin, I3C, DIM, ect) are great for PCT and can stimulate the HPTA and manage healthy estrogen metabolism, but they are not strong enough to prevent aromatization from high doses of aromatizing steroids. Don’t rely on these to prevent gyno during a cycle.

7. Reducing prolactin will reduce the overall stimulation on mammary growth. Suppressing prolactin is useful as a temporary method to help slow or stop gyno growth. However, continuing anti-prolactin treatment is not recommended to be continued beyond 8 weeks. Methods of suppressing prolactin include –

Vitex at 460mg/day
Vitamin B6 at 200-400mg/day
Mucuna Pruriens (15%-20% L-Dopa) 4-6g/day
Increasing DHT may also lower prolactin release (17)

8. Don’t fiddle with your nipples. This increases prolactin release which can make gyno worse.

9. IGF-1, GH, insulin and prolactin are all potent growth factors in gyno growth. Limiting these hormones will reduce the likelihood of experiencing gyno symptoms. “Bulking” (aka., eating-a-shitload-of-everything) will increase most of the growth factors listed above. Cutting calories (especially carbohydrates) will suppress insulin and IGF-1 therefore reducing the overall stimulatory effect on mammary growth. Ketogenic diet = less risk of gyno.

10. Body fat (adipose tissue) is the main site for androgens to convert to estrogens. Therefore, being overweight or having high body fat increases your gyno risk. This is another good reason to go on a cutting cycle if you are gyno prone. Reducing body fat will lower your rate of estrogen conversion from aromatizing steroids. (18)

11. Caffeine consumption can inhibit clearance of estrogen from the liver by competing for the P-450 oxidase system. Avoid caffeine if you are concerned about high estrogen levels.

12. Avoid supplements containing forskolin if concerned about gyno. Forskolin increases aromatase activity via cAMP modulation and can increase formation of estrogen. (23,24)

13. Increasing fiber intake (both soluble and insoluble) can enhance clearance of estrogens from the intestines. Research shows that increasing fiber intake in humans can reduce estrogen levels by up to 22%. (19)

14. Reducing estrogen below the normal range (such as over dosing arimidex, letrozol, aromasin or formestane) can eventually reduce SHBG levels, thus allowing more estrogen to freely circulate (by offsetting it from SHBG). Higher levels of freely circulating estrogen can amplify breast tissue growth (20). SHBG also appears to have anti-estrogenic effects at the cell receptor level. (21, 22) Avoiding over suppression of SHBG will reduce your gyno risk.

15. Don’t be afraid to lower the dose mid cycle. People have a tendency to panic at the first sign of gyno and drop everything. Generally, just lowering the dose of the afflicting steroid can offer gyno relief within 4-5 days.

16. Save SERM’s as your last resort against gyno. You do not need a SERM (tormifene, clomid or nolva) to avoid gyno from a properly planned cycle. If you are still having gyno problems after following the above points, consider the fact that you have a poorly planned cycle and you need to revaluate the compounds you have chosen.

By Eric M. Potratz

Eric M. Potratz has developed his education in the field of endocrinology and performance enhancement through years of research, counseling, and real world experience. Over the past five years he has been a private consultant for hundreds of athletes and bodybuilders alike, and is the founder & president of Primordial Performance


References –

1. Dihydrotestosterone may inhibit hypothalamo-pituitary-adrenal activity by acting through estrogen receptor in the male mouse.
Lund TD, et al.
Neurosci Lett. 2004 Jul 15;365(1):43-7.

2. Androgen-induced inhibition of proliferation in human breast cancer MCF7 cells transfected with androgen receptor.
Szelei J, et al.
Tufts University School of Medicine, Department of Anatomy and Cellular Biology, Boston, Massachusetts 02111, USA.

3. The non-aromatizable androgen, dihydrotestosterone, induces antiestrogenic responses in the rainbow trout.
Shilling AD, et al.
Agricultural and Life Sciences Building, room 1007, Oregon State University, Corvallis, OR 97331, USA.

4. The androgen 5alpha-dihydrotestosterone and its metabolite 5alpha-androstan-3beta, 17beta-diol inhibit the hypothalamo-pituitary-adrenal response to stress by acting through estrogen receptor beta-expressing neurons in the hypothalamus.
Lund TD, et al.
J Neurosci. 2006 Feb 1;26(5):1448-56.

5. Steroid modulation of aromatase activity in human cultured breast carcinoma cells.
Perel E, et al.
J Steroid Biochem. 1988 Apr;29(4):393-9.

6. Aromatase activity in the breast and other peripheral tissues and its therapeutic regulation.
Killinger DW, et al.
Steroids. 1987 Oct-Dec;50(4-6):523-36. Review.

7. The intracellular control of aromatase activity by 5 alpha-reduced androgens in human breast carcinoma cells in culture.
Perel E, et al
J Clin Endocrinol Metab. 1984 Mar;58(3):467-72.

8. FSH-induced aromatase activity in porcine granulosa cells: non-competitive inhibition by non-aromatizable androgens.
Chan WK, et al
J Endocrinol. 1986 Mar;108(3):335-41.

9. The effect of 5 alpha-reductase inhibitors on erectile function.
Canguven O, Burnett AL.
J Androl. 2008 Sep-Oct;29(5):514-23.

10. Comparative Pharmacokinetics of Three Doses of Percutaneous Dihydrotestosterone Gel in Healthy Elderly Men – A Clinical Research Center Study*
C. Wang et al.
Journal of Clinical Endocrinology and Metabolism Vol. 83, No. 8 (1998)

11. Successful percutaneous dihydrotestosterone treatment of gynecomastia occurring during highly active antiretroviral therapy: four cases and a review of the literature.
Benveniste O et al.
Clin Infect Dis. 2001 Sep 15;33(6):891-3.

12. Gynecomastia: effect of prolonged treatment with dihydrotestosterone by the percutaneous route.
Kuhn J et al.
Presse Med 12;21-25. (1983)

13. Percutaneous dihydrotestosterone (DHT) treatment. In: Nieschlag E, Behre HM, eds. Testosterone: action, deficiency substitution.
Schaison G, Nahoul K, Couzinet B.
Berlin: Springer Verlag; 155–164. (1990)

14. Transdermal dihydrotestosterone and treatment of ‘andropause’.
de Lignieres B.
Ann Med 1993;25: 235–41.

15. Metabolism and receptor binding of nandrolone and testosterone under invitro and invivo conditions.
Bergink et al.
Acta Endocrinol Suppl (Copenh). 271:31-7, 1985

16. Pharmacology of Reproduction
David E, et al.
Principles of Pharmacology (second edition) p. 510 (2008)

17. Antagonism of estrogen-induced prolactin release by dihydrotestosterone.
Brann DW, et al.
Biol Reprod. 1989 Jun;40(6):1201-7.

18. Aromatase – a brief overview
Simpson ER, et al
Annu Rev Physiol. 64:93-127, 2002

19. Dietary fiber intake and endogenous serum hormone levels in naturally postmenopausal Mexican American women: the Multiethnic Cohort Study.
Monroe KR et al.
Nutr Cancer. 2007;58(2):127-35.

20. Williams Textbook of Endocrinology.
Wilson, et al.
9th ED. Philadelphia: Saunders, 1997

21. Sex steroid binding protein receptor (SBP-R) is related to a reduced proliferation rate in human breast cancer.
Catalano MG, et al.
Breast Cancer Res Treat. 42(3):227-34, 1997

22. Biological relevance of the interaction between sex steroid binding protein and its specific receptor of MCF-7 cells under SBP and estradiol treatment.
Fissore F, et al.
Steroids, 59(11):661-7, 1994

23. Progestin-dependent effect of forskolin on human endometrial aromatase activity.
Tseng L, Malbon CC, Lane B, Kaplan C, Mazella J, Dahler H, Tseng A.
Hum Reprod. 1987 Jul;2(5):371-7.

24. Forskolin up-regulates aromatase (CYP19) activity and gene transcripts in the human adrenocortical carcinoma cell line H295R.
Watanabe M, Nakajin S.
J Endocrinol. 2004 Jan;180(1):125-33.
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Old 09-24-2010, 09:51 PM
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very useful post
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Old 09-24-2010, 11:59 PM
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Great post Bass...thanks for the info
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Old 10-21-2010, 07:56 AM
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topside


6. Natural anti-estrogens (resveratrol, chrysin, I3C, DIM, ect) are great for PCT and can stimulate the HPTA and manage healthy estrogen metabolism, but they are not strong enough to prevent aromatization from high doses of aromatizing steroids. Don’t rely on these to prevent gyno during a cycle.
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Old 10-21-2010, 07:59 AM
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doing a little research on resveratrol
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Old 09-13-2012, 03:36 AM
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hello Basskiller,

As you told [URL=""]Gynaecomasta surgery[/URL] may not give you a permanent solution for the issue. If all of the glandular/fibrous tissue of gynecomastia is removed then the treatment is permanent. If portions of the tissue are left behind and the source of the gynecomastia is continued (supplements, etc) then there is a chance for the gynecomastia to return. So consult plastic surgeons who are well experienced in this field.
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Old 09-13-2012, 07:21 AM
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"Topical testosterone applied to the scrotum" this is new to me. i wonder if Mila Kunis will help me with my application LOL
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Clomid & Nolvadex - The Dark Side

Quote:
By Eric M. Potratz (Email)

Eric M. Potratz has developed his education in the field of endocrinology and performance enhancement through years of research, counseling, and real world experience. Over the past five years he has been a private consultant for hundreds of athletes and bodybuilders alike, and is the founder & president of Primordial Performance.



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.

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)

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-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 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.

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.

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 the tamoxifen induced liver cancer make take years to manifest in a healthy male, its damaging effects could easily be exaggerated by other popular hepatotoxc , including 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 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 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.



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