The War on Female Hormones

Many readers of this book will have already used steroids in the past, or are currently on a cycle to reach one goal or another. These people may know a little about the female hormones termed ESTROGENS and drugs used to modify their actions/production within the male metabolism. In the following text I will go a little more in-depth than just cursory knowledge and hopefully not bore to death those that already have some comprehension of the basic facts.

Where are estrogens?

Just as any hormone that has the activity of TESTOSTERONE(such as DIHYDROTESTOSTERONEDHEAANDROSTENEDIONE, etc.), are classed as ANDROGENS, any hormone that has ESTRADIOLS’ or ESTRONES’ effects, are classed as estrogens. Many writers will go on about estrogen singly as if it was the only female hormone when there are in fact a group of such, the main ones being estradiol and estrone among others of lesser potency/concern.

Structurally, estradiol has a HYDROXY group at both the C3- and C17- structural positions, whereas estrone only differs in the type of groups at these same positions; namely KETO groups. Estradiol is always the most powerful of the natural estrogens (mg for mg), which can be manufactured within the male metabolism through the AROMATISATION of testosterone (artificial supplied OR naturally excreted) by the AROMATASE ENZYME, or from estrone already present via the 17β-HSD ENZYME. Estrone is the weaker of the two estrogens which can be produced from ANDROSTENEDIONE via the same aromatase enzyme, or from estradiol via the same HSD enzyme except working in reverse.

From an AAS using bodybuilders viewpoint, high estrogen levels can lead to a number of unwanted side effects (see relevant chapter for more in-depth info), such as GYNAECOMASTIA, inhibition of natural testosterone production and EDEMA (water retention) leading to bloating and increases in blood pressure…amongst others. Successful dieting can also be sabotaged by the presence of high estrogen levels and lead to possible development of female fat pattern distribution in males, i.e. on the hips, bum and thigh areas (READ: CELLULITE).

Estradiol has some nasty metabolites too (by-products), some of which are thought to be CARCINOGENIC, and some that can cause or aggravate existing conditions such as  HEPATIC CHOLESTASIS, which are blood filled cysts in the liver.

Mood can also be affected by high estrogen levels (ask your wife or girlfriend just before her period), be they from the aromatic conversion of testosterone, or from responsively high levels after AAS withdrawal (estrogen REBOUND). This is one of the reasons why athletes that are discontinuing high dose, more androgenic cycles, can sometimes suffer from mild estrogenic related DEPRESSION…and you thought you were pissed off from just losing all that bodyweight and strength!

Steroids that Aromatise

Many steroid using athletes believe they already know which steroids AROMATISE (convert to estrogens), and which do not. These assumptions are sometimes in error, as the PROGESTOGENIC activity (i.e. anything related to PROGESTERONE) of many steroids, can be easily mistaken for estrogenic activity (i.e. anything related to estrogens). This is very important as elevations of both progesterones AND estrogens (as mentioned previously), can both aggravate/cause gynaecomastia and/or excessive water retention. We see that steroids having the ability to activate the ANDROGEN RECEPTOR can also activate estrogen and progesterone receptors directly, without much differentiation of which is which. Androgens DO NOT‘convert’ to progesterone as testosterone can into estradiol, but rather uniquely they are able to act on the progesterone receptor WITHOUT any chemical changes in structure (such as is the case with NANDROLONES and TRENBOLONE).

In women, progesterone will up to a certain point increase sex drive and then have the opposite effect when blood concentrations get too high. In men too, progesterone can have this same action but the response is entirely dependent on an individual’s genetic makeup, progesterone receptor population and location.

Again, we have seen nandrolone and trenbolone proven as progestins, and it’s a point worth repeating…very important and often overlooked. Even moderate use of these compounds will actively lower estrogen levels through their reduction of natural testosterone due to limitation of LUTEINISING HORMONE; giving the aromatase enzyme less substrate to work on. Even with a reduction of estrogens, they can still cause gynaecomastia in some users due to their overt activity at the progesterone receptor itself (see Chapter 10 for more information on these specific compounds). Anti-estrogenic drugs will mostly have no purchase on the related side effects of nandrolone and trenbolone whatsoever in these cases, but ANTI-PROGESTERONES like CABERGOLINE might help in many.

ORAL TURINABOL, METHENOLONE, STANOZOLOL, OXANDROLONE, MESTEROLONE and DIHYDROTESTOSTERONE, cannot and will not aromatise, making anti-estrogen adjuncts to these compounds pointless when they are taken singly or stacked with one another.

Which steroids do aromatise? Study the last chapter of course, but in brief of particular concern are all the esters of testosterone, METHANDROSTENOLONEBOLDENONE, and FLUOXYMESTERONE (normally not problematic, as doses of fluoxymesterone are usually in the low mg range, and only used for short cycles due to toxicity concerns).

Estrogen receptor blockers (SERM’s)

Tamoxifen Citrate

Seen under the names: APO-TAMOX™, CEADON™, DEFAROL™, DURATAMOXIFEN™, EMBLON™, JENOXIFEN™, KESSAR™, LEDERTAM™, MANDOFEN™, MASTOFEN™, NOLTAM™, NOLVADEX™, NOLVADEX D™, NOLVADEX FORTE™, NONCARCINON™, NOURYTAM™, OXEPRAX™, T CELL PHARM™, T CITRATE™, T DUMEX™, TAMOXIFE-EBEWE™, E FARMOS™, T FERMENTA™, TAMOXIFEN HEXAL™, T HEUMANN™, T LACHEMA™, TADA™, TADEX™, TAFOXEN™, TAMAX™, TAMAXIN™, TAMCAL™, TAMEXIN™, TAMIFEN™, TAMOFEN™, TAMOFENE™, TAMOPLEX™, TAMOXAN™, TAMOXASTA™, TAMOX-GRY™, TAMOXIFEN™, TAMOXIFENO GADOR™, TAMOXIFEN LEIRAS™, TAMOXIFEN LEDERLE™, TAMOXIFEN MEDAC™, TAMOXIFEN MP™, TAMOXIFEN NM™, T ONKOLAN™, TPAN MEDICA™, TPHARBITA™, T SOPHARMA™, TAMOXIFEN TABLETTS™, TAMOXIFENO™, T FARMITALIA™, TAMOXIFENO FUNK™, TAMOXIFEN SEPTA™, T WASSERMANN™, TAMOXIFENUM™, TAMOXIFENUM GF™, TAMOXIFENUMPCH™, ZITAZONIUM ™ (Phew!).

Found in dosages: 10, 20, 30 and 40mg tablets

Presentation: Foil strips of 10 tablets (any dose), 1-5 strips per box; bottles of 20, 30, 50 or 100 tablets.

Tamoxifen citrate is classed as a non-steroidal anti-estrogenic drug, in the group known as SELECTIVE ESTROGEN RECEPTOR MODULATORS (or SERM’s for short). It is a chemical of the TRIPHENYLETHYLENE family, which possesses both estrogen agonist (booster) AND antagonist (reducer) properties at receptive sites. In simple terms this means that it can act like estrogen in tissues areas and/or block estrogen from doing its stuff at others. Most commonly accepted for its blocking action at the estrogen receptors in mammary gland tissue by bodybuilders (thus preventing or stopping development of gynaecomastia or ‘bitch tits), it was actually designed for doing this same job in women to prevent the growth of hormone receptive breast cancers. Developing swollen mammary glands in males is in the majority of cases non-life threatening, but that swollen gland can attract stubborn fat in the long-term, and might need surgical removal at a later date to rid the user of the unsightly lumps.

Many users of tamoxifen think that it will help reduce water retention caused by the use of aromatising steroids, but this thought is flawed. As an estrogen treatment drug it only BLOCKSthe attachment of estrogens at the mammary sites, IT DOES NOT REMOVE ESTROGENS FROM THE BODY. So it will not prevent water retention in the aromatising steroid user or lower blood pressure from the higher plasma content in the blood (caused by the rise in estrogens)

It has some other positive effects as well, and not just as a treatment of steroidal side effects. It possesses the ability to increase the production of FSH (FOLLICLE STIMULATING HORMONE) and LH (LUTEINISING HORMONE) in males. It does this feat by blocking the negative feedback caused by estrogens when they attach at their intended receptors at the HYPOTHALAMUS by attaching in their place WITHOUT stimulating them. This allows the hypothalamus to keep secreting GnRH (GONADOTROPHIN RELEASING HORMONE), which would otherwise have been shutdown in the presence of estrogens (this is somewhat similar to the way in which CLOMIPHENE CITRATE works too, but we’ll get into that next). Now since high LH levels in men normally stimulates the LEYDIG CELLS of the testes to secrete more natural androgen (testosterone), the drug is an obvious choice for part of the post cycle therapy protocol to get the old ‘nads’ back up and running again, but during a cycle will have little effect in this way since the massive supraphysiological level of androgens from ingested/injected steroids give a constant negative feedback effect. See more on this in the upcoming section on post cycle therapy.

Another positive for tamoxifen is that it acts like some other triphenylethylene compounds by acting as an estrogen in the liver cells. Estrogen action in the liver is VERY important in the regulation of blood cholesterol (LDL and HDL), by increasing the good stuff (HDL), and reducing the bad stuff (LDL). Since most steroids (particularly the ones modified to NOT aromatise), have a negative effect on blood lipids by ‘distracting’ the liver from one of its jobs (cholesterol management), some athletes compound this problem further by the adjunctive use of anti-aromatase inhibitors like ANASTROZOLE or LETROZOLE to reduce the side effects of estrogen in the body, which might lower the estrogens to a point where they further sabotage the management of blood fats in the liver…definitely not a good situation to be in. Rather than use the anti-aromatases to manage the estrogens, tamoxifen may be a better bet to keep the liver functioning normally, or even a low dose combination of both blockers and anti-aromatases to get the best of both worlds; slightly lower overall estrogen from the aromatase inhibitors AND some liver cell boosting effects to improve cholesterol from the tamoxifen. Please remember though that tamoxifen cannot eradicate the high impact that high doses of modified steroids or C17 alpha alkylated oral compounds might have on the livers management systems, it is used successfully in this way on weaker/low-dosed cycles only.

Tamoxifen was first synthesised in 1962 by chemical giant ICI. Initially used as a treatment for certain forms of female infertility, it became available on the commercial market in the U.S. within a few months of discovery…which goes to show how much sway the massive pharma companies have over the corrupt government departments (oooh…political). In 1971, clinical trials of the drug began investigating its possible use as a combatant against breast cancer. Two years later, ICI’s studies proved that there was a definite link between estrogens and some breast cancers, but it took another 4 years for the FDA to approve the drug as a breast cancer treatment. It was sold by ICI under the trade name of NOLVADEX™, and years later by ASTRAZENECA in the U.S., which became the new name for ICI. Many generic versions were to follow (see list above for just a few), and in 1998 the FDA also approved its use for breast cancer PREVENTION and not just treatment, especially in those with a genetic predisposition. Amazingly, even with all the proven successes with tamoxifen, AstraZeneca discontinued the sale of Nolvadex in the U.S., but it is still available under this name in this country, still by ICI.

I won’t talk about dosing schedules for treatment and prevention of breast cancer as it is very involved and beyond the scope and use of this small section. In bodybuilding, a preventative dose for gynaecomastia in men is 10-20mg per day. If a chap is not taking tamoxifen and develops swelling of the mammary gland, I suggest an immediate ingestion of 50mg or so to get the dose of tamoxifen up in the blood, then drop to 10-20mg for the rest of the cycle, or as long as the swelling persists.

Much anecdotal evidence has suggested that this compound can influence a marked reduction in GH and IGF-1 production in the body; two VERY important hormones that AAS users attempt to maintain or even increase to promote synergistic growth. Many athletes report minimised gains on light to moderate dosage AAS cycles when tamoxifen is used as an adjunct compared to when it is omitted entirely. Scientists have a theory that estrogens are actually needed in the body to keep the androgen receptors open (discussed elsewhere), making for larger gains in mass and strength. For these negative reasons, users must weigh up whether the estrogenic side effect of gynaecomastia or negative blood lipid balance are enough of a problem to warrant tamoxifen use, particularly in the lighter androgenic cycles where gains might become negligible. Many users actually wait until side effects become too problematic and then hit the tamoxifen at a relatively high dosage for one week (as mentioned above), then taper down to just 10-20mg per day for the remnants of their cycle, which should not limit the big gains too much and is also more economically viable. Please remember that I am talking with experience when I say that once gynaecomastia has started to develop it is almost impossible to regress its growth once initiated; the user must think very carefully before playing this hormonal form of Russian Roulette (but the letrozole is always there as a back-up…see later).

Stopping the use of tamoxifen abruptly at any point when estrogen levels are at higher than normal levels, can cause a severe rebound of side effects which will onset rapidly. If a user is taking tamoxifen as an adjunct when on a steroid cycle it is best to stop its use when estrogen levels are at a more acceptable range, i.e. 2-6 weeks post cycle, remembering that some injectable esters remain active in the blood for this length of time. Post cycle tamoxifen use ensures estrogen levels cannot exert their adverse effects at a time when they are most definitely NOT needed.

For bodybuilding use in women, tamoxifen has only really been employed in the run up to competition when estrogen blocking in females can help no end in attempts to reduce estrogenic fat burning ‘resistance’. Remember, estrogens are naturally present in the female metabolism in large amounts, so adding a small dose of tamoxifen can do some magical things with regard to fat loss (something which many ‘experts’ might disagree with, but something I have proven time and again with the female athletes I have worked with). This said though, please know that the female side effects for tamoxifen include hot flashes, vaginal bleeding (other than menses), vaginal discharge/itching, dizziness and hair-loss. Some other listed adverse effects are skin rashes, reduced white blood cell count and concurrent drop in immune system, visual disturbances, uterine fibroids and womb lining thickness changes, deep vein thrombosis leading to pulmonary embolism (DVT), changes in liver enzymes and changes in blood lipids. To top things off, some women using tamoxifen have had an increased incidence of endometrial cancer and uterine sarcoma, as well as possible birth defects in the unknowingly pregnant. So, a lady should think long and hard before adding tamoxifen into the mix just to get a little leaner or a little faster, especially when taking other drugs definitely not intended for use in the female metabolism.

MENS DOSAGE: 10-20mg taken once daily. Frontloading with 50-60mg if gynaecomastia is being initially treated.

WOMENS DOSAGE: No more than 10 mg daily for short period just prior to competition.

PRICE: £10-15 per 30 x 10mg tablets. £10-25 per 30-50 x 20mg tablets Black Market, £8-12 per 30 x 20mg tablets on the continent.

Please note that this excerpt is only a small sample of the book chapter it is taken from. A great deal more content is available on this and many other topics in the Break the Code book.

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