When talking about all the benefits of anabolic steroids I think it is
important to take a moment to talk about side effects and how to prevent them.
The biggest source of steroid related side effects comes from the impact
anabolic steroids have on your body's production of estrogen. So, here is a
quick biochemical over-view of estrogen. Estrogens regulate the growth,
differentiation, and functioning of diverse target tissues, both within and
outside of the reproductive system. Most of the actions of estrogens appear to
be exerted via the estrogen receptor (ER) of target cells, an intracellular
receptor that is a member of a large super family of proteins that function as
ligand-activated transcription factors, regulating the synthesis of specific
RNAs and proteins. This process is almost identical to the action by which
anabolic steroids affect protein synthesis.
Estrogen is also a steroid hormone, although not used for athletic enhancement.
However, estrogen plays a key role in the use of AAS. Certain steroids, at high
enough dosages, can convert via the enzyme aromatase into other hormones; in the
case of testosterone-based steroids this other hormone is usually estrogen.
Steroids with a dihydrotestosterone (DHT) base are not subject to aromatization;
as a metabolite of testosterone its structure is not affected by the aromatase.
Steroids with 17-alkylated structures generally convert into weaker estrogens.
Some steroids, such as nandrolone (deca-durabolin) or trenbolone convert into
High dosages of steroids for prolonged periods also shut down the body's natural
production of certain hormones (particularly testosterone) when steroid therapy
is stopped the body attempts to establish homeostasis by adjusting hormonal
levels. The average ratio of testosterone to estrogen in a healthy male is
100:1. When drugs increase the testosterone in the body, the body will respond
by increasing the estrogen in the body. Additionally, estrogen circulates in the
body bound to the protein SHBG (sex hormone binding globulin) as does the
testosterone. SHBG is produced in the liver and use of steroids increases the
production of this protein; which has a very high receptor affinity for
testosterone. With more SHBG in the body, more testosterone is bound, becoming
inactive as only free testosterone can activate an androgen receptor. SHBG,
however, has poorer receptor affinity for estrogen and more active free estrogen
circulates in the body, further altering the hormonal balance. These effects of
steroids (i.e. the potential for conversion into estrogen, as well as the
disruption of the hormonal balance in the body) can cause serious side effects
in male users. So, steroid users seek ways to block this estrogen from affecting
That is all a very nice and formal way of saying that you need to be taking
anti-estrogens when you are using steroids. See, without the anti-estrogens you
get all sorts of pleasant side effects, not limited to a nice pair of breasts
(with oh -so tender nipples) and extra body fat! This article will explore how
to effectively use anti-estrogens to prevent many of the side effects that
accompany anabolic steroid use.
These Drugs Are Your Friends
Oral clomiphene citrate (Clomid) is an ovulation stimulant used to treat ovulatory failure in women.
Oral tamoxifen citrate (Nolvadex) belongs to a class
of antineoplastics called antiestrogens. It is used to treat breast cancer. Body
builders use both of these drugs. Why on earth would they do that?
The answer is that both of these drugs are anti-estrogens. The term
anti-estrogen is a little inaccurate. This class of pharmaceutical does not
engage in some sort of matter/anti-matter reaction, annihilating estrogen in a
blinding burst of anabolic goodness. Rather, let us think of the classical
anti-estrogen drugs (such as nolvadex and clomid) as estrogen receptor
antagonists (ERA). These ERAs are chemicals that are close enough in structure
to estrogen to fit into the estrogen receptor site; however these chemicals do
not have the same chemical effect as estrogen. The result is that any estrogen
produced by the body or exogenous estrogen cannot find an open receptor site to
attach to. The free-floating estrogen then presents far less problems to
There is a lot of conflict over using nolvadex, clomid and other ERAs. The
regulation of estrogen-induced cellular effects is a multi-step molecular
process. The diversity of estrogen and anti-estrogen effects on cellular
functions is also modulated by tissue and gene specificity. This diversity of
reaction may be explained by different levels of molecular regulation, including
the presence of two distinct estrogen receptor isoforms (ER alpha and ER beta),
their binding to activator or co-repressor transcriptional proteins, and their
affinity to different DNA binding domains of target genes (estrogen responsive
element or API). These mechanisms may account for the specific responses to
estrogens or anti-estrogens according to tissue, cell or gene level.
Therefore, in English, a drug like nolvadex, which targets breast tissues, is
going to do a better job of preventing gynecomastia than is clomid. However
clomid has the benefit of boosting the levels of follicle stimulating hormone,
which helps restore the bodies natural testosterone levels and protects against
Many people stop using their ERA drugs when they end the cycle. That is a
terrible idea. Clomid, as we have already discussed, helps immensely with your
recovery processes. But remember, there is almost always an estrogen backlash to
having been using testosterone drugs for so long. Therefore, many symptoms of
high estrogen levels appear after the cycle. I would continue to use both Clomid
and Nolvadex for up to 3 weeks after the last of the drugs have left your body.
Remember, if on Friday you take 500 mg of a longer acting drug like Sustanon,
then don't consider the following few weeks as truly off time. That is why it is
important to know how long the drugs are effective in your body and yet another
reason to switch to faster acting drugs in the last few weeks of a cycle.
Effective dosages of these two drugs are debated. I personally would use the two
drugs be used together, Nolvadex at 20 mg per day, and clomid at 50 mg per day.
If Nolvadex is used by itself, 20-40 mg are sufficient. 50-100 mg of clomid can
be used if clomid is the only ERA drug. Clomid should be used for two weeks
after the last steroid injection to help return your body to its natural
hormonal state. Nolvadex and Clomid are not expensive, but very available
because they are not scheduled drugs and can be legally imported.
There is a second class of drug used to combat estrogen side effects from what
is grandly called steroid therapy; there are aromatase inhibitors. As mentioned
previously in this chapter, the body can convert testosterone into estrogen
using the enzyme aromatase. This second group of drugs, which I will call the
inhibitors, prevents this process from occurring at all. This class of
medication is generally only prescribed for severe conditions and is generally
more expensive then any of the ERA.
Teslac, (testolactone), has fallen out of favor for several reasons. First of
all, almost one gram daily is needed to achieve sufficient estrogen synthesis
inhibition. This makes this a very expensive drug to use. Also, it is currently
a scheduled drug because it is a testosterone derivate.
Cytadren (aminoglutethimide) is a better choice, requiring dosages of between
250-500 mg per day to suppress estrogen synthesis. 250mg cytadren doesn't cause
significant desmolase inhibition,
so there would still be cortisol and other steroids, while estrogen is
minimized! Cytadren is used therapeutically to combat Cushing's syndrome because
it also interferes with the body's ability to synthesis cortisol. Sounds like
fun, huh ... no cortisol, no estrogen. Perfect you say, well not really remember
Andreas Munzer! Cytadren can cause cysts as well as effect things like blood
clotting. It is reported that Munzer used 1-2g(!) of cytadren/day! Therefore
cytadren use should be done with precision.
Arimidex (anastrozole) is a drug designed to combat second stage breast cancer.
It is an extremely potent drug; one pill per day is sufficient to almost
entirely inhibit estrogen in the body. Its costs have come down thanks to the
production of this product in many underground pharmacies.
The final conclusion about inhibitors is that these are far more powerful drugs
then the ERA. All the drugs listed above effect a much wider hormonal spread
then the anti-estrogens and they are also going to cost you a lot more. Of all
the drugs mentioned, I think that Arimidex is the most useful drug for the body
Cytraden was promoted particularly because of its anti-catabolic ability to
suppress cortisol. But, this product is a double-edged sword. Too little
cortisol is painful to the joints and in the end, extremely dangerous. I would
not recommend the use of cytadren, but I have mentioned moderate dosage schemes
which have been used by friends with no ill effect.
Clomid - Taken daily during a cycle as an anti-estrogen, dosages range between
50-100 mg per day if used exclusively. If combined with Nolvadex, 50 mg per day
Nolvadex - If used alone then 20-40 mg are needed. Some athletes, because of
evidence that it negatively impacts various growth factors in the body, dislike
this drug. If combined with clomid, 10-20 mg are sufficient.
Proviron - This drug binds to androgen receptors but is also helps prevent
excess testosterone from converting into estrogen. I consider this effective
when stacked with either clomid or nolvadex. 1 pill will do if combined with
either 50 mg of clomid or 20 mg or nolvadex. On its own, I suggest at least 2
Arimidex - This is a very potent drug that prevents the body from converting
testosterone into estrogen. The drawback is that is very expensive. The minimum
effective dosage is around between a quarter and a half of a milligram/day. This
drug does not need to be combined with any other during the cycle; however I
recommend you begin using arimidex two weeks prior to commencing your cycle so
that the drug can effectively eliminate the enzyme that permits conversion of
testosterone to estrogen.
Now the bad part! - The scientific evidence that gave rise to this whole dispute
is that in addition to its anti-estrogenic action requiring estrogen receptors
(ER) and leading to growth arrest of breast cancers, studies have previously
shown that the anti-hormone tamoxifen (nolvadex) is able to block EGF, insulin
and IGF-I mitogenic activities in total absence of estrogens. Thus the excessive
use of anti-estrogens will actually result in a loss of some of the most
anabolic of hormones (insulin and insulin-like growth factor 1). Steroid
antagonists can inhibit not only the action of agonist ligands of the receptors
they are binding to, but can also modulate the action of growth factors by
decreasing their receptor concentrations or altering their functionality.
Bottom line is: Yes, you are probably compromising your anabolic state a bit by
using ERA. But does that mean they shouldn't be used? I've heard statements so
ridiculous as "Don't use anti-estrogens, they cut into your gains and cost too
much." Lovely, just brilliant, like needing surgery to remove the tumors from
your pecs isn't going to cut into your workouts or your gains and possibly ruin
the look of your chest in the process with scarring and possibly muscle tissue
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