Why Billy Has Breasts: Estrogen Story

YellowJacket

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Why Billy has Breasts: The Story of Estrogen
A Biochemical Over-View of Estrogen
By Grendel (From FreakyMuscle)

Meet poor Billy. Billy stands over 6 feet tall and
weighs around 270 pounds. Billy was born a healthy
normal man, but now Billy has an exciting career as an
exotic dancer thanks to his use of steroids without
anti-estrogens. To understand what happened to poor
Billy lets examine estrogen and its relationship to
male use of anabolic steroids.

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 effect 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 (parabolan, or in most people's cases
Finaplex) convert into progesterone.

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 Thus, steroid
users seek ways to block this estrogen from affecting
them.

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! Without anti-estrogens you will
end up like poor Bobby, shaking his titties in the
face of wealthy Japanese businessmen. No, seriously,
this article will explore how to effectively use
anti-estrogens to prevent many of the side effects
that accompany anabolic steroid usage.

The 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 homeostasis.

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 gynocomastia
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 testicular atrophy. It
also increases ejaculatory capacity; by the way, so
it's best to be considerate to those you care about
(or those you employ, I suppose). That was my public
service message for the month, by the way. I imagine
that this is has something to do with LSH and FSH
production in the body triggering the production of
more semen, but I am not sure. Ask Bill Roberts over
at the mighty TOSSED-OFF-TERONE.NET, or better yet,
contact Greg Zulak c/o MuscleMag.

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 are 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
would recommend that 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 mildly expensive, but very available
because they are not scheduled drugs and can be
legally imported. Check the Anabolic Extreme Forum for
the email address of one Mr. SBC who can help obtain
these vital drugs.

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 article, 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. What a fantastic
environment. Tell that to 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. However, the draw back is that this one pill per
day can cost you around ten dollars.

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 builder. Duchaine helped promote cytadren,
particularly because of its anti-catabolic ability to
suppress cortisol. But, even he acknowledged the
double-edged sword that this drug was. 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 provided the moderate dosage
schemes. The bottom line: These are not drugs to pop
like M&Ms.

The Argument Against Our Little Friends:
But these drugs decrease your gains right? Damn it. I
hate hearing that phrase clutched to…you guessed
it…peoples' breast like a mantra. First of all, there
is no way of telling what your gains would have been
like without nolvadex or clomid. The scientific
evidence that gave rise to this whole dispute (which I
believe Duchaine had a hand in too) 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.

Translation: Yes, you are probably compromising your
anabolic state by using ERA. But does that mean they
shouldn't be used? No. I have heard statements so
ridiculous as "Don't use anti-estrogens, they cut into
your gains and cost too much. Just get surgery".
Lovely, just fucking brilliant. Sure, like surgery
isn't going to cut into your workouts or your gains.
If you are swayed by the logic of just getting the
surgery, I have a recommendation. Go get a pair of
kitchen scissors. Ok, now, pull down your pants
exposing your atrophied testicles suspended in your
pimpled scrotum. Place the base of the scrotum
in-between the scissor blades and apply extreme force.
Thank you, you have helped the human race by ensuring
you cannot procreate and pass on your inferior
genetics…if you already have children please place
them in a sack and toss them into a lake to drown.

I hope this article has proved helpful to you. If only
poor Billy had spent those extra dollars on some
Nolvadex, then perhaps he would not be the top billing
at the local titty bar. This article may have gotten a
little heavy at times with the technical jargon, and I
apologize for that. Certainly, its not as much fun as
discussing getting huge or getting ripped so you can
get laid. But this an important topic if you are going
to responsibly use steroids. I do not think that
anyone should take their first shot or pill before
they have secured enough ERA and/or inhibitors. All
you have to do is look at almost any message board to
see a desperate plea for Nolvadex or clomid from
someone who is mid-cycle and has started to feel the
begins of a lump under his nipple. The telltale tumor,
you got to love it, huh Ronnie Coleman. There are
always those people who claim to never get any
problems no matter how much they take, that's great.
There are also people who get gyno from
androstenediol. I wouldn't want to find out I was a
member of the second group and not have the
appropriate drugs on hand. How do you know if you are
going to be effected? You really can't know until you
have some experience with heavy androgens. If you were
over-weight as a child (many men experience some
degree of gyno in puberty) you have a higher risk. But
the bottom line is that no one should begin a cycle
without having these drugs nearby. Surgery is not a
viable alternative to anti-estrogens.
 
Jarconis

Jarconis

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*presses breast agaisnt glass* oooooh biiiilly!
 
bigpetefox

bigpetefox

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Now, YJ.. Are you stating that I once danced in a said "titty bar", and that's why this article is in my honour?

Thanks, brother! :D

Mine are real, can't touch... Seriously, I plan to have more ERA's than research products, so I should be good.. ;)
 

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