ANABOLIC - ANDROGENIC Steroids - a basic description
This article will attempt to describe, in layman's terms, the fate of
Anabolic/Androgenic steroids (AAS) in the human body. The intent is to look at
steroids from a general view, not to describe the different individual steroids.
Of course, the author does not condone the use of steroids by anyone not under
the care and supervision of a qualified medical professional.
TYPES OF steroids
Anabolic/Androgenic steroids can be roughly classified into two types, oral and
injectable. When you eat food or consume anything orally, the great majority of
the ingested substances pass through the liver prior to entering the
bloodstream. For this reason, "injectable" AAS cannot be taken orally because
the liver will deactivate the steroids in this "first pass". Deactivation in the
liver usually involves the addition of one or more hydroxyl (OH) groups to
increase the solubility of the molecule in water, making excretion in the urine
more easily accomplished.
Oral steroids involve modification of the parent steroid to make it harder for
the liver to degrade the steroid molecules. This modification is almost always
the addition of an alkyl (methyl) group at the 17 position of the steroid ring.
The liver can still degrade the steroid, but not as effectively as the
un-modified steroid. Therefore, oral steroids make several cycles through the
bloodstream before being excreted. Most oral steroids are, to various degrees,
excreted from the body unchanged.
The injectable AAS are very effectively degraded in just a single pass through
the liver. If this is so, then how can the injectables be effective? The answer
is called a "depot" (or reservoir), which allows a regular release of steroid
into the bloodstream. As steroid is removed from the bloodstream by the liver,
more steroid is being released into the bloodstream from the depot. There are
several ways to provide such a reservoir of the steroid.
The first way is to use pure testosterone (a crystalline solid) suspended in
water. testosterone has a low solubility in water, and the crystals slowly
dissolve in the watery environment of the tissue in which it is injected. The
dissolved testosterone is carried throughout the body by the bloodstream. For
testosterone suspension, the "depot" is the actual physical site where the
injection is made. The crystals do not migrate to other parts of the body, and
the presence of the crystalline testosterone can cause some pain at the
injection site. The testosterone dissolves at a (relatively) constant rate, and
lasts for a few days in the body. Winstrol suspension is similar.
The other way to provide a depot of steroid is to use a water-insoluble form of
the steroid that can be converted in the body to the parent steroid, which has
some solubility in water (bloodstream). Most commonly, the parent molecule is
esterified with an organic acid, and the resulting ester is soluble in oil, but
only very slightly soluble in water. Commonly used organic acid groups are
acetate (C2), propionate (C3), enanthate (C7), decanoate (C10), and undecylenate
(C11). The longer the carbon chain of the acid, the more oil-soluble the ester,
and the longer it takes for the ester to turn into the parent steroid
(de-esterification). A type of enzyme that is found throughout the body
facilitates the de-esterification reaction to form the parent steroid from the
ester. The enzyme actually catalyzes the reaction in both directions, so it can
also attach an organic acid back onto the parent steroid. So, for example,
testosterone enanthate can actually be turned into testosterone palmitate. There
is some good evidence that steroid esters are, to some extent, stored in fat
It is commonly believed that esters form a depot of oil/ester that stays at the
injection site. This is not true. While the depot concept holds true for esters
(because they slowly release the parent steroid over time), the esters actually
disperse throughout the body after injection, prior to (and during) the
de-esterification reaction to form the parent steroid. They do not stay at the
injection site. For example, the ester testosterone enanthate has been found in
tissues throughout the body, including hair samples of subjects who have
injected T200. If a bio-contaminant is introduced at the time of injection
(non-sterile conditions), the body will attempt to encapsulate the contaminated
material, and an abscess will form. In this case it appears as if the ester has
remained at the injection site. But under normal sterile conditions, the oily
solution will disperse. Injecting too much at one site or injecting too
frequently at one site will not cause an abscess.
Transport of steroids in the Bloodstream
Once the steroid has been released from the depot (or the oral steroid has been
absorbed from the intestine), it is transported throughout the body in the
bloodstream. Carrier proteins (Albumin and Sex Hormone binding Globulin) bind
about 98% of testosterone under natural conditions. Thus, only 2% of the hormone
is free to carry out its actions. When exogenous steroid is present, the level
of free steroid is much higher than 2%. Bear in mind that the hormone is not
permanently bound to the some of the proteins, but is constantly binding and
un-binding from the protein. At any given time, about 2% of the hormone is
un-bound in the natural state. So, if the 2% unbound hormone were to magically
disappear, then the proteins would release more hormone such that 2% (of the
remaining total) would come unbound. The bloodstream is the mechanism by which
the hormones reach their target tissues (muscle).
ACTION OF Steroids
Androgen Receptor Activation
Once a free molecule of steroid reaches the muscle cell, it diffuses into the
cell. The diffusion can be with or without transport-protein assistance. Once in
the cell, the AAS is makes its way to the cell nucleus where it can bind with an
androgen receptor (AR), and activate the receptor. Two of these activated
receptor complexes join together to form the androgen response element (ARE).
The ARE interacts with DNA in the nucleus, and increases the transcription of
certain genes (such as muscle protein genes). As long as the ARE is intact, it
accelerates gene transcription. Remember, though, that the AAS and the receptor
are in a state of flux (binding and un-binding), just like with the Carrier
proteins. So the ARE can be deactivated just by losing one of the two AAS that
are bound to the AR's. This equilibrium situation explains why 1 gram per week
testosterone is more effective than 1/2 gram per week, even though 1/2 gram
appears to be more than enough to saturate all the AR's in the body. The higher
concentration makes it more likely that the receptors will be occupied by an
AAS, and the ARE will be intact for a longer period of time, on average.
Activation of the androgen receptor is a key mechanism in the action of AAS.
However, this mechanism by itself does not explain the differences between
steroids (i.e., nandrolone activates the AR better than testosterone, but is not
as good of a mass-building product). Other actions involve primarily the central
nervous system, and involve actions such as motor activation (muscle
coordination) and mood (i.e., aggressiveness). The mechanism by which AAS effect
these actions is not well understood at this time. Another effect occurs in the
liver, where some steroids cause the release of certain Growth Factors. The
different actions of the different AAS explains why a stack of two different
types of AAS is often better than one by itself.
Elimination of steroids
The liver is a primary route to deactivation of steroids, the chemical structure
is changed here to make the steroid more soluble in water for excretion through
the kidneys. A good portion of many steroids also are excreted as-is, without
any alteration by the liver, or by formation of the sulphate, which is more
water soluble. Many in the medical community have believed that AAS cause liver
damage because levels of certain enzymes (AST and ALT) are elevated when
steroids are used. Elevated levels of these enzymes are seen in patients with
liver damage from other causes, so the conclusion is that AAS must cause liver
damage because these enzymes are elevated. Recent work, however, has shown that
a true marker of liver damage, GGT, remains unchanged when some AAS are used,
and now it is questioned whether AAS are really damaging to the liver (the 17
alpha-alkylated AAS do cause damage in some rare cases, and this damage is
reversible upon cessation of steroid use). The same thought processes were used
to claim kidney damage, but that is unlikely as well.
One thing I'll say is 1 gram maybe better then 500mg, but the possibilities of
side effects would be higher too. Like he said 500mg "appears to be more than
enough to saturate all the AR's in the body." Once you go passed what your
receptors can handle, the chances of the juice converting to a side effect are
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