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Good basic AAS advice

May 21st, 2009 · No Comments

just found this article on a steroid article site thought it was intresting..

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.


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
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.

Injectable Steroids
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 cells. 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).


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.

Other Actions
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 very high.


Tip 1 – Do Your Research.
This is INCREDIBLY important. First, keep in mind that the accuracy of anything you read online will only be about 90% – that includes this article. Although much of my research has come from scientific papers and other very knowledgeable individuals – I can’t 100% say that anything, even the research experiments, are perfectly sound all of the time. You’ll have lots of self procalimed experts saying completely different things. One expert said that Nolvadex is useless to use as part of post cycle therapy and likened it to using suntan lotion in a snowstorm. Another expert said it is the preferred choice over it’s “weaker counterpart” clomid. Some experts will tell you that simple testosterone only cycles are best for the first cycle, while others will say that in order to optimize the benefits of any steroid cycle, you must properly stack any injectable steroids with their oral counterparts. I am a believer that testosterone should be the base of any steroid use, especially for those who have interest in doing further cycles in the future.
The main reason a testosterone only cycle is recommended for the first time users is because it is the building block of all future cycles – if it isn’t – it should be! By using testosterone initially you will get an idea of how your body will react to it. You will need to know if you are prone to gyno, how much fluid you will retain and how much your blood pressure will raise with the use of anabolic steroids as part of your training and nutrition program. These are very important things to be aware of.

Think about it like this – you’re doing a stack of testosterone enanthate and dianabol – you feel the signs and symptoms of gyno coming along. So you fix the problem by taking by taking 20-30 mg of Nolvadex or 100 mg of Clomid (which you intelligently kept on hand) daily until the problem subsides and a few days after just to be safe. So the next time you cycle – you use only testosterone enanthate to avoid the aromotization problems brought upon by the addition of the dianabol tabs the first time out. But guess what? It wasn’t the test that was aromatizing after all – it was the dianabol. Now with testosterone only, you are still getting the signs and symptoms of gyno and must once again control the substance with use of an anti estrogen. Had you known you were gyno prone with the testosterone you could have better planned this second cycle and worked out a stack to your advantage and possibly even eliminated or greatly reduced the risks of re-ocurring gyno. If you start cycling with a stack, you won’t have any way of knowing which steroids are causing which side effects.

Another reason why testosterone only is a good first cycle – it’s your first cycle! Why go overkill? You’ll grow like a weed off testosterone only with correct nutrition and training – hell, even without it! In a study done by Bhasin and co-workers1, men with no weight training whatsoever made increases in fat-free mass (4KG or 8.8 lbs), increases in triceps mass (400 mm or 1.6?), increases in quadriceps mass (600 mm or 2.4?), and added 10KG (22.2 lbs) on their bench press and 20KG (44.4 to their squat. It’s TESTOSTERONE after all. You’re injecting HORMONES into yourself. Don’t let the quantity fool you – a mL of cyanide will kill you the same way as minimal amounts of steroids will make you grow. Your virgin androgen receptors will eat it up. Why use more when you’ll get the same results off less? What’s the point? It’s just a big waste of time and money. The last thing you want to do is develop a tolerance so that you are required more quantity in the future.

Testosterone may be a strong androgen, but the side effects are very easily controlled for almost all of them with a few simple ancillaries.

With any steroids you take you are going to shut down your natural testosterone production and this can lead to short term impotence and testicular atrophy (short term if your post cycle therapy is sound!). Deca and Trenbolone are not the only ones that cause this (any drug can when not accompanied by testosterone). Deca and Trenbolone are just the most common and most complained about for this type of thing.

Tags: Anabolic Steroids · General · Steroids Cycles

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