Free testosterone vs. linked:
Actually, there is a very small amount of testosterone in a free state, where the interaction with cellular receptors is possible with the help of the best testosterone supplements. Most will bind to SHBG (steroid sex hormone-binding globulin, also called globulin sexual and globulin bound testosterone-estradiol bound) and albumin, which prevents the hormone exerts a forced activity. Steroid hormones actually bind more avidly to SHBG than albumin (approximately 1000-fold higher affinity), but the albumin is present at a level of 1000 times SHBG.
Therefore, the activity of both binding proteins in the body is relatively equal. The distribution of testosterone in men is typically 45% of testosterone bound to SHBG, and about 53% bound to albumin. The remaining 2% of the average blood concentration exists in a free state, without ligatures. In women the percentage of free testosterone is lower, it tends to be about 1%. A linker protein called ABP (androgen binding protein) also helps to mediate androgen activity in the reproductive system, although as located exclusively in these tissues is not relevant to muscle growth.
The level of free testosterone available in the blood is also an important factor mediating its activity since only a small percentage are actually active at any given time. We should also note that as we alter testosterone to form new anabolic/androgenic steroids, we also typically alter the affinity in which our steroid will bind to plasma proteins.
This is an important consideration because obviously the higher percentage we have of more active free hormone should be made on a milligram per milligram basis. And the variation can be extremely substantial between different compounds. Proviron® (1-methyl dihydrotestosterone) for example, binds with SHBG many times more avidly than the testosterona19 while mibolerone (7,17 dimethyl nandrolone) and bolasterone (7,17 dimethyl testosterone) show virtually no affinity for this protein at all. (Clear why these steroids are such potent androgens).
SHBG levels in the body are also variable and can be altered by a number of factors. The most prominent appears to be the concentration of estrogen and thyroid hormones in the blood. Usually, we see a reduction in the amount of this plasma binding protein as estrogen levels decline, and content of thyroid hormones in the blood, and an increase in SHBG as these values increase. It has also been shown that a high level of androgen because of the administration of anabolic/androgenic low levels of this protein considerably steroids.
This is clearly supported by a 1989 German study which showed a strong tendency for SHBG reduction with the oral anabolic steroid stanozolol (Winstrol) 20. After only three days of a dose of 0.2 mg/kg. body weight (such as 18 mg. for a man of 200 lbs) on the SHBG by almost 50% in normal subjects. Similar results were obtained using injectable testosterone enanthate, however milligram for milligram basis the effect of stanozolol was much higher compared to testosterone enanthate.
The administration form may have been important to achieve this level of response. Although the injectable version of stanozolol was not addressed in the German study, we can refer to others comparing the effect of oral estrogen vs. Transdermal. They show a much higher response to SHBG levels when the drug is given orally. This may be explained by the fact that SHBG is produced in the liver. Therefore we can not assume that the injectable (or injectable steroids in general) Winstol® show the same level of power in that matter.
Lowering the level of plasma binding protein is not the only mechanism that allows an increase in the level of free testosterone. Steroids that display a high affinity for these proteins may also increase the level of free testosterone competing with it for binding. Testosterone is obviously more difficult to locate available plasma proteins in the presence of the additional compound, more testosterone will be left in an unbound state.
A number of steroids including dihydrotestosterone, Proviron, and oral Turinabol (chlorodehydromethyltestosterone) show a strong tendency to this effect. Clearly, if the level of free testosterone can be altered by using different anabolic/androgenic steroids, there is also the possibility that a steroid can also enhance the potency of another through these same mechanisms. For example, the Proviron® is a poor anabolic, but its extremely high affinity for SHBG might make it useful by allowing the displacement of other steroids that are more active in these tissues.
We must not let this discussion lead us to think that binding proteins serve no valuable function. In fact, they play a vital role in the transport and operation of endogenous androgens. Binding proteins act to protect the steroid against rapid metabolism, ensure a concentration of hormones in the blood and facilitate more stable equal distribution of hormone to various body organs. The recent discovery of a specific receptor (SHBG SHBG-R) located on the surface of membrane steroid reactive cells also suggests a much more complicated for this transport protein hormone only role. It remains very clear, indeed, that manipulate the tendency of a hormone to exist in an unbound state is an effective way to alter drug potency.
