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This tissue may not be the most ideal one to use though, as it contains more androgen receptor than most skeletal muscles (the AR is still less abundant here than in target tissues such as the ventral prostate). An anabolic index greater than one indicates a higher tendency for anabolic effect, and therefore classifies the drug as an anabolic steroid. A measure lower than one in turn assesses the steroid as androgenic. There is some variance between experimental results and the actual real world experiences with humans, but (with a few exceptions) designations based on the anabolic index are generally accepted. Below are discussed a few factors that greatly affect anabolic/androgenic dissociation. The section of this book dealing with DHT conversion is important, because it helps us understand the anabolic steroid nandrolone and many of its derivatives. Nandrolone is identical to testosterone except it lacks a carbon atom in the 19th position, hence its other given name 19-nortestosterone. Nandrolone is very interesting because it offers the greatest ratio of anabolic to androgenic effect of the three natural steroids (see: Synthetic AAS Chemistry). This is because it is metabolized into a less potent structure (dihydronandrolone) in androgen target tissues with high concentrations of the 5-alpha reductase enzyme, which is the exact opposite of what happens with testosterone. Apparently the removal of the c4-5 double bond, which normally increases the androgen receptor binding capability of testosterone, causes an unusual lowering of this ability with nandrolone. Instead of becoming three to four times more potent, it becomes several times weaker. This is a very desirable trait if you want to target anabolic effects over androgenic. 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Where can i purchase anavar, cheap price buy anabolic steroids online gain muscle. Some early success with the creation of new structures convinced many scientists that they were on the right track. Unfortunately none of this progress led researchers their ultimate goal. By the mid-1950’s, well over one thousand testosterone, nandrolone, and dihydrotestosterone analogues had been produced, but none proved to be purely anabolic compounds. The failure to reach this goal was primarily due to an initial flawed understanding of testosterone’s action. Scientists had noticed high levels of DHT in certain tissues, and believed this indicated an unusual receptor affinity for this hormone. This led to the belief that the human body had two different androgen receptors. According to this theory, one receptor site would respond only to testosterone (eliciting the beneficial anabolic effects), while the other is activated specifically by the metabolite, dihydrotestosterone. With this understanding, eliminating the conversion of testosterone to DHT was thought capable of solving the problem of androgenic side effects, as these receptors would have little or none of this hormone available for binding. More recently, however, scientists have come to understand that only one type of androgen receptor exists in the human body. It is also accepted that no anabolic/androgenic steroid can possibly be synthesized that would participate only with receptors in tissues related to anabolism. DHT, which was once thought not to bind to the same receptor as testosterone, is now known to do so at approximately three to four times the affinity of its parent, and the unusual recovery of DHT from androgen responsive tissues is now attributed to the distribution characteristics of the 5a-reductase enzyme, where can i purchase anavar. FOR A LIST OF ANABOLIC STEROID ONLINE DISTRIBUTORS CLICK HERE. Synthetic Anabolic Steroids Development. In order to develop products that would be effective therapeutically, chemists needed to solve a number of problems with using natural steroid hormones for treatment. For example, oral dosing was a problem, as our basic steroids testosterone, nandrolone, and dihydrotestosterone are ineffective when administered this way. The liver would efficiently break down their structure before reaching circulation, so some form of alteration was required in order for a tablet or capsule to be produced. Our natural steroid hormones also have very short half-lives in the body, so when administered by injection, an extremely frequent and uncomfortable dosing schedule is required if a steady blood level is to be achieved. Therefore, extending steroid activity was a major goal for many chemists during the early years of synthetic AAS development. Scientists also focused on the nagging problems of possible excess estrogenic buildup in the blood, particularly with testosterone, which can become very uncomfortable for patients undergoing therapy. Methylated Compounds and Oral Dosing. Chemists realized that by replacing the hydrogen atom at the steroid’s 17th alpha position with a carbon atom (a process referred to as alkylation), its structure would be notably resistant to breakdown by the liver. The carbon atom is typically added in the form of a methyl group (CH3), although we see oral steroids with an added ethyl. A steroid with this alteration is commonly descirbed as a C-17 alpha alkylated oral, although the terms of methylated or ethylated oral steroid are also used. The alkyl group cannot be removed metabolically, and therefore inhibits reduction of the steroid to its inactive 17-ketosteroid form by occupying one of the necessary carbon bonds. Before long, pharmaceutical companies had utilized this advance (and others) to manufacture an array of effective oral steroids including methyltestosterone, Dianabol, Winstrol’, Anadrol 50′, Halotestin’, Nilevar, Orabolin, and Anavar.

 

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