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The Pharmacology Of Anabolic Steroids |
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Written by By Dan Gwartney, MD
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Wednesday, 28 January 2009 |
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Page 4 of 6
In the body, the various AAS do not provide identical responses to testosterone or each other. The major differences are generally believed to be due to whether the AAS used can be converted into estrogen via the aromatase pathway, DHT via 5a-reductase, both or neither.6 Even the non-steroidal SARMs (meaning they are not based upon testosterone) being developed by numerous pharmaceutical companies (still) seeking to dissociate anabolic from androgenic effects are believed to be less androgenic, because they are not affected by 5a-reductase.6 Drugs that 5a-reductase can convert are typically changed into more androgenic metabolites, leading to hair loss, acne and prostate enlargement. 19-Nortestosterone (nandrolone, Deca) is the exception to this rule, as it actually converts to a less androgenic compound.22 AAS that can be 5a-reduced typically provide less dramatic mass and strength gains, may be associated with joint pain, but tend to result in “higher quality” gains, as there is little water retention and fat loss appears to be enhanced.
AAS that can be aromatized tend to provide greater mass and strength gains, but also predispose users to increased water retention and fat gain. These effects could logically be anticipated, as skeletal muscle does not contain 5a-reductase but does produce aromatase, suggesting that the more androgenic DHT is not the preferred anabolic androgen, rather testosterone appears to be so. Also, the encoded production of estradiol in muscle suggests that aromatizable AAS provide supplementary stimuli, promoting growth that would not be generated by 5a-reduced or poorly aromatizable AAS. In fact, the poorly aromatizable 19-nortestosterone (Deca) provides lesser mass and strength gains than testosterone despite having a much higher anabolic:androgenic ratio.
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Research and Review 
