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Oxandrolone is a synthetic testosterone derivative administered orally. Due to the removal of the methyl group from the C-19 position, it has anabolic effects that are stronger than androgenic effects. Oxandrolone has anabolic potential that is between three and thirteen times more than that of testosterone and methyltestosterone. Oxandrolone is helpful for increasing weight gain after burns or trauma as well as in some disease states including COPD and AIDS when combined with enough calories. The increase in weight is mostly the result of elevated lean body mass as opposed to increased body fat, which is frequently seen with nutritional supplements. When a medicine is stopped, the positive effects on lean body mass are lost. In order to counteract the protein catabolism brought on by extended corticosteroid treatment, oxandrolone is employed. Supportive data also exist for the treatment of patients with Duchenne’s muscular dystrophy, constitutional delay of growth and puberty, HIV wasting syndrome and associated muscle weakness, and short stature associated with Turner’s syndrome. Conflicting evidence exists as to whether or not anabolic steroids significantly increase athletic performance by increasing muscle strength, but the NCAA and IOC currently prohibit their use by athletes. Oxandrolone is not ergogenic at labeled doses but athletes often use higher doses; athletic use should be discouraged due to the risk for dyslipidemia, potential hepatotoxicity, and other serious side effects. Oxandrolone was approved by the FDA in July 1964 and became a controlled substance in 1991.
Through a direct stimulant impact on testosterone or dihydrotestosterone receptors, enhanced androgen receptor expression in skeletal muscle, and intracellular amino acid reutilization, oxandrolone stimulates skeletal muscle protein synthesis. The same intracellular receptors that testosterone and dihydrotestosterone bind to are found in the reproductive system, bone, skeletal muscle, brain, liver, kidney, and adipocytes. Gene expression is regulated by receptor binding.
Oxandrolone works directly as an androgen, as it cannot be aromatized to estrogen. In addition to myotrophic effects from androgen receptor interaction in skeletal muscle, it appears that testosterone and oxandrolone have myotrophic effects caused by decreased protein catabolism through interaction with glucocorticoid receptors. It is hypothesized that anabolic-androgenic steroids displace glucocorticoids bound to the glucocorticoid receptor. Another hypothesis is that anabolic-androgenic steroids interfere with the glucocorticoid response element (DNA binding region). Improvement in lean body mass is a result of the drug’s myotrophic effect. Unlike growth hormone, which causes irreversible hyperplasia, anabolic steroids cause hypertrophy, a reversible event.
In addition to protein synthesis in muscle, increases in serum albumin, prealbumin, and transferrin concentrations have been noted with oxandrolone. Increased erythrocyte production is apparently due to enhanced production of erythropoietic stimulating factors.
Oxandrolone also causes osteolytic bone resorption stimulation, osteoblast proliferation, bone matrix protein production, and synthesis of growth factors and cytokines, which are mediated by androgen receptors on osteoblasts. These effects on bone are responsible for the growth-promoting effects of oxandrolone.
Oxandrolone causes suppression of pituitary gonadotrophins through negative feedback. Thus, endogenous testosterone p
