Human understanding of anabolic steroids began when Arnold Adolph Berthold (1849) demonstrated loss of male characteristics in testes-deprived cockerels. Experiments carried out in castrated dogs and later in humans demonstrated the anabolic effects of testosterone (Kochakian, 1936). Testosterone became the first ever synthetic anabolic steroid when created from cholesterol and from which all the steroids used currently are derived.
Anabolic steroids exert their anabolic effects on muscle and bone, and their androgenic effects on hair follicles in the skin, the liver and kidneys, and the haematopoietic, immune and central nervous systems (Mooradian et al.
, 1987). Thus their ergogenic properties promote human secondary sexual characteristics, such as muscular growth and physical strength (Evans, 2004). Steroids are relatively small molecules and they can passively diffuse into cells.
In target tissues, that is, the cells that contain steroid receptors, the hormone binds to the receptor ligand-binding domain, causing the receptor to change from an inactive to active state. In target tissues where intracellular enzymes are present, the action of testosterone is mediated by metabolism.
Testosterone is irreversibly converted by the enzyme 5a-reductase to 5a-dihydrotestosterone (DHT), which binds with greater affinity to the androgen receptor, or by aromatase to oestradiol, which binds to the oestrogen receptor (Shahidi, 2001).
Testosterone and DHT can be also converted to weaker androgens, again being dependent on whether the target tissue has the necessary enzyme activity, e. g. , 3a-hydroxysteroid dehydrogenase, 17ß-hydroxysteroid dehydrogenase. With structural modifications to testosterone, the anabolic effects of androgens can be enhanced but, even so, these cannot be divorced entirely from their androgenic effects. Hence, a more accurate term for anabolic steroids is anabolic–androgenic steroids [AAS] (Kuhn, 2002).
The widespread use of anabolic steroids started during World War II, when it was found that this artificial form of testosterone could be used to help malnourished soldiers gain weight and improve performance. After the war, athletes began to use steroids to enhance their performance in competitions. In the 1956 Olympics, Soviet athletes, especially wrestlers, performed at exceptionally high levels. After learning that those athletes were using testosterone, Dr. Zeigler, an American physician created a more selective form, of what we know as anabolic steroids.
From that point until the early 1970’s, steroids became increasingly popular among not just Olympic athletes, but also professional sports players and high school athletes. In 1975, the International Olympic Committee finally banned the use of steroids in Olympic competition. Although anabolic steroids are controlled substances in several countries, their use for cosmetic purposes such as development of bulging muscles and a well-toned figure is not uncommon since, it is considered a harmless manipulation.
Use of these AAS involves several risks that could cause problems in both the short and long term. Prolonged use of anabolic steroids increases one’s risk of sudden death due to serious conditions like ventricular hypertrophy, thrombo-embolism and cerebro-vascular disorders. However, the cardiovascular consequences of supra- physiological androgen levels had not been determined fully until now. A research study revealed that AAS caused the impairment of vascular reactivity.
It also revealed that abstention from AAS consumption, significantly improves vascular functions (Lane et al, 2006). Anabolic steroid use may also cause muscle and tendon tears, acne, liver cirrhosis, abnormal increase in cholesterol levels, and bipolar and aggressive behavior. Females undergo a deepening of the voice, increased hair loss, facial hair growth and depletion of female hormones, like estrogen and progesterone.
The most common problems for male users are reduced testosterone production, resulting in the shrinking of their testicles; erectile dysfunction, reduced sperm production and reduced sperm count. In teenagers, the continued use of AAS stops bone development (Kicman, 2008). Conversely, AAS also corrects physical problems and are employed in treatment of cachexia associated with chronic disease states, to increase testosterone levels and their effects in males whose levels are below ‘normal’ (Lew, 2007).
Only relatively recently that these agents are being revisited for clinical purposes and their efficacy still needs to be demonstrated in terms of improved physical function and quality of life. For clinical purposes, the administration of these drugs can be of therapeutic benefit and reasonably safe, with the physician making objective decisions based on the benefit/risk ratio in relation to a patient’s condition.
Hence it is important not to overstate the medical risks associated with anabolic steroid use (Hoffman and Ratamess, 2006) but to emphasize that the hazards to health are dependent on the sex, the dose, the duration of administration, whether hepatoxic 17a-alkylated steroids are being administered and the susceptibility of the individuals themselves to androgen exposure which is probably dependent on genetic factors, age and lifestyle.
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