Anabolic-androgenic steroids (AAS) can lead to testicular atrophy (shrinkage). Testosterone is synthesized and secreted by Leydig cells in the testes. Its release is regulated by the hypothalamic-pituitary-testicular axis (HPTA), a system highly sensitive to sex steroids. When anabolic steroids are administered, the HPTA recognizes the elevated hormone levels and responds by reducing testosterone synthesis. If the testes do not receive adequate stimulation over time, they atrophy, which may involve a reduction in testicular volume and size. This atrophy may not be noticeable to some individuals. In some cases, the testes may appear normal even with reduced function, while in other cases, the shrinkage is evident. Visible testicular atrophy is one of the most common side effects of steroid abuse, affecting over 50% of anabolic-androgenic steroid users.
Although testicular atrophy is common, it is also considered a reversible side effect. The gonads vary in size under the influence of hormones. Atrophy does not cause permanent damage. However, it may remain a persistent issue. After discontinuing steroids, it may take several weeks or months of luteinizing hormone (LH) stimulation to restore the original testicular volume. Testicular atrophy is often the underlying cause of delayed post-cycle hypogonadism. In extreme cases, full recovery may take over 12 months and may require medical intervention. Post-cycle therapy (PCT) using human chorionic gonadotropin (HCG), which mimics LH activity, can minimize this recovery period. Regular use of HCG during steroid administration is also effective in maintaining testicular mass. However, HCG must be used cautiously, as excessive use can desensitize the testes to LH, complicating HPTA recovery.
Some of the more potent anabolic-androgenic steroids, including testosterone, nandrolone, trenbolone, and oxymetholone, appear to suppress testosterone release more significantly than many other AAS drugs. This could be due to the inherent estrogenic or progestational activity of these steroids, as both estrogens and progestogens provide negative feedback inhibition of testosterone release. However, it is important to note that all anabolic-androgenic steroids can suppress testosterone secretion. This includes anabolic compounds such as stanozolol and oxandrolone, which are generally considered milder in this regard. While these compounds may be less suppressive of testosterone synthesis under some therapeutic conditions, significant atrophy and suppression are common when taken in supratherapeutic doses for physique or performance enhancement, with the distinction being less pronounced.
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