Anabolic steroid-induced hypogonadism (ASIH) is the functional incompetence of the testes with subnormal or impaired production of testosterone and/or spermatozoa due to administration of androgens or anabolic steroids.
Common complaints include depressive mood alterations, fatigue, lethargy, insomnia, and decreased libido. Also, common signs consistent with androgenic-anabolic steroids (AAS) use may be observed, such as acne, gynecomastia (enlarged male breast), testicular atrophy, skin striations, and alopecia (partial or complete absence of hair) should be noted if present. Spermatogenesis (sperm production) may also be impaired by ASIH, which, depending on the degree of severity, may result in partial or complete infertility.
Androgenic-anabolic steroids - i.e., the natural hormone testosterone and its synthetic relatives - are substances with both androgenic (responsible for developing and maintaining male characteristics) and anabolic (responsible for stimulating muscle hypertrophy) properties (Pic. 1).
According to the US Food and Drug Administration (FDA), “testosterone is a FDA-approved replacement therapy only for men with testicle, pituitary gland, or brain disorders that cause hypogonadism”. Therefore, the use of testosterone in the absence of these clinical conditions must be considered a misuse of AAS.
Use of AAS results in hypogonadotropic hypogonadism (gonadal failure due to abnormal pituitary gonadotropin levels) by feedback suppression of the hypothalamic-pituitary-gonadal (HPG) axis (control system that refers to the hypothalamus, pituitary gland, and gonadal glands) via impaired secretion of gonadotropins, including follicle stimulating hormone (FSH) and luteinizing hormone (LH), by the pituitary gland in the brain, and in turn decreased gonadotropin levels and a resultant lack of sex steroid production.
Initial diagnosis typically consists of a hormonal panel, complete blood cell count, lipid profile, prostate-specific antigen, and a comprehensive metabolic profile.
Treatment of ASIH depends on the type (testosterone, dihydrotestosterone, nandrolon) and duration of AAS use. Management of ASIH includes judicious use of testosterone replacement therapy, human chorionic gonadotropin (hCG), and selective estrogen receptor modulators (clomiphene, Tamoxifen).
Hypogonadism occurs when patient’s sex glands produce little or no sex hormones. Testosterone treatment is unequivocally needed in classical hypogonadism for releaving symptoms. These symptoms include decreased libido, erectile dysfunction, decreased vitality, decreased muscle mass, increased adiposity, depressed mood, osteopenia, and osteoporosis. In classical hypogonadism, testosterone production is usually clearly below the lower limit of normal and patients are highly symptomatic; the various symptoms are easily related to the deficiencies in various bodily systems where testosterone action is important.
Effect on organs
The use of AAS has well known adverse effects, namely to the cardiovascular system, endocrine system, and liver.
Behavioural and psychiatric effects
Regarding behavioural and psychiatric effects, AAS users are at greater risk than non-users to suffer from manic symptoms, such as irritability, aggressive behaviour, euphoria, delusions of grandeur, insomnia, hyperactivity, and reckless attitudes.
AAS also play a central role in muscle dysmorphia (an obsessive concern about the body, including a false belief that one’s own body is insufficiently muscular) and the pathological manipulation of body image. AAS use is a risk factor for substance use disorder (SUD), and possibly the other way round is also true. Most AAS users never report its use or seek help to stop using it. Mental health professionals tend to be less familiar with AAS than they are with other substances of abuse.
Stopping the use of large doses of anabolic steroids in the long term can lead to the development of withdrawal symptoms. They include: mood disorders (suicidal depression), insomnia, anorexia, decreased libido, fatigue, headache, muscle and joint pain and the desire to take more steroids. Drugs that are targeted to relieve these symptoms include antidepressants, non-steroidal anti-inflammatory and clonidine.
Immediate cessation of the use of AAS should be encouraged if complications occur.
Exogenous administration of testosterone synthesis derivatives induces negative feedback on the hypothalamic-pituitary axis and therefore inhibiting the secretion of both FSH and LH. Thus, if there is decreased production of FSH/LH, the testes do not perform their normal fertility function with the production of sperm in men alongside their role in producing the sex hormones.
Infertility after AAS abuse commonly presents as oligozoospermia (low sperm concentration) or azoospermia (absence of sperm in ejaculate), associated with abnormalities in sperm motility and morphology.
Depending upon the sperm count, the chance of conception can be lower than at a healthy man. The smaller sperm count is, the chance to conceive decreases. However, chances are very good if a female partner is fertile.
Erectile dysfunction and libido loss may also occur, especially after discontinuation, when endogenous testosterone levels are usually low.
Simply stopping the use of ASA may lead to the resumption of fertility in a certain proportion of male users. According to most reports, the quality of sperm tends to normalize spontaneously within 4–12 months after cessation of anabolic steroid abuse.
Patients may be treated by induction of spermatogenesis with gonadotropins or gonadoliberin analogues, including hCG intramuscular injections, human menopausal gonadotropin (hMG) or even recombinant FSH. The restoration of fertility has been reported, even in situations of persistent azoospermia (no sperm in semen) up to 5 years after the AAS stop.
Several different regimens are described including testosterone replacement therapy (TRT), Selective Estrogen Receptor Modulator (SERM) such as clomiphene citrate and tamoxifen. For resistant cases, injections of hCG can be used in association with SERM treatment.