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Anabolic-androgenic steroid use has emerged as a significant public health concern due to the expansion of use beyond professional athletes to broader populations. Anabolic-androgenic steroids encompass natural androgens, such as testosterone, as well as synthetic derivatives designed to replicate the effects of endogenous male hormones. Etiologically, anabolic-androgenic steroid misuse is driven by motivations that include enhancement of athletic performance, increased endurance, and augmentation of muscle mass with minimal fat accumulation. Risk factors for misuse include male sex, younger age, body image concerns, and participation in strength- or appearance-focused sports. At the cellular level, anabolic-androgenic steroids act via androgen receptors to promote protein synthesis and muscle hypertrophy, while dysregulating the hypothalamic-pituitary-gonadal axis and affecting cardiovascular, hepatic, and neuroendocrine systems. Clinically, individuals may present with mood disturbances, aggression, gynecomastia, acne, and altered libido. Diagnosis relies on patient history, physical examination, and, in some cases, detection of exogenous androgens in the laboratory. Management emphasizes cessation, psychological support, and monitoring for medical complications such as cardiomyopathy, hepatic dysfunction, and infertility. Prognosis varies, with early identification and intervention improving outcomes, whereas prolonged use increases the risk of persistent adverse effects. This activity for healthcare professionals is designed to enhance the learner's competence when evaluating and managing anabolic-androgenic steroid use disorder. Participants advance their mastery of the condition's etiology, risk factors, pathophysiology, clinical presentation, and evidence-based diagnostic and therapeutic approaches. Improved skills equip clinicians to collaborate with interprofessional teams caring for affected individuals. Objectives: Screen at-risk individuals for anabolic-androgenic steroid use disorder based on established diagnostic criteria, noting history, physical signs, and laboratory findings. Apply evidence-based interventions for anabolic-androgenic steroid use disorder, encompassing cessation strategies, hormonal restoration, and management of withdrawal symptoms and psychiatric comorbidities.

Screen at-risk individuals for anabolic-androgenic steroid use disorder based on established diagnostic criteria, noting history, physical signs, and laboratory findings. Apply evidence-based interventions for anabolic-androgenic steroid use disorder, encompassing cessation strategies, hormonal restoration, and management of withdrawal symptoms and psychiatric comorbidities. Improve awareness of the long-term health effects and support resources for patients and families affected by anabolic-androgenic steroid use disorder. Collaborate with the interprofessional healthcare team to improve detection, counseling, treatment adherence, and long-term outcomes for individuals affected by anabolic-androgenic steroid use disorder. Access free multiple choice questions on this topic.

The term anabolic describes metabolic processes that consume energy to promote tissue growth and constructive metabolism. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision, does not provide a standalone diagnosis for anabolic steroid use. Clinically, problematic anabolic-androgenic steroid (AAS) use is coded under Other (or Unknown) Substance Use Disorder, with specification of AAS. AASs constitute a heterogeneous group of steroidal compounds derived from or structurally related to testosterone, including endogenous hormones and synthetic analogs designed to enhance anabolic and androgenic effects. Although these agents have well-established therapeutic roles in specific medical conditions, their nonmedical use has expanded substantially beyond elite athletic settings, representing a significant and evolving public health concern.[1][2] Epidemiologic evidence from the past decade indicates that AAS exposure is no longer restricted to competitive sports. Contemporary meta-analyses and population-based studies estimate the global lifetime prevalence of AAS use at approximately 1% to 5%, with higher prevalence among males, especially in regions characterized by strong gym-based fitness cultures.[3] A notable proportion of individuals report initiation for aesthetic or lifestyle-related reasons rather than athletic competition, highlighting a shift in the demographic profile of AAS misuse.[4] Regulatory responses to AAS misuse reflect the recognized abuse potential of these agents and associated medical risks. In the United States, testosterone and many synthetic derivatives are classified as Schedule III controlled substances under the Controlled Substances Act, with comparable regulatory approaches adopted in multiple countries. Despite these measures, widespread availability persists through informal distribution networks, online marketplaces, and loosely regulated clinical environments, compromising effective surveillance and increasing the risk of unsupervised exposure.[5]

Regulatory responses to AAS misuse reflect the recognized abuse potential of these agents and associated medical risks. In the United States, testosterone and many synthetic derivatives are classified as Schedule III controlled substances under the Controlled Substances Act, with comparable regulatory approaches adopted in multiple countries. Despite these measures, widespread availability persists through informal distribution networks, online marketplaces, and loosely regulated clinical environments, compromising effective surveillance and increasing the risk of unsupervised exposure.[5] From a clinical perspective, androgens are essential for the development and maintenance of male secondary sexual characteristics and are prescribed for evidence-based indications, including hypogonadism, delayed puberty in adolescent boys, and select catabolic conditions. In women, therapeutic use occurs in limited contexts, such as certain malignancies and severe muscle-wasting disorders. Nonmedical AAS use typically involves supraphysiologic dosing intended to enhance lean muscle mass, physical performance, or body image, frequently without medical oversight.[6][7] This distinction is critical, as dosing regimens and pharmacologic exposures associated with misuse differ fundamentally from those employed in standard testosterone replacement therapy. In recent years, AAS exposure pathways have diversified to include treatment at anti-aging clinics, unsupervised testosterone supplementation, and internet promotion of novel androgenic compounds and peptide-steroid combinations marketed as wellness or rejuvenation therapies. These developments complicate clinical recognition, as many individuals do not self-identify as engaging in substance misuse and may present with delayed, organ-specific complications rather than overt features of steroid abuse. Sociocultural factors, such as body image dissatisfaction, aging-related performance anxiety, and digital fitness media influence, have contributed to the normalization of androgen use among nonathletic populations.[8]

In recent years, AAS exposure pathways have diversified to include treatment at anti-aging clinics, unsupervised testosterone supplementation, and internet promotion of novel androgenic compounds and peptide-steroid combinations marketed as wellness or rejuvenation therapies. These developments complicate clinical recognition, as many individuals do not self-identify as engaging in substance misuse and may present with delayed, organ-specific complications rather than overt features of steroid abuse. Sociocultural factors, such as body image dissatisfaction, aging-related performance anxiety, and digital fitness media influence, have contributed to the normalization of androgen use among nonathletic populations.[8] Contemporary AAS misuse demonstrates pharmacologic heterogeneity, including cyclic administration, concurrent use of multiple agents (stacking), and prolonged exposure to supraphysiologic doses. Evidence increasingly links these practices to persistent cardiometabolic, endocrine, and neuropsychiatric sequelae, some persisting long after cessation.[9] These observations support recognition of AAS misuse as a dependence-like syndrome characterized by tolerance, withdrawal, and continued use despite harm.[10] Withdrawal manifestations include fatigue, depressed mood, anhedonia, insomnia, libido changes, severe depression, and suicidality.[11][12]

The etiology of AAS use disorder is multifactorial, arising from interactions among sociocultural, occupational, psychological, and neurobiological influences. Population-based estimates indicate that several million individuals in the US have been exposed to AASs for nonmedical purposes, most frequently to increase muscle mass, enhance physical appearance, or improve perceived strength and performance rather than gain a competitive athletic advantage alone. This widespread exposure highlights the shift of AAS use from elite sports into broader community and occupational settings. Certain occupational groups demonstrate elevated rates of AAS misuse, particularly individuals in roles emphasizing physical dominance, intimidation, or endurance. Fighters, bodybuilders, nightclub security personnel, and bouncers constitute higher-risk populations in whom AAS use may be reinforced by workplace expectations and peer norms regarding muscularity and strength.[13] Slang terminology such as steroids, roids, gear, or juice reflects the normalization of AAS use within these environments and contributes to the underestimation of associated risks. Psychological vulnerability contributes significantly to the initiation and maintenance of AAS misuse. Muscle dysmorphia, a body image disorder defined by a persistent perception of insufficient muscularity despite objectively adequate muscle mass, demonstrates strong associations with AAS initiation and progression to problematic use. Individuals with muscle dysmorphia often engage in compulsive resistance training, strict dietary control, and persistent preoccupation with body appearance, with increased AAS use serving as a maladaptive strategy to achieve perceived physical adequacy and reinforce identity.[14] Longitudinal evidence suggests that muscle dysmorphia frequently precedes AAS exposure and predicts escalation to higher doses and prolonged use.[15]

Psychological vulnerability contributes significantly to the initiation and maintenance of AAS misuse. Muscle dysmorphia, a body image disorder defined by a persistent perception of insufficient muscularity despite objectively adequate muscle mass, demonstrates strong associations with AAS initiation and progression to problematic use. Individuals with muscle dysmorphia often engage in compulsive resistance training, strict dietary control, and persistent preoccupation with body appearance, with increased AAS use serving as a maladaptive strategy to achieve perceived physical adequacy and reinforce identity.[14] Longitudinal evidence suggests that muscle dysmorphia frequently precedes AAS exposure and predicts escalation to higher doses and prolonged use.[15] Behavioral and neuropsychological mechanisms further influence etiology. Reinforcement learning processes, such as rapid gains in muscle mass, social validation, and improved self-esteem, may promote continued use despite awareness of health risks. Over time, tolerance, withdrawal symptoms, and affective disturbances reinforce dependence-like patterns, blurring the boundary between appearance-driven use and substance use disorder. Peer modeling within gym-based subcultures and online fitness communities amplifies the risk of initiation, particularly when adverse effects are minimized or reframed as manageable. The contemporary digital environment has substantially modified etiologic pathways. Unregulated online markets, social media influencers, and direct-to-consumer hormone vendors lower barriers to access while circumventing traditional medical oversight. These platforms frequently promote AASs and related compounds as lifestyle enhancers or anti-aging interventions, facilitating initiation among younger individuals and nonathletic populations.[16]

The epidemiology of AAS misuse has evolved substantially over the past 2 decades, with evidence indicating a steady increase in prevalence and diversification of populations exposed to AAS. Large-scale meta-analytic data identify male sex and participation in strength-oriented physical activity as the strongest demographic predictors of AAS exposure. Pooled prevalence estimates suggest that lifetime AAS use approaches 6% to 7% among males, compared to approximately 1% to 2% among females; however, these figures likely underestimate true exposure due to underreporting and inconsistent surveillance methodologies. Competitive athletics historically represented the primary context for AAS misuse. However, contemporary epidemiologic studies demonstrate a marked shift toward recreational gym users and noncompetitive bodybuilders. Population-based analyses indicate that most individuals who misuse AAS do so for appearance-related or personal fitness goals rather than organized sport performance.[17] This transition broadens the at-risk population and diminishes the effectiveness of sport-centered monitoring systems traditionally used to detect steroid misuse. Age-specific patterns further highlight changing epidemiology. AAS misuse is most frequently reported among young adult men in their 20s and 30s. However, initiation increasingly occurs during late adolescence. Cohort and survey studies involving secondary school– and university-aged populations confirm that AAS exposure persists among adolescents, often associated with body image dissatisfaction, supplement misuse, and concurrent substance use behaviors.[18][19][20] These observations indicate shared epidemiologic pathways between AAS misuse and other forms of substance use rather than isolated experimentation. Geographic and healthcare-related factors also influence prevalence estimates. European studies of fitness-center populations report high rates of access to AAS through informal or semimedical channels, including nonspecialist healthcare providers and anti-aging clinics, blurring distinctions between prescribed and nonmedical use. Globally, growing reliance on internet-based distribution further complicates epidemiologic assessment by circumventing conventional medical and regulatory controls.[21]

Geographic and healthcare-related factors also influence prevalence estimates. European studies of fitness-center populations report high rates of access to AAS through informal or semimedical channels, including nonspecialist healthcare providers and anti-aging clinics, blurring distinctions between prescribed and nonmedical use. Globally, growing reliance on internet-based distribution further complicates epidemiologic assessment by circumventing conventional medical and regulatory controls.[21] Routes of administration remain relatively consistent across regions, with injection representing the predominant method of use. Observational studies continue to document unsafe injection practices among a subset of patients with AAS exposure, including needle reuse and shared equipment, raising the risk of blood-borne infections and exacerbating the public health burden associated with AAS misuse.[22][23] Collectively, these epidemiologic trends emphasize the expanding scope of anabolic steroid exposure and underscore the need for enhanced detection strategies within primary care, sports medicine, and mental health settings.

A substantial subset of individuals chronically exposed to AAS develop dependence-like patterns, characterized by continued use despite harm.[24] According to a model of AAS dependence, stage 1—termed the myoactive phase—involves high-dose AAS use combined with dietary control and rigorous weight training. Stage 2 is defined by chronic, high-level AAS use, resulting in reward pathway sensitization and promoting abuse and dependence.[25] Hypogonadism is a hallmark of AAS abuse and can produce profound effects on the reproductive system. Most individuals with longstanding AAS exposure exhibit low gonadotropin and testosterone levels even after discontinuation of AAS.[26] Administration of exogenous AAS suppresses the hypothalamic-pituitary-gonadal axis, reducing endogenous testosterone production and impairing testicular function in men, including decreased testicular volume and sperm output. In a retrospective study, 21% of 382 men with hypogonadism receiving testosterone treatment reported prior use of exogenous androgens. In men with a history of androgen use, sperm counts typically recover within approximately 4 months to 1 year after discontinuation, with older men requiring longer recovery periods than younger men. Androgen intake may result in low sperm count, small testes, elevated hemoglobin and hematocrit, suppressed or nondetectable serum luteinizing hormone, and reduced sex hormone–binding globulin. These laboratory and clinical findings should raise suspicion for exogenous androgen use, particularly among men participating in competitive sports. Cardiovascular risks associated with AAS abuse include myocardial dysfunction, coronary atherosclerosis, hypercoagulopathy, hepatic dysfunction, hypertension, life-threatening arrhythmias, and sudden death.[27][28][27] Concentric left ventricular hypertrophy is frequently observed in individuals with prolonged exposure to AAS, even after discontinuation of the inciting agent.[29] Long-term AAS use also elevates low-density lipoprotein and reduces high-density lipoprotein, increasing the risk of cardiac events. AAS misuse is associated with psychiatric and behavioral disturbances.[30] An observational study by Christoffersen et al reported increased aggression, violent behaviors, and a 9-fold higher risk of criminal behavior and imprisonment among individuals with AAS abuse.[31]

Cardiovascular risks associated with AAS abuse include myocardial dysfunction, coronary atherosclerosis, hypercoagulopathy, hepatic dysfunction, hypertension, life-threatening arrhythmias, and sudden death.[27][28][27] Concentric left ventricular hypertrophy is frequently observed in individuals with prolonged exposure to AAS, even after discontinuation of the inciting agent.[29] Long-term AAS use also elevates low-density lipoprotein and reduces high-density lipoprotein, increasing the risk of cardiac events. AAS misuse is associated with psychiatric and behavioral disturbances.[30] An observational study by Christoffersen et al reported increased aggression, violent behaviors, and a 9-fold higher risk of criminal behavior and imprisonment among individuals with AAS abuse.[31] Long-term complications of AAS use in females include hirsutism, acne, temporal male-pattern hair recession, voice deepening, and clitoromegaly.[32] Some women develop oligomenorrhea or amenorrhea, as well as breast atrophy, reflecting disruption of normal reproductive hormone balance. Supraphysiologic AAS exposure alters central neurotransmitter systems involved in reward processing, impulse control, and affect regulation. Experimental and clinical studies demonstrate dysregulation of dopaminergic and serotonergic signaling, accompanied by structural and functional changes in the limbic and prefrontal cortical regions. These neurobiological alterations may account for persistent compulsive use, impaired judgment, and mood instability observed in patients with prolonged AAS exposure. AAS-induced oxidative stress, endothelial dysfunction, and myocardial fibrosis appear to act synergistically, contributing to long-term cardiovascular remodeling independent of traditional risk factors. Emerging evidence indicates that these neurocardiovascular changes may be only partially reversible after cessation, particularly following prolonged or high-dose exposure.[33][34]

Diagnosis of AAS abuse requires a detailed history and a thorough physical examination. Clinical suspicion should arise in children or adolescents exhibiting premature onset of secondary sexual characteristics, decreased height, or premature closure of epiphyses. In female patients, indicators include temporal hair recession, hirsutism, acne, irregular menses, breast atrophy, irreversible deepening of the voice, clitoromegaly, decreased total body fat, and increased muscle mass. In male patients, signs suggestive of AAS misuse include rapid increases in muscle mass and strength, gynecomastia, small testes, low sperm count, impotence, and acne. Recognition of these characteristic features facilitates early identification and supports further evaluation and intervention.

Exogenous androgen use should be suspected in individuals participating in competitive sports or activities who exhibit behavioral changes such as aggression, depression, or irritability, or laboratory abnormalities, including suppressed luteinizing hormone concentration, elevated hematocrit, and reduced sex hormone–binding globulin.[35] Gynecomastia in male patients and hirsutism in female patients warrant further investigation to exclude AAS misuse.

No formal, dedicated clinical practice guideline from the Endocrine Society currently exists for the management of AAS misuse. Existing recommendations are primarily derived from expert reviews, consensus statements, and emerging clinical frameworks. Current evidence indicates that the most effective treatment of AAS misuse involves discontinuation of androgen use, management of withdrawal symptoms, behavioral therapy, and symptomatic interventions. Therapeutic decisions depend on the duration of use, risk of withdrawal, patient-specific treatment goals, and risk-benefit considerations. In 2019, Anawalt outlines 4 management strategies for chronic AAS exposure—cessation without medical therapy; cessation with initiation of clomiphene therapy; cessation with initiation of human chorionic gonadotropin therapy; and conversion of nonprescription AAS to prescription testosterone. In individuals with less than 1 year of AAS use, testosterone levels typically return to baseline within 6 months of discontinuation. Patients with chronic AAS exposure frequently exhibit prolonged hypogonadism and persistently low testosterone levels.[36] Restoration of hormonal balance is essential to prevent long-term hypogonadism. Androgen use in athletes must be discontinued immediately, despite the expectation of withdrawal symptoms. Initiation of testosterone replacement therapy for hypogonadism requires prior therapeutic use exemptions from the appropriate regulatory agencies. Clomiphene or human chorionic gonadotropin therapy may be indicated in men with chronic high-dose AAS use.[37] Concurrent management of behavioral and mental health comorbidities is necessary.[38] Anxiety and depression should be addressed with antidepressants and cognitive-behavioral therapy. Patients with conduct disorder or other substance use disorders require targeted behavioral interventions and appropriate referrals.[39] Fertility concerns must be addressed promptly.[40] Withdrawal symptoms require careful monitoring and active management to reduce complications and support recovery.

Investigation of AAS misuse is warranted in middle-aged and young men presenting with gynecomastia, hirsutism, coronary artery disease, or left ventricular dysfunction.[41] Assessment should also include screening for comorbid mental health disorders and other substance use disorders.

Abrupt discontinuation of AAS in individuals with dependence potential induces withdrawal symptoms, including anxiety and depression. Additional manifestations include fatigue, sleep disturbances, decreased appetite, reduced libido, and steroid cravings. Severe depressive symptoms constitute a significant withdrawal risk and may result in suicidal ideation or suicide attempts. Observational studies indicate that individuals misusing AAS may concurrently use other illicit substances to mitigate withdrawal-related effects such as depression, anxiety, irritability, and insomnia.[45][46][47]

AAS misuse is associated with a broad spectrum of systemic complications affecting cardiovascular, endocrine, hepatic, musculoskeletal, neuropsychiatric, and behavioral domains. Many adverse effects are dose-dependent and may persist or progress even after discontinuation, particularly following prolonged exposure to supraphysiologic androgen levels. Collectively, these findings underscore that AAS misuse represents a multisystem disorder with potentially irreversible health, psychological, and social consequences. Cardiovascular Sequelae Cardiovascular toxicity constitutes one of the most serious and well-documented consequences of chronic AAS misuse. Observational and imaging studies consistently demonstrate associations with left ventricular hypertrophy, impaired systolic and diastolic function, endothelial dysfunction, hypertension, and accelerated atherosclerosis.[48] Dyslipidemia, characterized by reductions in high-density lipoprotein cholesterol and elevations in low-density lipoprotein cholesterol, is a common biochemical abnormality and contributes to long-term cardiovascular risk. Emerging evidence suggests that these alterations may not be fully reversible, even after cessation of steroid use. Endocrine and Reproductive Complications Exogenous androgen administration suppresses the hypothalamic-pituitary-gonadal axis, frequently resulting in secondary hypogonadism upon discontinuation. Clinical manifestations include decreased libido, erectile dysfunction, infertility, testicular atrophy, and mood disturbances.[49] Recovery of endogenous testosterone production may be delayed or incomplete, requiring medical intervention. In female individuals, AAS misuse can cause virilization, menstrual irregularities, clitoromegaly, and voice deepening, some of which may be irreversible. Neuropsychiatric and Behavioral Effects

Exogenous androgen administration suppresses the hypothalamic-pituitary-gonadal axis, frequently resulting in secondary hypogonadism upon discontinuation. Clinical manifestations include decreased libido, erectile dysfunction, infertility, testicular atrophy, and mood disturbances.[49] Recovery of endogenous testosterone production may be delayed or incomplete, requiring medical intervention. In female individuals, AAS misuse can cause virilization, menstrual irregularities, clitoromegaly, and voice deepening, some of which may be irreversible. Neuropsychiatric and Behavioral Effects Neuropsychiatric complications constitute central features of AAS misuse. Manifestations include mood instability, irritability, aggression, impulsivity, anxiety, depressive symptoms, and, in severe cases, psychotic manifestations. Epidemiologic and clinical studies demonstrate associations between nonmedical AAS use and increased engagement in high-risk behaviors, including substance misuse, unsafe sexual practices, and violent or criminal activity.[50] These behavioral effects appear to result from androgen-related modulation of central neurotransmitter systems and may be amplified during withdrawal.[51] Substance Use and Risk-Taking Behaviors AAS misuse frequently co-occurs with other substance use behaviors. Population-based studies in adolescents and young adults demonstrate strong correlations between AAS exposure and alcohol misuse, tobacco use, stimulant use, and illicit drug consumption, suggesting shared vulnerability pathways rather than isolated steroid use.[52] Injectable administration further introduces risks from unsafe injection practices, including needle reuse and sharing, which increase susceptibility to blood-borne infections such as hepatitis B, hepatitis C, and HIV. Sports and Regulatory Consequences AASs are universally prohibited in competitive sports, both in-competition and out-of-competition. International and national governing bodies, including the World Anti-Doping Agency, the International Olympic Committee, the United States Anti-Doping Agency, and the National Collegiate Athletic Association, classify anabolic steroids as banned substances, with violations carrying professional, legal, and reputational consequences.[53] These sanctions compound the psychosocial burden associated with AAS misuse.

The potential adverse effects of AAS misuse are significant and often chronic. Healthcare providers must recognize individuals at risk for this condition. Ongoing patient education regarding adverse effects is essential for individuals receiving androgens for therapeutic purposes. Early identification of AAS misuse and timely referral for appropriate treatment are strongly indicated.

AAS use disorder represents a growing and underrecognized public health concern with substantial endocrine, cardiovascular, psychiatric, and behavioral consequences. Presentation is often delayed, with nonspecific symptoms or complications such as hypogonadism, cardiomyopathy, mood disturbances, or infertility. Early recognition and comprehensive management are essential to reduce morbidity, prevent relapse, and address coexisting mental health and substance use disorders. Effective management requires a coordinated interprofessional approach. Primary care clinicians, emergency physicians, and sports medicine specialists support early identification through targeted screening, thorough history-taking, and recognition of characteristic physical and laboratory findings. Endocrinologists provide expertise in hormonal assessment, management of hypogonadism, and restoration of the hypothalamic-pituitary-gonadal axis. Psychiatrists and psychologists diagnose and treat comorbid mood disorders, body dysmorphic symptoms, and substance use disorders using evidence-based psychotherapeutic and pharmacologic interventions. Nurses and allied health professionals reinforce patient education, monitor treatment adherence, and provide counseling on harm reduction, injection safety, and management of withdrawal symptoms. Pharmacists ensure medication safety, identify inappropriate androgen use, and provide guidance regarding drug interactions and adverse effects. Referral to addiction specialists, cardiologists, or reproductive health experts may further optimize clinical outcomes. Clear communication, shared decision-making, and coordinated follow-up allow the interprofessional healthcare team to improve early detection and facilitate safe discontinuation strategies. These interventions reduce complications and support long-term recovery in individuals with AAS use disorder.