Introduction

Anabolic-androgenic steroids (AAS) comprise testosterone and a diverse group of synthetic derivatives developed to exploit its anabolic and androgenic properties. Beyond approved indications, these agents are widely used to enhance muscularity, physical performance, perceived well-being, and cosmetic appearance, and now represent one of the most prevalent forms of substance misuse among appearance- and performance-enhancing drugs [1].

The isolation and synthesis of testosterone from cholesterol in 1935 by Butenandt and Ruzicka was a landmark in andrology and reproductive endocrinology and earned them the 1939 Nobel Prize in Chemistry [2]. Subsequent characterization of testosterone’s anabolic and androgenic actions stimulated the development of numerous derivatives from the 1950s onward, aimed at improving oral bioavailability, extending duration of action, and modifying tissue selectivity. These efforts were based on targeted alterations of the testosterone steroid nucleus, generating compounds with distinct pharmacokinetic and pharmacodynamic profiles [3].

Epidemiologic data indicate that nonmedical AAS use is a global public health concern. A meta-analysis of 187 studies estimated a global lifetime prevalence of 3.3%, with higher prevalence in males (6.4%) than females (1.6%), and significantly elevated rates among athletes and recreational gym users compared with the general population [4]. In the United States, Pope et al. combined age-of-onset distributions from nine studies with four national youth surveys to estimate that 2.9–4.0 million Americans aged 13–50 have used AAS, and approximately 1 million have developed AAS dependence [5]. Notably, although initiation is predominantly post-adolescent, ~22% of initiations occur before age 20, representing an estimated 640,000 to 880,000 individuals and highlighting a substantial adolescent and late-teen subgroup that warrants targeted prevention and early detection strategies [5].

AAS abuse has been associated with multi-system toxicity, reflecting the widespread expression of androgen receptors and the impact of sustained supraphysiologic exposure. Reported adverse outcomes encompass reproductive and endocrine dysfunction (hypogonadotropic hypogonadism, infertility), cardiovascular disease, hepatic injury, renal impairment, adverse lipid and metabolic profiles, musculoskeletal and tendon complications, cutaneous manifestations, hematologic alterations, and a spectrum of neuropsychiatric and dependence-related disorders [1, 6,7,8]. These concerns, together with the scale and pattern of use, underscore the need for an evidence-based, clinically oriented appraisal.

Recently, Grant et al. published a narrative review summarizing the multisystem risks and adverse effects of androgen abuse in men [9]. In contrast, the present review is framed more specifically from a sexual-medicine and andrology perspective, with particular emphasis on sexual dysfunction, reproductive sequelae, and the clinical evaluation and management of recovery after cessation. Accordingly, this review aims to [1] summarize and appraise the available literature on the adverse health consequences of nonmedical AAS use in men, with emphasis on sexual and reproductive health, and [2] propose a pragmatic, evidence-informed framework for the evaluation and management of men with a history of AAS use or dependence in clinical practice.

This narrative review was based on a targeted search of the PubMed/MEDLINE and Scopus databases for English-language literature on AAS abuse and its health consequences, with particular emphasis on sexual and reproductive outcomes. Priority was given to recent systematic and narrative reviews, relevant clinical guidelines, and key observational studies addressing cardiovascular, hepatic, hematologic, musculoskeletal, neuropsychiatric, dermatologic, and reproductive sequelae, as well as management after cessation. Reference lists of selected articles were also screened to identify additional relevant publications. The final selection was based on relevance to the clinical scope of this review and the authors’ judgment regarding the importance of individual studies.

Physiology of testosterone and supraphysiologic androgen effects

Under physiological conditions, testosterone secretion is governed by the hypothalamic–pituitary–gonadal (HPG) axis [10]. Pulsatile hypothalamic Gonadotropin-releasing hormone (GnRH) release stimulates pituitary Luteinizing hormone (LH) and Follicle-stimulating hormone (FSH), which in turn drive testicular testosterone production and spermatogenesis. In circulation, testosterone is distributed among three fractions: a small free component, a bioavailable albumin-bound fraction, and a larger Sex Hormone-Binding Globulin (SHBG)-bound fraction, of which only the free and albumin-bound forms are biologically active [11] (Fig. 1). This binding equilibrium buffers fluctuations in androgen levels and governs tissue exposure. Testosterone is further metabolized to dihydrotestosterone (via 5α-reductase) and estradiol (via aromatase), both of which participate in endocrine feedback at the hypothalamus and pituitary to maintain homeostasis [10, 11].

Fig. 1: Testosterone homeostasis.
Fig. 1: Testosterone homeostasis.The alternative text for this image may have been generated using AI.
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Physiologic considerations governing testosterone homeostasis GnRH gonadotropin-releasing hormone, DHT dihydrotestosterone, LH luteinizing hormone, E2 estradiol, SHBG sex hormone-binding globulin.

Supraphysiologic androgen exposure, as occurs with AAS use, profoundly disrupts the HPG axis. Elevated circulating androgens exert strong negative feedback at both the hypothalamus and pituitary, leading to near-complete suppression of GnRH, LH, and FSH secretion even at relatively modest supraphysiologic levels [12]. This results in a marked fall in intratesticular testosterone to levels far below the threshold required to sustain spermatogenesis and rapidly induces secondary hypogonadism. At these concentrations, SHBG-binding sites become partially saturated, increasing the proportion of biologically active free testosterone, which amplifies the suppressive signal to the HPG axis [13]. Enhanced conversion of testosterone to estradiol and dihydrotestosterone further reinforces negative feedback. The combined effect is a sustained shutdown of gonadotropin production, impaired spermatogenesis, and testicular atrophy, forming the central endocrine mechanism underlying AAS-associated reproductive and sexual dysfunction.

Pharmacology of AAS

Following the isolation and synthesis of testosterone, extensive medicinal chemistry efforts produced a broad range of synthetic derivatives with diverse pharmacokinetic and pharmacodynamic profiles. Given the breadth and complexity of these chemical modifications, a comprehensive discussion is beyond the scope of this manuscript; however, the most common structural alterations are summarized in Fig. 2 [1, 3, 14].

Fig. 2: Common aterations to the testosterone molecule.
Fig. 2: Common aterations to the testosterone molecule.The alternative text for this image may have been generated using AI.
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Most common structural modifications to the testosterone molecule: description with resulting effect.

From a functional perspective, AAS are often categorized according to aromatization potential and relative potency [3, 14, 15]. Aromatizable steroids (e.g., testosterone, methandrostenolone) exhibit balanced androgenic and anabolic actions but are associated with estrogen-mediated adverse effects such as gynecomastia and fluid retention [12]. Non-aromatizable steroids (e.g., stanozolol, oxandrolone, trenbolone) produce minimal direct estrogenic effects yet may display pronounced androgenic, metabolic, or hepatic toxicity [16]. “Highly potent” AAS (e.g., trenbolone, oxymetholone, fluoxymesterone) induce profound HPG-axis suppression and carry a high risk of systemic toxicity, whereas “milder” agents (e.g., oxandrolone, methenolone, mesterolone), although often perceived as safer, remain suppressive with chronic or high-dose use and are not devoid of risk [15, 17].

AAS abusers, who are they?

Contemporary evidence indicates that most individuals who use AAS are not elite athletes but recreational strength-training men, motivated primarily by appearance enhancement, muscularity, and perceived well-being, with competitive performance goals playing a secondary role [18,19,20]. In the Anabolic 500 survey of 506 male AAS users (mean age 29 years) and 771 non-users (mean age 25.2 years), Ip et al. [18] reported that approximately 70% of users endorsed recreational or cosmetic motives, and that users frequently engaged in polypharmacy with multiple AAS and other performance- and image-enhancing drugs. Compared with non-users, AAS users were significantly more likely to meet criteria for a substance dependence disorder (23.4% vs 11.2%), report an anxiety disorder (10.1% vs 6.1%), report recent cocaine use (11.3% vs 4.7%), and disclose a history of sexual abuse (6.1% vs 2.7%), highlighting a subgroup characterized by broader psychosocial and psychiatric vulnerability [18].

Data from a large, nationally representative household survey of Swedish men aged 15–64 years further demonstrate that AAS use is not merely a function of gym exposure or opportunity, but rather clusters with a poly–substance-use phenotype and is shaped by socioeconomic and educational factors [19]. Using hierarchical logistic regression in two complementary models, Håkansson et al. [19] first compared lifetime AAS users with all nonusers and found that AAS use was independently associated with lifetime illicit drug use, misuse of prescribed psychoactive medications, intensive physical training, and lower educational level. In a second model restricted to men who had been offered AAS, only illicit drug use and prescription drug misuse remained significant predictors of actual AAS use, indicating that while strength-training environments facilitate exposure and access, co-occurring substance-use behaviors are the key factors distinguishing individuals who progress from opportunity to use.

Patterns of procurement reinforce the normalization of extra-medical use within non-elite, gym-based communities. In a large U.S. web-based survey of 1955 non-medical AAS users, Cohen et al. [21] reported that more than half (52.7%) obtained AAS via the Internet, followed by local sources (16.7%), friends or training partners (15.0%), physicians’ prescriptions (6.6%), and importation from abroad (5.8%), underscoring the central role of online and informal markets in facilitating access.

Similarly, Parkinson and Evans’ survey of 500 users found that nearly 4 out of 5 were non-competitive bodybuilders or non-athletes using AAS mainly for cosmetic reasons, commonly at high cumulative doses and with extensive stacking [20]. The majority self-administered injectable preparations, and approximately 10–13% reported unsafe injection practices (needle reuse, sharing needles or multidose vials), while almost all respondents (99.2%) reported at least one perceived adverse effect, illustrating both the intensity of use and the potential for injection-related and systemic harm [20].

A critical question is whether users experiencing such adverse effects engage with formal healthcare. This was systematically examined by Amaral et al. [22], who conducted a systematic review and meta-analysis of 36 studies including 10,101 AAS users to estimate the prevalence of help-seeking from physicians. The pooled proportion of users who had ever sought medical support related to AAS use was 37.1% (95% CI 29.7–44.5), indicating that only about one in three users had any contact with medical services. Subgroup analyses showed substantial heterogeneity, with higher help-seeking among needle and syringe program clients and in some Australian cohorts (≈54%–67%), and notably lower rates among adolescents (≈17%), recreational gym users, and online-recruited samples, all can be considered as populations most likely to remain hidden from routine clinical care. The authors concluded that this reflects a major treatment and engagement gap driven by stigma, fear of legal or sporting consequences, limited clinician expertise, and reliance on peer and online “underground” guidance, and emphasized the need for accessible, non-judgmental, evidence-based services tailored to AAS users [22].

Together, these data portray AAS users as predominantly male, often socially integrated and gym-focused, commonly engaged in high-dose, polysubstance regimens, with non-trivial burdens of psychiatric comorbidity and parallel substance use. These characteristics are directly relevant to risk stratification, case-finding, and the design of targeted harm-reduction and management strategies.

Adverse effects of AAS abuse

Nonmedical AAS use is associated with multi-system toxicity driven by supraphysiologic dosing, long cumulative exposure, polypharmacy with other performance- and image-enhancing drugs, and the ubiquity of androgen receptors across tissues (Figs. 3 and 4). Evidence is primarily observational (cohort, case–control, imaging, registry, and case series), but convergent data from multiple settings support clinically significant risks across major organ systems.

Fig. 3: Suppression of the HPG axis.
Fig. 3: Suppression of the HPG axis.The alternative text for this image may have been generated using AI.
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Sexual and reproductive adverse effects of AAS abuse: HPG-axis suppression leading to hypogonadism and altered testosterone-to-estradiol balance. T testosterone, E2 estradiol, T/E2 testosterone:estradiol ratio.

Fig. 4: Adverse eff ects of AAS abuse.
Fig. 4: Adverse eff ects of AAS abuse.The alternative text for this image may have been generated using AI.
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Multi-system adverse effects of AAS abuse.

Sexual consequences of anabolic–androgenic steroid abuse

AAS abuse is closely linked to clinically significant sexual dysfunction, particularly decreased libido, erectile dysfunction (ED), and gynecomastia (Fig. 3). These manifestations predominantly arise from suppression and dysregulation of the HPG axis, disruption of the androgen–estrogen balance, and secondary vascular and neuropsychological effects. They often persist beyond cessation of AAS exposure and may represent key clinical entry points for case detection in otherwise healthy-appearing young men.

With respect to libido, during active AAS use, many individuals report an initial, dose-dependent increase in sexual drive. However, chronic supraphysiologic androgen exposure induces potent negative feedback at the hypothalamic and pituitary levels, resulting in markedly reduced endogenous testosterone production. On discontinuation or dose reduction, users frequently transition abruptly from sustained supraphysiologic exposure to a hypogonadal state, which often will affect their sex drive. Corona et al. [23] provide quantitative support for this association: in their meta-analysis of AAS abusers, reduced libido was reported in up to approximately one-third of users (31%), based on pooled data from seven studies. Importantly, longitudinal data indicate that HPG axis recovery may be delayed or incomplete in a subset of men after prolonged or repeated cycles, supporting AAS-induced hypogonadism as a potential cause of persistent loss of libido [24].

ED associated with AAS abuse reflects an interplay between endocrine, vascular, and psychosexual mechanisms. Endocrinologically, post-cycle hypogonadism is central. Testosterone levels falling below the threshold required for normal nitric oxide synthase expression, cavernosal smooth muscle integrity, and libido directly impair erectile physiology [25, 26].

Corona et al. [23] highlight that, across six studies included in their meta-analysis, ED was reported in up to 19% of AAS users, despite heterogeneity in study designs and limited systematic assessment of sexual outcomes.

Chronic AAS exposure may also induce structural and functional vascular alterations relevant to penile hemodynamics, including endothelial dysfunction, atherogenic dyslipidemia, increased hematocrit, and prothrombotic tendency [27, 28]. These changes could theoretically impair penile hemodynamics in susceptible individuals. In parallel, mood disturbances, anxiety, anhedonia, and relationship stress are frequently reported during AAS use and withdrawal and may further compromise erectile function through psychogenic pathways [29].

Gynecomastia is one of the most characteristic endocrine complications of AAS abuse and reflects disruption of the local estrogen-to-androgen balance in male breast tissue. Contemporary reviews and guidelines agree that pathological gynecomastia arises when estrogens are increased, and/or androgens are reduced, at the systemic or intramammary level, tipping the equilibrium toward glandular proliferation [30]. In the context of AAS use, aromatizable androgens such as testosterone esters are converted by aromatase to estradiol and estrone, while exogenous androgens simultaneously suppress endogenous testosterone, removing its physiological anti-proliferative effect at the breast [31]. Older literature and AAS-specific reviews further suggest that some 19-nortestosterone derivatives display progestogenic activity, which may potentiate estrogen-driven breast changes and contribute to the hormonal milieu favoring glandular overgrowth [32, 33].

In a prospective cohort from an Indian tertiary plastic surgery center (2019–2022) including all patients operated for gynecomastia, Beniwal et al. found that the true prevalence of AAS-associated gynecomastia, based on detailed postoperative reassessment, was 39.2%, compared with only 4.1% detected from preoperative history alone [32]. AAS abusers often attempt to mitigate this specific side effect through unsupervised use of selective estrogen receptor modulators (SERMs) such as tamoxifen and clomiphene, and aromatase inhibitors (AIs) [34]. Nonetheless, evidence indicate that these medications may be effective during the early tender glandular phase, whereas long-standing gynecomastia becomes increasingly fibrotic and less amenable to medical therapy [35].

Effects of anabolic–androgenic steroid abuse on male reproductive function

AAS abuse impairs male fertility primarily through suppression of the HPG axis which causes marked reductions in intratesticular testosterone to concentrations insufficient to support normal spermatogenesis [24]. This is accompanied by reduced Sertoli cell activity and inhibin B, leading to oligozoospermia or azoospermia in a substantial proportion of users [36]. Experimental male hormonal contraceptive trials with injectable testosterone undecanoate demonstrate that pharmacologic androgen exposure can reliably induce severe oligozoospermia or azoospermia in most healthy men, with recovery of sperm counts to the fertile range typically occurring within 6–24 months after discontinuation, underscoring that androgen-induced suppression is in principle reversible when exposure is time-limited and regimens are standardized [37].

Recent literature focusing specifically on non-medical AAS use suggests a more heterogeneous and, in some cases, less favorable reproductive trajectory. In a current-concepts review, de Ronde and Smit summarized emerging cohort data and concluded that androgen abuse consistently produces complete suppression of LH and FSH, marked reductions in sperm concentration and testicular volume, and that recovery of endocrine parameters is generally faster than recovery of spermatogenesis [36]. In the HAARLEM prospective cohort, most men with normal baseline gonadal function recovered normal testosterone within three months after stopping AAS, whereas total sperm counts required approximately 48–69 weeks to return to baseline; men with higher cumulative lifetime exposure showed incomplete recovery and biochemical evidence of persistent Leydig cell dysfunction [38].

These findings are reinforced by Shankara-Narayana et al. [39], who studied 41 current users, 31 past users (median ~10 months since cessation), and 21 non-users. Current users exhibited profound suppression of reproductive hormones and semen parameters compared with non-users. Past users showed near-normal LH, FSH, testosterone, and semen parameters but persistently reduced testicular volume. Modeling suggested that recovery of AMH, LH, and FSH occurred over approximately 7–11 months, whereas recovery of sperm output required about 14 months and was slower with longer durations of abuse [39].

Systematic synthesis further supports a substantial, but not uniformly complete, reversibility of AAS-related infertility. In a 2023 systematic review and meta-analysis of 32 studies including 9371 men (2671 AAS users), Mulawkar et al. [24] reported that AAS users had significantly lower LH, FSH, and total testosterone, smaller testicular volume, and worse semen parameters, particularly sperm concentration and motility, than non-users. Recovery of semen quality after cessation was variable and often incomplete within available follow-up, leading the authors to conclude that the adverse impact on male fertility is only partially reversible in many individuals.

Guideline-level evidence echoes these observations. The updated AUA/ASRM guideline on male infertility notes that exogenous testosterone and AAS suppress spermatogenesis and that some men fail to fully recover sperm production despite cessation of therapy, particularly after prolonged exposure [40]. Taken together, contemporary data indicate that AAS-induced infertility is primarily mediated by HPG-axis suppression but that the depth and duration of gonadal toxicity are strongly dose- and time-dependent. In most users, spermatogenesis recovers over 6–24 months once androgens are withdrawn; however, a clinically relevant subset experiences delayed, incomplete, or possibly persistent impairment of testicular function, with important implications for counseling and management of men who present with AAS-related infertility.

Cardiovascular effects of anabolic–androgenic steroid abuse

The cardiovascular system is a major target of AAS toxicity, with data supporting myocardial remodeling, vascular dysfunction, and prothrombotic changes that increase long-term risk of cardiomyopathy and ischemic events [41]. In the HAARLEM imaging study, a typical supraphysiologic cycle (median ~16 weeks; ~900 mg testosterone equivalents weekly) was associated with increased LV mass (~28 g), increased wall thickness (~0.9–1.2 mm), reduced LV ejection fraction (~5%), and worsened diastolic indices, with normalization after discontinuation, suggesting reversible remodeling in many users [42]. In the FIDO-DK cohort, cumulative lifetime exposure was independently associated with coronary atherosclerosis and biventricular dysfunction; each additional year of use increased the odds of a positive coronary calcium score (adjusted OR 1.23; 95% CI 1.09–1.39) and non-calcified plaques (adjusted OR 1.17; 95% CI 1.05–1.30), and most men with > 5 years exposure had cardiac parameters outside the median of the normal range [43]. Population-level registry data further demonstrate excess clinical events, including increased risks of myocardial infarction, revascularization, venous thromboembolism, arrhythmias, cardiomyopathy, and heart failure among sanctioned AAS users compared with controls [44].

Hepatic toxicity of anabolic–androgenic steroid abuse

The liver is a primary target of AAS toxicity, especially with 17α-alkylated oral agents, with a spectrum ranging from enzyme elevations to severe cholestasis, vascular lesions (e.g., peliosis hepatis), and neoplasia in long-term exposure [45]. Mechanistic syntheses implicate hepatocellular injury, oxidative stress, mitochondrial dysfunction, and interference with bile salt transport, with 17α-alkylation strongly linked to cholestatic phenotypes [46, 47]. Solimini et al. [47] describe three predominant clinical patterns in doping populations: prolonged cholestatic injury (often “bland cholestasis”), vascular lesions (peliosis/sinusoidal dilatation), and hepatic adenomas (rarely carcinoma), with typically slow but possible recovery after withdrawal and clinically important risks in advanced presentations. Additional reports highlight toxicant-associated steatosis/steatohepatitis-like patterns as an emerging phenotype [48].

Hematologic consequences of anabolic–androgenic steroid abuse

AAS abuse is consistently associated with androgen-driven erythrocytosis and a prothrombotic milieu, plausibly contributing to thromboembolic and cardiovascular risk [49,50,51,52]. Testosterone/AAS stimulate erythropoiesis via increased erythropoietin signaling and hepcidin suppression with enhanced iron utilization, effects that may be amplified at supraphysiologic doses [49]. In AAS users, higher hemoglobin/hematocrit and red cell mass have been reported with partial normalization after cessation, consistent with a reversible exposure effect [50, 51]. Hemostasis studies suggest alterations across coagulation and fibrinolysis rather than a single dominant defect; prospective HAARLEM data showed reversible changes in multiple procoagulant/anticoagulant factors, higher D-dimer, and prolonged clot lysis time during cycles with return toward baseline after discontinuation [52], aligning with mechanistic findings of impaired fibrinolysis in active users [53].

Musculoskeletal consequences of anabolic–androgenic steroid abuse

Epidemiologic data indicate a higher lifetime prevalence of tendon rupture among long-term AAS users compared with strength-trained controls, particularly involving upper-body tendons [54]. A leading hypothesis is a mismatch between rapid muscle hypertrophy and slower tendon adaptation, predisposing to injury under high loads [55]. Experimental models support altered tendon material properties (stiffer but mechanically weaker) and disordered collagen architecture with AAS exposure, potentially mediated by dysregulated extracellular matrix turnover, including changes in MMP activity and impaired physiologic collagen remodeling [56,57,58]. Clinically, this risk is relevant to counseling and injury prevention, particularly in high-intensity resistance training settings.

Neuropsychiatric and neurologic consequences of anabolic–androgenic steroid abuse

Neuropsychiatric effects are frequently reported in AAS users, including depressive symptoms, anxiety, irritability, sleep disruption, and anhedonia, with persistence in a subset after cessation [59,60,61,62]. Associations with aggression and violent or antisocial behavior appear more variable, with larger effects reported in individuals with pre-existing vulnerabilities (e.g., impulsivity, personality traits) [63, 64]. Neuroimaging and neurocognitive studies suggest possible long-term structural and functional brain changes in heavy users, including signals of accelerated brain aging/cortical thinning and impairments in learning and memory; reviews link these findings to alterations in prefrontal/limbic regions and hippocampal-related pathways [65,66,67]. While causality is difficult to establish, the consistency across study designs supports clinical vigilance for mood and cognitive symptoms in current and former users.

Cutaneous consequences of anabolic–androgenic steroid abuse

Cutaneous manifestations are common and include acne (sometimes severe), seborrhea, androgenic alopecia, hirsutism, and striae, reflecting androgen-driven sebaceous gland hypertrophy and increased sebum production with downstream follicular occlusion and inflammation [68, 69]. Injection-site reactions and atypical lesions may occur in chronic users. Although many dermatologic effects improve with dose reduction or cessation, scarring acne, striae, and patterned hair loss may be only partially reversible [70].

Management options

From a therapeutic standpoint, the cornerstone of managing men with AAS–induced hypogonadism is complete cessation of non-medical AAS use. Recovery of the HPG axis, testicular volume and spermatogenesis is contingent on withdrawal of exogenous androgens, and recent reviews and practice guidelines emphasize that counselling around discontinuation, relapse prevention and harm reduction should be the first priority in any management plan [71, 72]. After complete cessation, however, the natural history of recovery is heterogeneous. Prospective and review data indicate that many men with relatively short, cyclic AAS exposure regain near-normal testosterone and gonadotropin levels within about 3–12 months, whereas a substantial minority—particularly those with long-term, high-dose, near-continuous use—remain biochemically and symptomatically hypogonadal for much longer [38, 73, 74]. This variability underpins the central management dilemma: whether to adopt an expectant, watchful-waiting strategy in anticipation of spontaneous recovery, or to initiate pharmacological treatment aimed at inducing earlier recovery of endogenous function, despite limited data on its long-term efficacy and safety.

This uncertainty faced by clinicians is highlighted by a 2023 survey of UK endocrinologists managing AAS-induced hypogonadism. Grant et al. reported wide practice variation, with most respondents advising observation and lifestyle measures while roughly one in five prescribed endocrine therapies including SERMs, human chorionic gonadotropins (hCG), AIs, or testosterone in selected cases [75]. Many clinicians perceived that patients remained symptomatic at follow-up and reported low confidence in their own management strategies, underscoring the absence of evidence-based guidelines. Parallel work surveying 470 AAS users showed that unsupervised “post-cycle therapy” which usually constitute combinations of SERMs, hCG and AIs obtained on the black market, was self-reported to reduce withdrawal symptoms and suicidal thoughts, but the heterogeneity and uncontrolled design preclude firm conclusions and emphasize the need for properly designed clinical trials [20].

In the absence of robust trial data, a pragmatic, patient-centered approach can be structured around three key domains: exposure history, baseline endocrine status and fertility intentions (Fig. 5). First, the duration, dose and pattern of AAS use are major determinants of recovery. Men with relatively short cumulative exposure and clearly demarcated cycles appear more likely to normalize testosterone and gonadotropin levels within the first year after cessation, whereas those with multi-year, high-dose, near-continuous regimens are prone to develop persistent hypogonadism and may warrant earlier consideration of active endocrine treatment rather than prolonged observation alone [38, 73, 74]. A careful history should therefore document total years of use, typical weekly dose, number of different compounds used concurrently, and whether there were drug-free intervals.

Fig. 5: Selection scheme for spontaneous versus induced recovery.
Fig. 5: Selection scheme for spontaneous versus induced recovery.The alternative text for this image may have been generated using AI.
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Proposed decision criteria for selecting induced recovery versus spontaneous recovery following AAS cessation.

Second, baseline hormonal status should be reassessed once exogenous androgens have cleared to distinguish men with potentially reversible suppression from those with underlying primary or secondary hypogonadism. Morning total testosterone, SHBG, LH and FSH are the minimum; where available, measurement of inhibin B and assessment of testicular volume may further inform prognosis [40]. Men with very low testosterone and inappropriately low or normal gonadotropins after several months of abstinence, particularly if there is evidence of pre-existing androgen deficiency or significant comorbidity, are less likely to recover fully and may ultimately require long-term management as for classical hypogonadism rather than short-term “recovery” strategies.

Third, fertility intentions are central to treatment decisions. In men who desire paternity in the near term, preservation or restoration of spermatogenesis is the principal goal; in this context, exogenous testosterone should be avoided because it further suppresses gonadotropins and intratesticular testosterone, and treatment should instead focus on stimulating endogenous pituitary–testicular function. Conversely, in men with no short- or medium-term fertility plans, especially older individuals with pronounced, persistent symptoms despite a period of abstinence, conventional testosterone replacement may be appropriate after careful counselling about its implications for future fertility and the uncertainty surrounding spontaneous recovery once long-term replacement has been established. Across all groups, shared decision-making that explicitly weighs symptom burden, recovery prospects, fertility goals and the off-label nature of available interventions is essential.

Available pharmacologic options for induced recovery can be considered along these lines. SERM such as clomiphene citrate and tamoxifen increase endogenous LH and FSH, thereby stimulating testicular testosterone production and, in many men, spermatogenesis. hCG acts as a LH analogue, directly stimulating Leydig cells and constituting a mainstay of therapy in hypogonadotrophic hypogonadism. Non-steroidal AIs such as anastrozole and letrozole block the conversion of androgens to estradiol, lowering circulating estradiol and thereby reducing negative feedback at the hypothalamus and pituitary. This can increase LH/FSH and endogenous testosterone and improve the testosterone–estradiol ratio, but at the expense of reduced estrogen action in bone and other tissues. It is important to note that none of these medications are specifically licensed for the management of AAS-induced hypogonadism and their use in this setting is entirely off-label.

The existing evidence base is limited and derives largely from small series using combinations of these agents. A 16-week open-label pilot in 10 men with long-term AAS-induced hypogonadism found that clomiphene 25 mg on alternate days, with optional adjunct hCG, increased LH and FSH and brought total testosterone into the reference range in about half of participants, with only mild adverse effects [76]. In a retrospective series of 45 men with azoospermia or severe oligospermia after AAS use, a standardized regimen combining clomiphene with hCG for 3–6 months led to the reappearance of sperm in most patients, but normozoospermia was achieved in only a minority, underscoring both the potential and the limitations of such SERM–hCG–based therapy [77]. A systematic review of aromatase inhibitor use in men reports modest improvements in testosterone and sperm parameters in selected hypogonadal or subfertile populations, but identifies no controlled trials in AAS users and concludes that their role in this context remains uncertain [78].

Beyond endocrine recovery, many men with a history of AAS use present with ED and other organ-specific complications. Because no dedicated guideline-based pathway exists for men presenting with ED after cessation of AAS, we propose a pragmatic clinical algorithm to support evaluation and management in this setting (Fig. 6). This approach combines standard stepwise ED care with focused assessment of prior AAS exposure, hormonal status, and fertility intentions, allowing treatment to be individualized according to the likelihood of spontaneous recovery, the need for fertility preservation, and the appropriateness of testosterone replacement. Psychiatric and psychosexual factors should also be considered in men presenting with ED after AAS cessation, as persistent sexual symptoms may not be solely explained by endocrine disruption. Referral for psychiatric or psychosexual assessment may be appropriate in patients with prominent depression, anxiety, irritability, body-image disturbance, dependence-related features, withdrawal symptoms, or persistent distress disproportionate to the degree of hormonal abnormality [29, 79]. Such cases often require multidisciplinary management, particularly when psychological factors appear to contribute substantially to ongoing sexual dysfunction. Other organ-specific complications should continue to be managed according to existing evidence-based guidelines, with emphasis on sustained AAS cessation and multidisciplinary follow-up.

Fig. 6: Proposed clinical algorithm for the evaluation and management of erectile dysfunction in men with prior AAS use after cessation.
Fig. 6: Proposed clinical algorithm for the evaluation and management of erectile dysfunction in men with prior AAS use after cessation.The alternative text for this image may have been generated using AI.
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Men presenting with erectile dysfunction after discontinuation of anabolic–androgenic steroids should undergo a structured assessment including conventional ED risk factors, detailed AAS exposure history, fertility intentions, and targeted laboratory evaluation. Initial management should incorporate standard stepwise ED therapy, including counseling, lifestyle modification, and phosphodiesterase type 5 inhibitors where appropriate. In men with persistent symptomatic hypogonadism, subsequent management should be guided primarily by fertility goals and time since cessation. Testosterone replacement therapy should generally be avoided in men desiring fertility, whereas expectant or pharmacologically induced recovery may be considered in selected cases. In men without fertility goals, testosterone replacement therapy may be considered after an adequate period of observation if recovery of the hypothalamic-pituitary-gonadal axis does not occur. The algorithm is intended as a pragmatic clinical framework rather than a formal guideline.

Conclusion

Non-medical AAS use can result in clinically relevant hypogonadism that may persist after cessation, with adverse reproductive, metabolic, cardiovascular, and neuropsychiatric sequelae. While discontinuation of AAS remains the cornerstone of management, recovery of the hypothalamic–pituitary–gonadal axis and spermatogenesis is highly variable, and evidence guiding the choice between expectant and pharmacological management is limited. Current treatment strategies are largely based on physiological principles and small observational studies, supporting an individualized approach that considers AAS exposure characteristics, baseline endocrine status, symptom burden, and fertility intentions. However, the evidence base remains constrained by the predominance of observational studies, marked heterogeneity in exposure definitions, compounds used, cumulative dose, and duration of use, as well as the paucity of randomized controlled trials evaluating interventions intended to accelerate recovery. As such, current recommendations should be interpreted with appropriate caution. Well-designed prospective studies, standardized diagnostic definitions, and long-term outcome registries are needed to inform evidence-based guidelines and optimize care for this population.