madman
Super Moderator
Anabolic-androgenic steroid (AAS) and performance-enhancing drug (PED) use is a prevalent medical issue, especially among men, with an estimated 2.9–4 million Americans using AAS in their lifetime. Prior studies of AAS use reveals an association with polycythemia, dyslipidemia, infertility, hypertension, left ventricular hypertrophy, and multiple behavioral disorders. AAS withdrawal syndrome, a state of depression, anhedonia, and sexual dysfunction after discontinuing AAS use, is a common barrier to successful cessation. Clinical resources for these patients and training of physicians on management of the patient using AAS are limited. Many men are hesitant to seek traditional medical care due to fear of judgment and lack of confidence in physician's knowledge base regarding AAS. While proposed approaches to weaning patients off AAS are published, guidance on harm reduction for actively using patients remains sparse. Medical education regarding the management of AAS use disorder is paramount to improving the care of this currently underserved patient population. Management of these patients must be non-judgmental and focus on patient education, harm reduction, and support for cessation. The approach to harm reduction should be guided by the specific AAS/ PEDs used.
INTRODUCTION
Anabolic-androgenic steroids (AAS) and performance-enhancing drugs (PEDs) represent multiple classes of compounds used to enhance one’s physique and/or improve physical performance. These include testosterone esters, synthetic androgens, aromatase inhibitors (AIs), selective estrogen receptor modulators (SERMs), selective androgen receptor modulators (SARMs), human growth hormone (hGH), fat-burning compounds, and myriad other compounds. The use of AAS has become widespread in the USA, with an estimated 2.9–4 million Americans using AAS at some point in their lifetime.1 Worldwide, the lifetime prevalence of AAS use is estimated at 1–5%.2 Several case series of male gym attendees found the prevalence of AAS use to be 15–30% in this population.3–5 While AAS use is often associated with professional athletics, the majority of adults using AAS are nonprofessionals taking these compounds recreationally.4,6,7 Despite widely reported cardiovascular, reproductive, hematologic, and neuropsychiatric effects described with these agents, there exist no guidelines or evidence-based harm reduction approaches to men actively using AAS.
It is estimated that over 98% of those using AAS are male.1 These compounds have become readily available through illicit internet sources.8 Men are commonly motivated to use AAS to improve their muscularity and strength.7 An increasing societal emphasis on body image is believed to have contributed to increasing AAS use among men.9,10 Many of these men may be prone to developing muscle dysmorphia, a pathologic preoccupation with muscularity and body image that may impair quality of life.8,10 AAS use has also been correlated with a history of poor self-esteem, depression, suicidality, and previously experienced physical or sexual abuse.11–13
Common consequences of AAS/PED use include dyslipidemia, hypertension, left ventricular hypertrophy (LVH), arrhythmia, atherosclerosis, polycythemia and thrombosis, infertility, endocrine dysfunction, tendon rupture, and sexual dysfunction.6,14–18 Those attempting to discontinue AAS use often experience AAS withdrawal syndrome, a state of depression, anhedonia, and sexual dysfunction which challenges prolonged cessation.6 The lack of long-term data, medical education, and national initiatives addressing AAS use is highlighted in several recent reviews, stressing the need for swift action to prevent the worsening of this growing issue.2,8 With limited public health resources available to men using AAS,6 and general distrust of clinicians among many of these patients,19 men often rely on other men using AAS and online sources for advice regarding the use and procurement.7,20
A major effect of extended AAS use is anabolic steroid-induced hypogonadism (ASIH), which refers to the disruption of the hypothalamic-pituitary-testicular (HPT) axis from prolonged exposure to supraphysiologic doses of testosterone esters, synthetic androgens, and accessory performance– enhancing drugs.21 Men using AAS often attempt to prevent ASIH by taking various compounds such as SERMs and hCG, an unproven strategy referred to as “post-cycle therapy” or “PCT.” ASIH is proving to be a significant cause of male hypogonadism, with 20.9% of 6033 hypogonadal men reporting prior AAS use in a recent retrospective study.22 The development, degree, and duration of ASIH are highly dependent on factors such as age, dosages used, duration of use, and compounds used.23
While several authors have addressed the proposed management of men ready to stop AAS use with symptomatic ASIH2,23,24 (Table 1), harm reduction guidance for men actively using these agents remains limited. To begin, an example of a common clinical experience for the patient using AAS/PEDs is described to highlight the challenges faced by both clinician and patient. Next, the approach to caring for such patients, review of specific AAS/PED compounds, and strategies for harm reduction are described.
*Clinical Example. A 39-year-old man presents to his primary-care clinic to discuss having blood work checked. Vitals are notable for a blood pressure of 142/90 mmHg and a body mass index (BMI) of 31 kg/m2 . On exam, he has above-average muscularity and mild acne. He hesitantly discloses he has been using steroids to improve his physique and describes his regimen (Table 2). He obtains the steroids from the internet and a friend at the gym helps him plan his “cycle.” He has concerns regarding his use and wants to make sure his liver function and blood counts are “okay.”
The clinician discusses the dangers of AAS use and recommends he discontinue. The patient expresses multiple concerns with stopping, including concern over losing strength and muscularity. The clinician tells him “it is important for your health that you stop using. Why don’t you stop for a few weeks before we check labs?”
Frustrated with the lack of understanding and lack of assistance from his physician, he resorts to following the advice of other men using AAS. Despite multiple attempts to wean his use, he struggles with severe depression from acute AAS withdrawal. Due to his prior experience with his healthcare provider, he continues to self-manage his care and rely on others using AAS rather than seeking medical care.
*Initial Approach to Men Using AAS Seeking Healthcare
The presented vignette highlights a common situation: A concerned patient using AAS who is unsure how to best monitor his health, seeking guidance from a well-intentioned clinician with has limited experience in assisting such patients. While the patient did not state willingness to cease use, he demonstrated concern for his health by seeking care. His clinician intended to help, but unintentionally promoted preconceived beliefs the patient had regarding the healthcare system, ultimately discouraging him to seek further care.
A recent systematic review of AAS use found common reasons for seeking medical care were overall health concerns, blood test monitoring, and prescription substances. Help with discontinuing AAS use was not a top priority.25 Clinicians should certainly discourage AAS use, but the initial interaction should serve to obtain a better understanding of why the patient is using AAS, what concerns they have, and why they are seeking care. Doing so in a non-judgmental and supportive manner is essential. Open-ended questions may reveal the motivations of the patient, such as fertility or side effect avoidance. Identifying these factors creates opportunities to build rapport, minimize harm, and eventually progress to cessation.
Alternatively, no such motivation may be identified. In this situation, harm reduction labs may be even more useful. For example, identifying previously undiagnosed dyslipidemia or cardiac disease may serve as motivation for some patients to consider cessation. The following sections will provide background, side effects, and harm reduction strategies for commonly used AAS/PEDs.
*ANABOLIC ANDROGENIC STEROIDS AND PERFORMANCE ENHANCING DRUGS OF MISUSE: (TABLES 3 AND 4)
Injectable Androgenic Anabolic Steroids
Background. Dating back to the 1950s, numerous injectable testosterone compounds were used by elite athletes for strength and muscle gain. By the 1980s, AAS were in use by the general public.9 There are three main classes of AAS compounds: testosterone esters, 19-nortestosterone and related derivatives, and dihydrotestosterone (DHT) derivatives26,27 (Table 5). Each class is believed to have somewhat unique anabolic and/or androgenic effects.26
The foundations of most AAS regimens are testosterone esters and synthetic testosterone compounds taken in supraphysiologic doses. Reported doses commonly range between 500 and 1000 mg of testosterone per week,7 which is 5–10 times the accepted treatment dose for male hypogonadism.28
It is common for men using AAS to utilize injectable AAS for 8–16 weeks at a time, often referred to as a “cycle”. 27 “Stacking” refers to the use of multiple AAS/ PEDs during a cycle. A cycle is commonly followed by a period of weeks to months where users either decrease their AAS dose or abstain completely to allow recovery of their hypothalamic-pituitary-testicular (HPT) axis.23 Additional AAS nomenclature is available in Table 6.
Adverse Effects. Cardiovascular effects of AAS are the most frequently reported and have the highest quality of data supporting their association. A recent cross-sectional study of 86 males with over 2 years of AAS exposure was found to have reduced left ventricular ejection fraction (LVEF), impaired diastolic relaxation, increased left ventricular mass, and higher volumes of coronary artery plaque compared to age-matched non-users.15 Post-mortem studies revealed increased rates of cardiomegaly, left ventricular hypertrophy, and myocardial fibrosis compared to non-users.29–31 Increases in LDL and decreases in HDL were supported by a meta-analysis examining 11 studies on dyslipidemia in men using AAS14; the same study found an association with AAS use and atrial fibrillation and ventricular arrhythmia. Coronary artery calcium (CAC) testing of 14 male professional bodybuilders using AAS found that 7 patients had CAC scores greater than the 90th percentile expected for their age, 3 of which were under 40 years old.32
AAS use has been shown to cause infertility and ASIH in retrospective studies.17 Restoration of fertility and endogenous testosterone production is more likely in men who engaged in shorter (generally under a year) and less-extreme AAS use.2,23 Estrogenic side effects are common due to the aromatization of exogenous androgens, causing issues such as gynecomastia.33 Exogenous testosterone is also shown to accelerate the growth of existing metastatic prostate cancer.34
A wide range of behavioral effects are reported with AAS use including impulsivity, hypomanic/manic symptoms, aggression, and anxiety.6,35 Multiple retrospective and cross-sectional studies found an association of AAS use with concurrent illicit substance use disorder, and body image disorders such as muscle dysmorphia.10,36,37 AAS withdrawal syndrome is reported in men abruptly stopping AAS use and involves significant symptoms of depression, libido dysfunction, and anhedonia.2,6
Other notable adverse effects include dose-dependent erythropoiesis and polycythemia,38 thromboses,16 development of focal segmental glomerular sclerosis (FSGS),39 acute kidney injury (AKI),40, and upper extremity tendon rupture.
Harm Reduction Strategies. Initial screening should include blood pressure assessment, review of family history of cardiovascular disease, lipid profile testing, a comprehensive metabolic panel, and electrocardiogram (ECG) testing. Hypertension and dyslipidemia should be treated according to national guidelines. Given the increased prevalence of LVH in this population,14 we favor angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) for the treatment of hypertension. Obtaining a transthoracic echocardiogram (TTE) is reasonable if there is clinical concern for cardiac dysfunction, chronic AAS use (over 1 year), and/or strong family history of cardiovascular disease. CAC testing should also be considered if additional atherosclerotic cardiovascular disease (ASCVD) risk factors are identified.
We suggest prostate stimulating antigen (PSA) screening in this population the same way it is recommended in men receiving testosterone replacement therapy per Endocrine Society guidelines.28 Screening involves assessing PSA in men aged 55–69 years old (or beginning at age 40 if high risk) in those agreeable to prostate cancer screening. Referral to urology is recommended in situations of abnormal prostate exam, PSA > 4 ng/mL, sudden worsening of lower urinary tract symptoms, or a confirmed PSA increase of greater than 1.4 ng/mL over a 12-month period. Testosterone levels with gonadotropins may be useful in quantifying the degree of androgen use and HPT-axis suppression, or if AAS use is suspected but uncertain.
Due to the high prevalence of behavior disorders and concurrent substance use,13,36,37 we suggest early referral to a behavioral health specialist, ideally having experience regarding substance use disorders and body image disorders. The association between AAS use and increased psychological distress and impaired executive function41 is one possibility as to why these issues are more frequently seen among this population.
Oral AAS/Pro-hormones
Background. Oral AAS compounds, such as metandienone (Dianabol), oxandrolone (Anavar), and stanozolol (Winstrol) are commonly used in conjunction with injectable AAS during steroid cycles for added muscle size and strength benefits.42 These agents gained popularity in the 1970s and continue to be common additions to user-designed AAS cycles.2
Adverse Effects. Alkylated oral compounds are associated with hepatotoxicity due to the presence of the 17-methyl group, which prevents degradation by first-pass hepatic metabolism when dosed orally.43
Harm Reduction Strategies. In addition to the approach advised for injectable AAS, obtaining liver function tests is of benefit due to the high prevalence of hepatotoxicity from oral alkylated AAS. Reviewing concurrent substances, medications, or supplements that may cause additional hepatic injury is advised.
Aromatase Inhibitors
*Background
*Adverse Effects
*Harm Reduction Strategies
Selective Estrogen Receptor Modulators
*Background
*Adverse Effects
*Harm Reduction Strategies
Human Chorionic Gonadotropin
*Background
*Adverse Effects
*Harm Reduction Strategies
Phosphodiesterase-5 Inhibitors
*Background
*Adverse Effects
*Harm Reduction Strategies
Fat Burning Compounds (T3, Clenbuterol, and DNP)
*Background
*Adverse Effects
*Harm Reduction Strategies
Site Enhancement Oils
*Background
*Adverse Effects
*Harm Reduction Strategies
Insulin
*Background
*Adverse Effects
*Harm Reduction Strategies
Diuretics
*Background
*Adverse Effects
*Harm Reduction Strategies
Human Growth Hormone and Related Peptides
*Background
*Adverse Effects
*Harm Reduction Strategies
Dopamine Agonists
*Background
*Adverse Effects
*Harm Reduction Strategies
Selective Androgen Receptor Modulators
*Background
*Adverse Effects
*Harm Reduction Strategies
Compassionate care is paramount. It is essential that cessation of AAS use is routinely discussed with the patient. These regular discussions should be non-judgmental and caring, much like with smoking cessation. The authors strongly oppose the prescribing of medications with potential anabolic uses in patients who are currently using illicit AAS/PEDs. For example, we discourage prescribing an AI or SERM to a patient on illicit AAS who wishes to decrease his estrogen levels. In men who present with sexual dysfunction, not ready to work towards discontinuing AAS use, we discourage the use of PDE-5 inhibitors or other related treatments because the clinician-supervised cessation of AAS improves/resolves this issue. We strongly support the screening and treatment of AAS-related cardiovascular conditions, behavioral disorders, and hematologic disorders to further reduce self-harm during AAS use. Once a patient acknowledges he is ready to discontinue AAS use, we currently favor a personalized approach as outlined in reviews by Anawalt2 and Rahnema et al.,23 as no randomized control trials on this subject have been conducted.
We believe harm minimization would not only reduce adverse effects of AAS but also serve as a bridge to cessation. For example, many men using AAS are relatively young and have no prior health issues. A medical assessment revealing hypertension, dyslipidemia, and LVH may serve to have such a patient reconsider further use and consider cessation. In some men, the desire to continue AAS use will predominate despite the diagnosis of serious adverse effects. In these cases, the authors recommend continued close clinical surveillance in addition to prompt referral to appropriate behavioral health specialists. This will allow for continued health monitoring and management of adverse effects, while further building rapport and presenting ongoing opportunities to reconsider cessation.
LIMITATIONS
Most of the reviewed literature consisted of cross-control studies, retrospective reviews, and case series. The lack of randomized controlled data and limited prospective data are significant limitations. The guidance provided is based upon the current literature and the clinical experience of the authors.
CONCLUSIONS
A harm reduction approach, with a strong emphasis on reducing cardiovascular risk, should be taken with men actively using AAS who decline current cessation.
INTRODUCTION
Anabolic-androgenic steroids (AAS) and performance-enhancing drugs (PEDs) represent multiple classes of compounds used to enhance one’s physique and/or improve physical performance. These include testosterone esters, synthetic androgens, aromatase inhibitors (AIs), selective estrogen receptor modulators (SERMs), selective androgen receptor modulators (SARMs), human growth hormone (hGH), fat-burning compounds, and myriad other compounds. The use of AAS has become widespread in the USA, with an estimated 2.9–4 million Americans using AAS at some point in their lifetime.1 Worldwide, the lifetime prevalence of AAS use is estimated at 1–5%.2 Several case series of male gym attendees found the prevalence of AAS use to be 15–30% in this population.3–5 While AAS use is often associated with professional athletics, the majority of adults using AAS are nonprofessionals taking these compounds recreationally.4,6,7 Despite widely reported cardiovascular, reproductive, hematologic, and neuropsychiatric effects described with these agents, there exist no guidelines or evidence-based harm reduction approaches to men actively using AAS.
It is estimated that over 98% of those using AAS are male.1 These compounds have become readily available through illicit internet sources.8 Men are commonly motivated to use AAS to improve their muscularity and strength.7 An increasing societal emphasis on body image is believed to have contributed to increasing AAS use among men.9,10 Many of these men may be prone to developing muscle dysmorphia, a pathologic preoccupation with muscularity and body image that may impair quality of life.8,10 AAS use has also been correlated with a history of poor self-esteem, depression, suicidality, and previously experienced physical or sexual abuse.11–13
Common consequences of AAS/PED use include dyslipidemia, hypertension, left ventricular hypertrophy (LVH), arrhythmia, atherosclerosis, polycythemia and thrombosis, infertility, endocrine dysfunction, tendon rupture, and sexual dysfunction.6,14–18 Those attempting to discontinue AAS use often experience AAS withdrawal syndrome, a state of depression, anhedonia, and sexual dysfunction which challenges prolonged cessation.6 The lack of long-term data, medical education, and national initiatives addressing AAS use is highlighted in several recent reviews, stressing the need for swift action to prevent the worsening of this growing issue.2,8 With limited public health resources available to men using AAS,6 and general distrust of clinicians among many of these patients,19 men often rely on other men using AAS and online sources for advice regarding the use and procurement.7,20
A major effect of extended AAS use is anabolic steroid-induced hypogonadism (ASIH), which refers to the disruption of the hypothalamic-pituitary-testicular (HPT) axis from prolonged exposure to supraphysiologic doses of testosterone esters, synthetic androgens, and accessory performance– enhancing drugs.21 Men using AAS often attempt to prevent ASIH by taking various compounds such as SERMs and hCG, an unproven strategy referred to as “post-cycle therapy” or “PCT.” ASIH is proving to be a significant cause of male hypogonadism, with 20.9% of 6033 hypogonadal men reporting prior AAS use in a recent retrospective study.22 The development, degree, and duration of ASIH are highly dependent on factors such as age, dosages used, duration of use, and compounds used.23
While several authors have addressed the proposed management of men ready to stop AAS use with symptomatic ASIH2,23,24 (Table 1), harm reduction guidance for men actively using these agents remains limited. To begin, an example of a common clinical experience for the patient using AAS/PEDs is described to highlight the challenges faced by both clinician and patient. Next, the approach to caring for such patients, review of specific AAS/PED compounds, and strategies for harm reduction are described.
*Clinical Example. A 39-year-old man presents to his primary-care clinic to discuss having blood work checked. Vitals are notable for a blood pressure of 142/90 mmHg and a body mass index (BMI) of 31 kg/m2 . On exam, he has above-average muscularity and mild acne. He hesitantly discloses he has been using steroids to improve his physique and describes his regimen (Table 2). He obtains the steroids from the internet and a friend at the gym helps him plan his “cycle.” He has concerns regarding his use and wants to make sure his liver function and blood counts are “okay.”
The clinician discusses the dangers of AAS use and recommends he discontinue. The patient expresses multiple concerns with stopping, including concern over losing strength and muscularity. The clinician tells him “it is important for your health that you stop using. Why don’t you stop for a few weeks before we check labs?”
Frustrated with the lack of understanding and lack of assistance from his physician, he resorts to following the advice of other men using AAS. Despite multiple attempts to wean his use, he struggles with severe depression from acute AAS withdrawal. Due to his prior experience with his healthcare provider, he continues to self-manage his care and rely on others using AAS rather than seeking medical care.
*Initial Approach to Men Using AAS Seeking Healthcare
The presented vignette highlights a common situation: A concerned patient using AAS who is unsure how to best monitor his health, seeking guidance from a well-intentioned clinician with has limited experience in assisting such patients. While the patient did not state willingness to cease use, he demonstrated concern for his health by seeking care. His clinician intended to help, but unintentionally promoted preconceived beliefs the patient had regarding the healthcare system, ultimately discouraging him to seek further care.
A recent systematic review of AAS use found common reasons for seeking medical care were overall health concerns, blood test monitoring, and prescription substances. Help with discontinuing AAS use was not a top priority.25 Clinicians should certainly discourage AAS use, but the initial interaction should serve to obtain a better understanding of why the patient is using AAS, what concerns they have, and why they are seeking care. Doing so in a non-judgmental and supportive manner is essential. Open-ended questions may reveal the motivations of the patient, such as fertility or side effect avoidance. Identifying these factors creates opportunities to build rapport, minimize harm, and eventually progress to cessation.
Alternatively, no such motivation may be identified. In this situation, harm reduction labs may be even more useful. For example, identifying previously undiagnosed dyslipidemia or cardiac disease may serve as motivation for some patients to consider cessation. The following sections will provide background, side effects, and harm reduction strategies for commonly used AAS/PEDs.
*ANABOLIC ANDROGENIC STEROIDS AND PERFORMANCE ENHANCING DRUGS OF MISUSE: (TABLES 3 AND 4)
Injectable Androgenic Anabolic Steroids
Background. Dating back to the 1950s, numerous injectable testosterone compounds were used by elite athletes for strength and muscle gain. By the 1980s, AAS were in use by the general public.9 There are three main classes of AAS compounds: testosterone esters, 19-nortestosterone and related derivatives, and dihydrotestosterone (DHT) derivatives26,27 (Table 5). Each class is believed to have somewhat unique anabolic and/or androgenic effects.26
The foundations of most AAS regimens are testosterone esters and synthetic testosterone compounds taken in supraphysiologic doses. Reported doses commonly range between 500 and 1000 mg of testosterone per week,7 which is 5–10 times the accepted treatment dose for male hypogonadism.28
It is common for men using AAS to utilize injectable AAS for 8–16 weeks at a time, often referred to as a “cycle”. 27 “Stacking” refers to the use of multiple AAS/ PEDs during a cycle. A cycle is commonly followed by a period of weeks to months where users either decrease their AAS dose or abstain completely to allow recovery of their hypothalamic-pituitary-testicular (HPT) axis.23 Additional AAS nomenclature is available in Table 6.
Adverse Effects. Cardiovascular effects of AAS are the most frequently reported and have the highest quality of data supporting their association. A recent cross-sectional study of 86 males with over 2 years of AAS exposure was found to have reduced left ventricular ejection fraction (LVEF), impaired diastolic relaxation, increased left ventricular mass, and higher volumes of coronary artery plaque compared to age-matched non-users.15 Post-mortem studies revealed increased rates of cardiomegaly, left ventricular hypertrophy, and myocardial fibrosis compared to non-users.29–31 Increases in LDL and decreases in HDL were supported by a meta-analysis examining 11 studies on dyslipidemia in men using AAS14; the same study found an association with AAS use and atrial fibrillation and ventricular arrhythmia. Coronary artery calcium (CAC) testing of 14 male professional bodybuilders using AAS found that 7 patients had CAC scores greater than the 90th percentile expected for their age, 3 of which were under 40 years old.32
AAS use has been shown to cause infertility and ASIH in retrospective studies.17 Restoration of fertility and endogenous testosterone production is more likely in men who engaged in shorter (generally under a year) and less-extreme AAS use.2,23 Estrogenic side effects are common due to the aromatization of exogenous androgens, causing issues such as gynecomastia.33 Exogenous testosterone is also shown to accelerate the growth of existing metastatic prostate cancer.34
A wide range of behavioral effects are reported with AAS use including impulsivity, hypomanic/manic symptoms, aggression, and anxiety.6,35 Multiple retrospective and cross-sectional studies found an association of AAS use with concurrent illicit substance use disorder, and body image disorders such as muscle dysmorphia.10,36,37 AAS withdrawal syndrome is reported in men abruptly stopping AAS use and involves significant symptoms of depression, libido dysfunction, and anhedonia.2,6
Other notable adverse effects include dose-dependent erythropoiesis and polycythemia,38 thromboses,16 development of focal segmental glomerular sclerosis (FSGS),39 acute kidney injury (AKI),40, and upper extremity tendon rupture.
Harm Reduction Strategies. Initial screening should include blood pressure assessment, review of family history of cardiovascular disease, lipid profile testing, a comprehensive metabolic panel, and electrocardiogram (ECG) testing. Hypertension and dyslipidemia should be treated according to national guidelines. Given the increased prevalence of LVH in this population,14 we favor angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) for the treatment of hypertension. Obtaining a transthoracic echocardiogram (TTE) is reasonable if there is clinical concern for cardiac dysfunction, chronic AAS use (over 1 year), and/or strong family history of cardiovascular disease. CAC testing should also be considered if additional atherosclerotic cardiovascular disease (ASCVD) risk factors are identified.
We suggest prostate stimulating antigen (PSA) screening in this population the same way it is recommended in men receiving testosterone replacement therapy per Endocrine Society guidelines.28 Screening involves assessing PSA in men aged 55–69 years old (or beginning at age 40 if high risk) in those agreeable to prostate cancer screening. Referral to urology is recommended in situations of abnormal prostate exam, PSA > 4 ng/mL, sudden worsening of lower urinary tract symptoms, or a confirmed PSA increase of greater than 1.4 ng/mL over a 12-month period. Testosterone levels with gonadotropins may be useful in quantifying the degree of androgen use and HPT-axis suppression, or if AAS use is suspected but uncertain.
Due to the high prevalence of behavior disorders and concurrent substance use,13,36,37 we suggest early referral to a behavioral health specialist, ideally having experience regarding substance use disorders and body image disorders. The association between AAS use and increased psychological distress and impaired executive function41 is one possibility as to why these issues are more frequently seen among this population.
Oral AAS/Pro-hormones
Background. Oral AAS compounds, such as metandienone (Dianabol), oxandrolone (Anavar), and stanozolol (Winstrol) are commonly used in conjunction with injectable AAS during steroid cycles for added muscle size and strength benefits.42 These agents gained popularity in the 1970s and continue to be common additions to user-designed AAS cycles.2
Adverse Effects. Alkylated oral compounds are associated with hepatotoxicity due to the presence of the 17-methyl group, which prevents degradation by first-pass hepatic metabolism when dosed orally.43
Harm Reduction Strategies. In addition to the approach advised for injectable AAS, obtaining liver function tests is of benefit due to the high prevalence of hepatotoxicity from oral alkylated AAS. Reviewing concurrent substances, medications, or supplements that may cause additional hepatic injury is advised.
Aromatase Inhibitors
*Background
*Adverse Effects
*Harm Reduction Strategies
Selective Estrogen Receptor Modulators
*Background
*Adverse Effects
*Harm Reduction Strategies
Human Chorionic Gonadotropin
*Background
*Adverse Effects
*Harm Reduction Strategies
Phosphodiesterase-5 Inhibitors
*Background
*Adverse Effects
*Harm Reduction Strategies
Fat Burning Compounds (T3, Clenbuterol, and DNP)
*Background
*Adverse Effects
*Harm Reduction Strategies
Site Enhancement Oils
*Background
*Adverse Effects
*Harm Reduction Strategies
Insulin
*Background
*Adverse Effects
*Harm Reduction Strategies
Diuretics
*Background
*Adverse Effects
*Harm Reduction Strategies
Human Growth Hormone and Related Peptides
*Background
*Adverse Effects
*Harm Reduction Strategies
Dopamine Agonists
*Background
*Adverse Effects
*Harm Reduction Strategies
Selective Androgen Receptor Modulators
*Background
*Adverse Effects
*Harm Reduction Strategies
Compassionate care is paramount. It is essential that cessation of AAS use is routinely discussed with the patient. These regular discussions should be non-judgmental and caring, much like with smoking cessation. The authors strongly oppose the prescribing of medications with potential anabolic uses in patients who are currently using illicit AAS/PEDs. For example, we discourage prescribing an AI or SERM to a patient on illicit AAS who wishes to decrease his estrogen levels. In men who present with sexual dysfunction, not ready to work towards discontinuing AAS use, we discourage the use of PDE-5 inhibitors or other related treatments because the clinician-supervised cessation of AAS improves/resolves this issue. We strongly support the screening and treatment of AAS-related cardiovascular conditions, behavioral disorders, and hematologic disorders to further reduce self-harm during AAS use. Once a patient acknowledges he is ready to discontinue AAS use, we currently favor a personalized approach as outlined in reviews by Anawalt2 and Rahnema et al.,23 as no randomized control trials on this subject have been conducted.
We believe harm minimization would not only reduce adverse effects of AAS but also serve as a bridge to cessation. For example, many men using AAS are relatively young and have no prior health issues. A medical assessment revealing hypertension, dyslipidemia, and LVH may serve to have such a patient reconsider further use and consider cessation. In some men, the desire to continue AAS use will predominate despite the diagnosis of serious adverse effects. In these cases, the authors recommend continued close clinical surveillance in addition to prompt referral to appropriate behavioral health specialists. This will allow for continued health monitoring and management of adverse effects, while further building rapport and presenting ongoing opportunities to reconsider cessation.
LIMITATIONS
Most of the reviewed literature consisted of cross-control studies, retrospective reviews, and case series. The lack of randomized controlled data and limited prospective data are significant limitations. The guidance provided is based upon the current literature and the clinical experience of the authors.
CONCLUSIONS
A harm reduction approach, with a strong emphasis on reducing cardiovascular risk, should be taken with men actively using AAS who decline current cessation.
