Anabolic-Androgenic Steroid Use in Sports, Health, and Society : Medicine & Science in Sports & Exercise

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Anabolic-Androgenic Steroid Use in Sports, Health, and Society


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Medicine & Science in Sports & Exercise 53(8):p 1778-1794, August 2021. | DOI: 10.1249/MSS.0000000000002670



This consensus statement is an update of the 1987 American College of Sports Medicine (ACSM) position stand on the use of anabolic-androgenic steroids (AAS). Substantial data have been collected since the previous position stand, and AAS use patterns have changed significantly. The ACSM acknowledges that lawful and ethical therapeutic use of AAS is now an accepted mainstream treatment for several clinical disorders; however, there is increased recognition that AAS are commonly used illicitly to enhance performance and appearance in several segments of the population, including competitive athletes. The illicit use of AAS by competitive athletes is contrary to the rules and ethics of many sport governing bodies. Thus, the ACSM deplores the illicit use of AAS for athletic and recreational purposes. This consensus statement provides a brief history of AAS use, an update on the science of how we now understand AAS to be working metabolically/biochemically, potential side effects, the prevalence of use among athletes, and the use of AAS in clinical scenarios.


 This consensus statement is an update of the previous position stand from the American College of Sports Medicine (ACSM), published in 1987 (1). Since then, a substantial amount of scientific data on anabolic-androgenic steroids (AAS) has emerged and the circumstances of AAS use has evolved in the athletic, recreational, and clinical communities. The objective of this consensus statement is to provide readers with a brief summary of the current evidence and extend the recommendations provided in the 1987 document (1). Key topics discussed are the brief history of AAS, epidemiology, methods, and patterns of AAS use, androgen physiology and ergogenic effects, side effects of AAS, and clinical uses of AAS (see Box 1). The writing group used the rating system of the National Heart Lung and Blood Institute (Table 1) and a consensus approach to synthesize the available evidence from clinical trials and case reports, narrative and systematic reviews, and meta-analyses (3). The recommendations represent the consensus of the writing panel, the ACSM, and incorporate guidance from other professional organizations with expertise in the area.

TABLE 1 - Evidence categories.
Evidence Category Sources of Evidence Definition
A RCT (rich body of data) Evidence is from endpoints of well-designed RCT (or trials that depart only minimally from randomization) that provide a consistent pattern of findings in the population for which the recommendation is made. Category A therefore requires substantial numbers of studies involving substantial numbers of participants.
B RCT (limited body of data) Evidence is from endpoints of intervention studies that include only a limited number of RCT, post hoc or subgroup analysis of RCT, or meta-analysis of RCT. In general, Category B pertains when few randomized trials exist, they are small in size, and the trial results are somewhat inconsistent, or the trials were undertaken in a population that differs from the target population of the recommendation.
C Non-RCT and observational studies Evidence is from outcomes of uncontrolled or nonrandomized trials or from observational studies.
D Panel consensus judgment Expert judgment is based on the panel’s synthesis of evidence from experimental research described in the literature and/or derived from the consensus of panel members based on clinical experience or knowledge that does not meet the above-listed criteria. This category is used only in cases where the provision of some guidance was deemed valuable but an adequately compelling clinical literature addressing the subject of the recommendation was deemed insufficient to justify placement in one of the other categories (A through C)
Modified from (2).
RCT, randomized controlled trial.

BOX 1. ACSM Consensus Statements and Recommendations Summary.

Consensus Statements and Recommendations

  • 1. The administration of AAS in a dose-dependent manner significantly increases muscle strength, lean body mass, endurance, and power. The effects are primarily seen when AAS use is accompanied by a progressive training program. Evidence Category A.
  • 2. Historically, AAS use was primarily seen in competitive athletes and aspiring bodybuilders and powerlifters. Recreational AAS use appears to have surpassed athletic AAS use indicated by survey prevalence estimates demonstrating that recreational trainees are the leading consumers of AAS. The ACSM deplores the illicit use of AAS for recreational purposes. Evidence Category C.
  • 3. AAS are classified as schedule III drugs, banned by several sport governing bodies, and are illegal to use for athletic purposes. The ACSM deplores the illicit use of AAS for recreational use and performance enhancement in athletes. Evidence Category D.
  • 4. Coaches, trainers, and medical staffs should monitor and be cognizant of visible signs of AAS use and abuse. These include (but are not limited to): a substantial increase in muscle mass, strength, and power in a relatively short period of time (or the reverse which could denote AAS withdrawal); acne that is resistant to medical treatment; development of unexplainable rash, gynecomastia, increased body hair, and prominent increases in surface vascularity; changes in temperament, mood, and aggressive behavior (severe depression or suicidality could indicate AAS withdrawal); facial masculinization and fluid retention; and muscle mass that appears disproportionate to body structure or pubertal status in young athletes. In addition, the presence of AAS-related materials (books, articles, websites, dealer information, needles, vials) on the individual could reflect intent and may warrant further dialogue from the coaching, trainer, and medical staffs. Medical staff should be aware of regulations and documentation requirements regarding use of AAS for athletes with medical indications for their use. Evidence Category C.
  • 5. Use and abuse of AAS is associated with several notable adverse effects in men and women including (but not limited to) suppression of the hypothalamic-pituitary-gonadal axis, psychological changes, immunosuppression, and unhealthy cardiovascular, hematological, reproductive, hepatic, renal, integumentary, musculoskeletal, and metabolic effects. Several adverse effects may be reversible upon discontinuation but some could pose health risks beyond the duration of AAS use. Evidence Category B.
  • 6. Use of AAS in prepubertal and peripubertal children may lead to early virilization, premature growth plate closure, and reduced stature. Evidence Category C.
  • 7. Coaches, trainers, and medical staffs should be cognizant of the reasons for AAS use and abuse and deter use when possible. Prevention programs based on education may assist; and providing the individual with scientific nutrition and training advice is a recommended strategy to mitigate the temptation of AAS use. Evidence Category D.
  • 8. Androgen replacement therapy is approved for the medical treatment of several clinical diseases and abnormalities. The ACSM acknowledges the lawful and ethical use of AAS for clinical purposes and supports the physicians’ ability to provide androgen therapy to patients when deemed medically necessary. The reader is referred to guidelines established by the Endocrine Society (4). Evidence Category C.


Anabolic-androgenic steroids are drugs chemically and pharmacologically related to testosterone (T) that promote muscle growth and are not estrogens, progestins, or corticosteroids. An androgen is any natural or synthetic steroid hormone capable of promoting the development of male primary and secondary sexual characteristics via binding to androgen receptors at the tissue level. The term anabolic describes a hormone or other substance capable of enhancing the growth of somatic tissue, such as skeletal muscle and bone. In a sport-related setting, this is typically used to describe the enhancement of skeletal muscle. Table 2 presents nomenclature associated with AAS. In the United States, AAS are classified as Schedule III controlled substances (5). Although AAS have legitimate medicinal use, nontherapeutic use among athletes and recreationally active young men and women is performed to improve strength, power, increase muscle mass, and improve appearance. Athletic and recreational (i.e., noncompetitive) use of AAS has been widespread over the last 50 yr, creating considerable interest by the scientific and medical communities, as well as sport governing bodies, in examining the potential medical, legal, and ethical issues surrounding the use of these substances. All major national and international sports organizations have banned the illicit use of AAS by athletes.

TABLE 2 - Definition of terms associated with AAS.
Testosterone Hormone with strong anabolic and androgenic effects. produced by the testes in males. lesser quantities are produced by ovaries in women and by the adrenal glands in both sexes. the hypothalamus and pituitary regulate testosterone production in humans.
Testosterone derivative Chemically altered testosterone resulting in changes in solubility, pharmacokinetics, and/or clinical effects.
Testosterone esters Testosterone derivative with an ester group bound to testosterone to enhance oil solubility. This slows testosterone absorption and increases duration of effect, and allows for depot injections of testosterone
SARM Drugs designed to optimize anabolic tissue growth, while minimizing androgenic side effects. No current clinical applications, but research suggests potential therapeutic benefit in cancer, prostatic hyperplasia, and hypogonadism
Designer anabolic-androgenic steroids Synthetic steroids fabricated with intent to evade drug testing, or current laws prohibiting nonprescribed use
Testosterone enhancers/boosters Variety of substances purported to increase testosterone levels or effects, usually by increasing endogenous testosterone production or decreasing metabolism
HCG An analog to LH. Stimulates Leydig cells in the testes. Increases testosterone levels and sperm production
Clomiphene citrate (Clomid) Estrogen receptor modulator. Increases LH production. Has been shown relieve hypogonadal symptoms and maintain testosterone levels in men with symptomatic hypogonadism for up to 3 yr
Kisspeptins Peptide that appears to be important for onset of puberty and regulation of sperm production. Current evidence not definitive in regards to effects on androgen production in humans.
SARM, selective androgen receptor modulators; HCG, human chorionic gonadotropin.


Anabolic-androgenic steroids use has been examined extensively in various chapters, books, meta-analyses, and reviews (5–12). The effects of testicular extracts and castration on animals and humans have been a source of fascination for thousands of years (13,14). Suggestions that the consumption of testis tissue could improve impotence were noted ~140 BC (13). The mid 1700s to late 1800s marked a time where interest in testicular endocrinology increased (14). Table 3 depicts a brief historical timeline of some key events in AAS use in athletes. Testosterone was synthesized and biochemically described in the late 1920s and 1930s, and a host of different synthetic variations have been developed since (5,15,16). Testosterone or AAS use by athletes began in the 1940s and 1950s, and increased considerably thereafter, culminating in high usage during the 1968 Olympic Games (5,6). It has been speculated that the first appearance of AAS use among female athletes dates back to the late 1950s/early 1960s in Soviet track and field athletes (17).

TABLE 3 - Timeline of some key historical events related to AAS use.
Year Event
1889 Brown-Sequard suggest increases in muscle strength and endurance can occur following the injection of testicular extracts over a span of 2 wk
1896 Zoth and Pregel first suggested androgen use in athletes and investigated effects of testicular extracts on muscular strength and athletic performance
1927 Fred Koch and Lemuel McGee (University of Chicago) isolated an impure but potent form of T by pulverizing several tons of bull testicles
1928 The IAAF were first to ban doping agents
1935 Testosterone was isolated and the first two papers on testosterone synthesis were published—oral and injectable preparations were available to the medical community shortly thereafter—Kochakian reported T stimulates anabolism and suggested therapies could be useful for several disorders
Early 1940s Case studies suggested that human subjects were given testosterone in Germany and undocumented reports suggested AAS was administered to German soldiers during World War II
1942 Samuels, Henschel, and Keys published “Influence of methyl testosterone on muscular work and creatine metabolism in normal young men” in the Journal of Clinical Endocrinology and Metabolism—an early study investigating AAS in men
1945 De Kruif published “The Male Hormone” and suggested interest in athletes using testosterone to see the beneficial effects
Late 1940s West Coast bodybuilders began experimenting with T preparations
1952 Legendary strength athlete and coach Bob Hoffman of York Barbell speculates that Soviet athletes were using hormones during the Olympic Games
1954 Dr. John Ziegler was told by Soviet coaches that Soviet Weightlifters were using testosterone—he returned to United States and experimented on himself along with some weightlifters
1958 Ciba Pharmaceutical Company manufactured Dianabol—soon thereafter Dr. Ziegler began administering the drug to some of the York Barbell Weightlifting team
1963 Reports of NFL players first using AAS
1964 Androgen use increased greatly primarily in strength and power sports
1965 Oral Turinabol was synthesized by a German state-owned pharmaceutical company
A few scientists gained interest in studying AAS and performance in men as 2 studies were published between 1965 and 1969
1967 The IOC established a medical commission and developed a list of prohibited substances and methods
1968 Large increases in AAS use was seen including stacking and doses exceeding 2–5 times therapeutic doses—estimated that at least 1/3 of US track & field team and most of the German team used drugs in the 1968 Olympics
1969 The editor of Track & Field News (John Hendershott) called AAS the “Breakfast of Champions”
1973–1974 First testing procedures for androgens proposed radioimmunoassay and gas chromatography and mass spectrometry (RIA, GC-MS) and used in 1974 at the Commonwealth Games in Auckland New Zealand where 9 of 55 samples testing positive for androgens
1976 Drug testing instituted at the Olympic Games in Montreal—only 8 of 275 tests were deemed positive despite the majority of athletes admitting to using AAS in training—athletes began shifting to T from AAS as a result of drug testing
1976 The ACSM National Conference included a symposium and roundtable meeting on AAS in sports—two polarized groups evolved: those who thought AAS were “fool’s gold” or “myth” versus those who understood the ergogenic potential of the drugs—the prevailing medical opinion was that AAS were ineffective until the 1980s (possibly to dissuade use in part) which lead to mistrust between athletes and the medical community leading athletes to the black market for drugs and information
1977 The ACSM publishes the “Position statement on the use and abuse of anabolic-androgenic steroids in sports”—concluded that “… there is no conclusive evidence that extremely large doses of anabolic-androgenic steroids either aid or hinder performance …”
1980 Dr. Manfred Donike developed a method for testing testosterone—the 6:1 T:E ratio
1981 1st edition of the Underground Steroid Handbook (by Dan Duchaine [nicknamed “The Steroid Guru”]) was published
1982–1983 Methods to circumvent T:E ratio (i.e., use of hCG, clomiphene, epitestosterone, and timing of T administration) were used to enable doping without detection
1984 ACSM National Conference included symposium on “Drug Use in Sports” with >12 scientific presentations with several focusing on AAS in athletes
1987 The ACSM publishes an updated position stand “The use of anabolic-androgenic steroids in sports”—revised position to AAS in the presence of an adequate diet and training can contribute to increases in lean body weight and muscular strength
1988 Testing for masking agents and diuretics begins—US government passes the Anti-Drug Abuse Act which made distribution or possession of AAS for nonmedical reasons a federal offense
1990 US government passes Anabolic Steroid Control Act—inserted 27 AAS and related drugs as Class III drugs where simple possession could result in incarceration
1994 US Congress passes Dietary Supplement Health and Education Act to protect consumers from certain substances
2001 The WADA was formed
2002 The advent of designer AAS began
2004 The Anabolic Steroid Control Act is revised to include 26 new compounds including prohormones
2005 T:E ratio lowered to 4:1 by WADA for a positive doping test
Constructed from various sources (1,5,6,9,12,15,16).
E, epitestosterone; IAAF, International Amateur Athletics Federation.

The sophistication of AAS use by athletes in the late 1960s was characterized by a host of different “stacking routines” (i.e., the consumption of two or more drugs in an attempt to improve the response) using various oral and injectable AAS preparations (5). Initially, many physicians did not believe AAS improved performance, and the International Olympic Committee (IOC) did not include AAS on the banned substance list. The ACSM adopted this position in their first AAS position stand in 1977 but later corrected in the 1987 publication (1). Although the 1970s marked a time where AAS use was known mostly among competitive athletes, the 1980s marked a time where AAS use spread well beyond athletics to gyms, health clubs, and public awareness of AAS use increased. The Anti-Drug Abuse Act (1988), Anabolic Steroid Control Act (1990, 2004), and Dietary Supplement Health and Education Act (1994) were enacted, in part, to stem the growing use of AAS. Only a few studies (~17) on AAS use and strength/hypertrophy increases were conducted before the 1980s, and these cumulatively showed minimal effects in untrained men, but significant responses in trained men, despite doses less than that used by many athletes (6,7,10). The sophisticated protocols and array of drugs used recreationally and by athletes remained a “black box” from a research perspective.

Of current concern is the ease by which AAS users may obtain AAS via the Internet and the proliferation of men’s health clinics. In addition to the use of AAS by competitive athletes, a growing segment of AAS users are nonathletes. Management of men with damaged hypothalamic-pituitary-gonadal regulatory pathways became a new area of medicine resulting in indiscriminate AAS use (18). Interest in AAS persists as research identifies new information regarding the performance and health aspects of the drugs and through stories of purported use in the sports world. The World Anti-Doping Agency (WADA) has developed new antidoping measures, including blood sampling, guidelines for international information gathering and sharing and revamping their “Athlete Biological Passport” guidelines. While AAS use in sports continues, increases in AAS use in the general population appear to have outpaced athletic use in the last decade (19).


Peer-reviewed studies examining the frequency of illicit AAS use have declined in the past decade despite concern over the growing AAS epidemic in the United States. These studies often rely on self-reports and are fraught with sampling bias, small sample sizes, possible confusion regarding supplement and AAS use, and suboptimal ascertainment (5). Many AAS users are secretive, with one survey finding that 56% of respondents would not disclose their physicians’ use (20). Athletes may be unwilling to discuss their use with researchers even when anonymity and confidentially are guaranteed for fear it may jeopardize their career; thus, leading to differences in what athletes reported on surveys versus their actual activities (21).

In 2014, the National Institute on Drug Abuse estimated that 1.3 million Americans were AAS users, while the Endocrine Society estimated between 2.9 and 4.0 million Americans have used AAS at some point in their lives (18,22,23). Other reports showed that the number of users might be as high as 4 million men in the United States, with ~100,000 new AAS users annually (6,23,24). The age of onset of use begins later than most drugs, with only 6% of users starting before 18 (23).

Although the general public and medical communities attribute AAS use primarily to competitive athletes (6), research does not support this misperception. Muscle dysmorphia (“megarexia”) is a dominant risk factor for illicit AAS use and indicates that AAS use is often used in pursuit of a more muscular appearance rather than for enhanced athletic performance (25). Recreationally active individuals age 15 to 24 yr are more likely to use AAS than athletes participating in organized sport (26). However, reports on the prevalence of illicit AAS use in athlete and nonathlete populations are widely variable. Anabolic-androgenic steroids have been reported in 9% to 67% of elite athletes, while reports of AAS use among gym attendees ranged from 3.5% to 80% (27). In all areas, men report higher prevalence than women, although the prevalence in women is increasing (28). Studies in girls have shown prevalence rates between 0.4% and 1.0% in adolescents, ~1.2% in collegiate athletes, and ~10.3% in elite athletes (27). Others have reported AAS use in young athletes ranging between 0.6% and 6.6% in teenage boys, 0.0% to 3.3% in teenage girls, and between 0.8% and 9.1% for collegiate male athletes (29–32). Peer-reviewed studies report the highest prevalence of use in weightlifters, powerlifters and bodybuilders, with rates ranging from 33.3% to 79.5% (31,33).

Several studies have examined sport and activity participation among self-reported AAS users. A survey study of >500 male AAS users (mean age of 29) showed ~70% were recreational exercisers versus 12% competitive bodybuilders, 8% competitive weightlifters, and 9% competitive athletes in other sports (34). Participation in high school sports was not associated with an increased risk of AAS use (34). A survey of 12 female AAS users indicated that 33% of the women were recreational users, while 67% participated in competitive bodybuilding and weightlifting. These women used a polypharmacy approach, but their weekly dose was lower than male AAS users (35). Female users were less likely to stack, more likely to pyramid and less likely to inject AAS than male users (35).

Rates of AAS use in athletes are sometimes inferred from rates of positive doping tests. However, this data has some inherent limitations, including ongoing updates to banned substances lists, variable drug testing methodologies, and variable lists of targeted substances tested by organizations that do not follow WADA protocols. It has been estimated that drug testing alone may underestimate drug use in elite athletes by 8-fold (21). The Anti-Doping Administration and Management System maintained by WADA now allows any sports body to share drug testing information. While AAS use in particular divisions, such as men’s vs women’s and underage athletes is still difficult to obtain, the testing databases now include much larger numbers of athletes than in the past. Anabolic agents constitute 87% of atypical findings reported by WADA and 46% of all adverse analytical findings (International Amateur Athletics Federation) (36,37). Stanazolol and nandrolone have the highest number of AAF at 20% and 14%, respectively, while an “unidentified anabolic agent” (e.g., “designer” AAS) was the third most common at 11% (36).

The true nature of AAS use and abuse in athletes and recreationally trained individuals is difficult to discern and is often underestimated. In addition to surveys and doping results, other sources of information on AAS use include investigated journalism and government hearings. Unfortunately, all of these methods have significant methodological issues that reduce their estimation accuracy (17). Journalists have interviewed current and former athletes, coaches, team physicians, and trainers whose estimate of AAS use in sports is much higher than survey reports. There has been an inconsistency between the number of individuals demonstrating signs of AAS use and the statistical prevalence generated via surveys. Drug testing is often limited by circumventing positive tests and has done little to quantify “real-life” use or dissuade AAS use at high levels of competition. Obtaining accurate measures of AAS use in athletes is difficult given the challenges of reducing bias; testing issues, and sincerity needed during interviews and survey completion, for example, fear of accountability, fear of loss of potential income or suspension, or fear of being perceived as a cheater or athlete who needed drugs to be successful.

Attempts have been made to identify the type of individual prone to using AAS (38–40). Hildebrandt et al. (39) reported 4 clusters of users from highest to lowest risk, each with different levels of motivation for AAS use: 1) polypharmacy (i.e., use of multiple drugs) approach with high risk (~11%); 2) fat burning (~17%); 3) muscle building (~21%); and 4) low-risk use designed to reduce fat and build muscle (~52%). Others have reported a four-level typology: 1) expert type (exemplifies controlled risk-taking, is knowledgeable about AAS and fascinated with effects on the human body, is scientific and may be focused on muscularity); 2) athlete type (interested in performance enhancement and is competitive); 3) well-being type (interested in looking and feeling good with low risk-taking); and 4) YOLO “You Only Live Once” type (is haphazard using risky behavior, quick improvements, impressing others and peer recognition is important) (38,40). Despite the typology, athletes’ motivation to use AAS is multi-faceted and influenced by many factors (Table 4).

TABLE 4 - Reported motivators for AAS use by athletes.
↑ muscle mass, strength, power, endurance, speed, fitness levels, energy, blood volume, BMD Encouragement from friends, family, coaches to do so
↑ sex drive ↑ recovery between workouts and competitions, pain tolerance
↑ athletic success, chances of winning, individual performance, strive to maximize potential Fear their opponents are using and they must use AAS in order to maintain competitive balance
↑ social recognition, peer acceptance, self-confidence, aggression, mental intensity and alertness Lack of fear in getting caught or being held accountable by sport governing bodies
↑ financial gain, chance at scholarship, notoriety ↓ body fat and injury risk, ↑ weight loss
Improve appearance, self-esteem, mood, personal protection ↓ aging effects, likelihood of muscle dysmorphia
Modified from (34,41).

Several extensive, national studies indicate an overall downward trend in lifetime AAS use among adolescents since peaking in the early 2000s (42). Monitoring the Future (MTF) is administered annually to a sample of 8th, 10th, and 12th grade students (43). The MTF reported peak prevalence rates for lifetime AAS use in 2000 to 2002 of 3% to 4% compared with 2018 data in Table 5 (i.e., ~1%–3%). The Youth Risk Behavior Survey (YRBS) is administered annually to a sample of high school students and reports an overall prevalence of 2.9% in 2017 (See Table 6), after peaking in 2001 at 5% (44). Although the YRBS is widely cited, concern has been raised that the term “steroid” is vague and potentially conflated with corticosteroids or steroid-like dietary supplements (45). Surveys that delineate the type of steroid show usage rates that are markedly lower than those seen in the YRBS data (45). Although AAS use rates in adolescents are low, ~1 in 8 AAS users initiates their use before age 18 (23). Several correlates of increased AAS use risk in this group include fitness-related activity (46,47); weight-related concerns (perceptions of very underweight or overweight status) (48,49); sexual preference and gender identity (25,44); and race and ethnicity (43,44). Some view current AAS use as an epidemic given the emergence of AAS availability through internet/mail order and “backroom” laboratories (18,50).

TABLE 5 - Lifetime prevalence data from the 2018 MTF survey based on answers to the following query: “Anabolic steroids are prescription drugs sometimes prescribed by doctors to treat certain conditions. Some athletes, and others, have used them to try to increase muscle development.” The question then asks, “on how many occasions have you taken steroids on your own—that is, without a doctor telling you to take them?”
8th Grade 10th Grade 12th Grade
Overall 1.1% 1.2% 1.6%
Male 1.0% 1.3% 2.2%
Female 1.1% 0.9% 0.9%
White 1.0% 1.1% 1.4%
African American 1.2% 1.3% 2.9%
Hispanic 1.1% 1.0% 1.3%

TABLE 6 - Lifetime prevalence data from the 2017 YRBS survey based on answers to the following query: “During your life, how many times have you taken steroid pills or shots without a doctor’s prescription?”
Overall Females Males
Ever used steroids 2.9% 2.4% 3.3%
By race/ethnicity
 Black 2.2% 1.8% 2.7%
 White 3.6% 2.6% 4.6%
 Hispanic 3.5% 3.1% 3.8%
By sexual contact
 Opposite sex only 3.9% 2.6% 4.9%
 Same sex or both sexes 8.0% 7.2% 10.1%
 No sexual contact 0.7% 1.0% 0.5%


Patterns of AAS use in athletes and resistance-trained populations vary greatly and depend upon: AAS type, self-administration routes, dosages, cycling patterns and durations, and ancillary drugs. A “polypharmacy approach” is commonly used where supraphysiologic doses of injectable and oral AAS are stacked and pyramided progressively in cycles, while ancillary drugs are consumed to minimize side effects, promote other areas of health and fitness, and/or enhance T levels during off-cycles, or periods in between cycles (Table 7). Figure 1 depicts survey results from two studies on usage patterns for >2400 predominately male AAS users (34,41). These studies indicated that 99.2% of users reported using injectable AAS or a combination of oral and injectable AAS, and >40% used ancillary drugs, such as antiestrogens (41). Ip et al. (34) reported that 79% of AAS users “stacked” drugs, 18% used the “pyramid” approach (i.e., where drug intake is progressively increased, plateaus, and then is decreased or tapered until the end of the cycle), and only 9% thought physicians and pharmacists were knowledgeable about AAS. Interestingly, AAS users spent an average of 268 ± 472 h researching AAS prior to use (34).

TABLE 7 - AAS and ancillary drugs used by athletes.
Anabol 4–19 (norclostebol acetate) Myagen (bolasterone)
Anadrol (oxymetholone) Parabolan (trenbolone hexahydrobenzylcarbonate)
Anavar (oxandrolone)
Cheque drops (mibolerone) Primobolan (methenolone)
Dianabol (methandrostenolone) Primobolan depot (methenolone enanthate)
Deca durabolin (nandrolone decanoate) Proviron (mesterolone)
Durabolin (nandrolone phenylproprionate) Testosterone (androderm, AndroGel, Striant, testoderm)
Dynabol (nandrolone cypionate)
Dynabolan (nandrolone undecanoate) Testosterone blend (Sustanon, Omnadren, Equitest, Sten, Testoviron)
Equipoise (boldenone undecanoate)
Finajet (trenbolone acetate) Testosterone cypionate (Depo-Testosterone)
Genabol (norbolethone) TE (Delatestryl)
Halotestin (fluoxymesterone) Testosterone proprionate (Oreton)
Madol (desoxymethyltestosterone) Testosterone suspension (Andronaq)
Masteron (drostanolone) Tetrahydrogestrinone
Metandren (methyltestosterone) Trenabol (trenbolone enanthate)
Metribolone (methyltrienolone) Turinabol (chlorodehydromethyltestosterone)
Miotolan (furazabol) Winstrol (stanozolol)
Banned Prohormone/OTC Steroids
1-Testosterone Epi-DHT
4-Hydroxytestosterone 19-Norandrostenediol
Boldione 19-Norandrostenedione
Androstenediol, 1-,4-Androstenediol Halodrol
Androstenedione, 1-, 5-Androstenedione Superdrol
1-Androsterone Methylhydroxynandrolone
Androstanolone Prostanozol
Epiandrosterone, 1-Epiandrosterone
Andarine (S4) RAD-140 (testolone)
Ligandrol (LGD-4033) YK-11
Ostarine (enobosarm)
Arimidex (anastrozole) Faslodex (fulvestrant)
Aromasin (exemestane) Femara (letrozole)
Clomid (clomiphene citrate) Fertodur (cyclofenil)
Cytadren (aminoglutethimide) Lentaron (formestane)
Evista (raloxifene) Nolvadex (tamoxifen citrate)
Fareston (toremifene citrate) Teslac (testolactone)
Ancillary Drugs
Accutane (isotretinoin) Lasix (furosemide)
Cardarine Cytomel (liothyronine sodium)
Abuterol Synthroid (levothyroxine sodium)
Clenbuterol Human growth hormone (somatotropin, protropin, nutropin, humatrope, genotropin, norditropin)
Catapres GHRH secratogues (CJC-1295, Mod GRF 1–29, Egrifta [tesamorelin acetate], Geref [sermorelin acetate])
Aldactone (spironolactone)
Dyrenium (triamterene)
Hydrodiuril (hydrochlorthiazide) Growth hormone releasing peptides (Lenomorelin [Ghrelin]. GHRP-1 to  GHRP-6, hexarelin [examorelin], ipamorelin,  ibutamoren mesylate [MK-677])
Probenecid (masking agent)
Synthol (site enhancer)
GH fragments (HGH fragment 176–191, AOD-9604)
IGF-1 and variants (Increlex [mecasermin])
Mechano growth factor
THG, tetrahydrogestrinone.

Usage patterns of steroids in predominantly male AAS users; data from (34,41).


Testosterone is the principal androgen and has both androgenic (masculinizing) and anabolic (tissue building) effects. Testosterone is synthesized from cholesterol via the Δ-4 or Δ-5 pathways through the sequential action of several enzymes (Fig. 2). In men, >95% of T is synthesized in the Leydig cells of the testes (with smaller adrenal contributions) under control of the hypothalamic-anterior pituitary-gonadal axis where gonadotropin-releasing hormone stimulates the release of luteinizing hormone (LH). Healthy men produce ~4 to 9 mg of T per day (10–35 nmol·L−1) whereas women have approximately 0.5 to 2.3 nmol·L−1 of circulating T in the blood (5). Gonadotropin-releasing hormone function is under the control of hypothalamic neuropeptides, such as kisspeptins, neurokinin-B, dynorphin-A, and phoenixins (51). In women, androgens are produced primarily by the ovaries and adrenal glands (52). Skeletal muscle produces small amounts of androgens (53). Testosterone circulates in the blood bound to sex hormone-binding globulin (44%–60%), albumin, orosomucoid, and cortisol-binding globulin. Testosterone and other 19-carbon androgens can be converted to 5α-dihydrotestosterone (DHT) by the action of steroid 5α-reductase or converted to estradiol or estrone by the aromatase enzyme. The liver inactivates T, and the resultant metabolites are excreted in the urine.

Testosterone (and related steroid hormones) biosynthesis from cholesterol (File:Steroidogenesis.svg [Internet]. Wikimedia Commons, the free media repository; 2020 Sep [cited 2020 Sep 30]. Available at:

Androgens perform many ergogenic, anabolic, and anticatabolic functions in skeletal muscle and neuronal tissue, leading to increased muscle strength, power, endurance, and hypertrophy in a dose-dependent manner (54). A meta-analysis concluded that short-term AAS use increases muscle strength substantially more than placebo and that strength gains and muscle hypertrophy are greater in trained individuals than in nontrained individuals (55). Gains in body mass and lean body mass (LBM) of ~5% to 20% from AAS use have been reported (56). Figure 3 depicts some physiological ramifications of androgens that could affect physical performance. However, the findings of controlled clinical trials of T and other AAS may differ from the practical experience of athletes due to the inclusion of mostly untrained subjects in controlled clinical trials; the use of lower doses of T or AAS in clinical trials than those used by many athletes; the use of multiple AAS in stacks with other drugs over long periods; and differences in nutritional patterns, training programs, and study design (5,27).

Physiological and molecular-level consequences of AAS usage that may affect physical performance. NT, neurotransmitter; CSA, cross-sectional area; AR, androgen receptor; GC, glucocorticoid; GH, growth hormone; Acvr2b, activin receptor type-2B; TG, triglyceride; RBC, red blood cell; Hgb, hemoglobin; S6K1, ribosomal protein S6 kinase beta-1; ERK1/2, extracellular signal-regulated kinase 1 and 2; PI3, phosphoinositide 3-kinase; AKT, protein kinase B; Ankrd1, ankyrin repeat domain 1; MuRF1, muscle RING-finger protein-1; MGF, mechanogrowth factor; MCT1/4, monocarboxylate transporter 1 and 4; RFD, rate of force development.

Exogenous androgens are often administered orally or parenterally but are also available in cream, nasal spray, buccal, subcutaneous pellets, patches, and gel. Orally administered T is absorbed well but is degraded rapidly. The esterification of the 17-beta-hydroxyl group (e.g., T enanthate, cypionate, decanoate, undecanoate, propionate) makes the androgen more hydrophobic, causing a slow release from the muscle into circulation, increasing the duration of action. When administered intramuscularly, the androgen ester is slowly absorbed into the circulation, where it is then rapidly de-esterified by esterase enzymes to T. Intrinsic potency, bioavailability, and rate of clearance from the circulation are determinants of the biological activity. Other oral and injectable AAS are T, DHT, or 19-nortestosterone derivatives (e.g., methyltestosterone, methandrostenolone, fluoxymesterone, nandrolone decanoate, oxandrolone, trenbolone, stanozolol, and other designer-AAS).

An important and relevant question is how long the effects of a dose of AAS would last in an athlete? That is, how long would potential strength gains or gains in muscle mass persist? The answer to the question is undoubtedly complex and dependent on the AAS being used and their potency (see Fig. 1), the history of AAS in the athlete (57), the athlete’s training age, sex (58,59), and potentially the developmental stage of the athlete relative to puberty and adulthood (i.e., 18 yr of age). The literature in this area is, unsurprisingly, sparse, but some studies suggest that the effects of AAS persist for weeks after taking the steroids, but at ~12 wk after taking AAS that the effects, at least insofar as strength and muscle mass are concerned, are largely absent (55,60). For example, Giorgi et al. (61) showed that testosterone enanthate (TE) (3.5 mg·kg−1) administration for 12 wk during training resulted in greater increases in strength, muscle girth, and muscle thickness than a group given a placebo. However, after 12 wk without TE administration, but while still training, there was a reversion of strength and muscle in the TE group to levels no different from the placebo group. In contrast, others have observed preservation of AAS-induced gains in strength and LBM that persist after AAS usage has ceased, at least in the short-term (62).

Persistent and long-term (at least 5 yr) AAS use in a mixed sample of strength (strongman and powerlifters) and aesthetic sport (bodybuilding) athletes has been reported, in comparison to non-AAS, to result in persistent (i.e., in comparison to a matched group) elevations in LBM, muscle fiber area, capillary density, myonuclei density, and strength that were dose-dependent (57). The observation that long-term AAS use results in increased myonuclei density (57) suggesting that a much longer ‘muscle memory’ is perhaps possible in AAS users, particularly those who use AAS early in life. Evidence for such a mechanism comes from preclinical models (10), where young mice were exposed to AAS and subsequently increased their myonuclear content, resulting in a substantial hypertrophic advantage later in life. The authors of this work (63) even went so far as to suggest, “… the benefits of even episodic drug [AAS] abuse might be long lasting, if not permanent, in athletes. Our data suggest that the World Anti-Doping Code calling for only 2 yr of ineligibility after… [a doping violation for AAS] use… should be reconsidered.” Support for whether an AAS-induced increase in myonuclear number in humans is lacking; however, if present, then AAS-induced increases in myonuclei are theoretically advantageous to an athlete even if strength and lean mass advantages have been lost.

Residual effects of endogenous testosterone exposure in testosterone-suppressed transgender females are areas of active study and debate. These effects vary greatly depending upon the developmental stage of treatment initiation and will be much less when treatment is initiated before pubertal onset. There is a dichotomy when looking at measures of prepubertal athletic performance. Studies evaluating age-group athletic records report no significant differences in top age-group performances between boys and girls younger than 10 to 12 yr old (64–66). However, some studies evaluating more specific measures of strength and aerobic capacity reveal an 8% to 10% advantage in prepubertal biologic males relative to females, even after normalizing for body size (67,68). These performance differences may be residual effects from higher testosterone levels during early infancy (e.g., “mini-puberty”) and/or nonandrogenic genetic factors. Currently, there are no data on the durability of these performance differences in transgender females who start gender-affirming treatment before puberty.

Postpubertal testosterone suppression has variable impacts on performance-related parameters. Within 3 months of starting hormone suppression, hematocrit decreases by 4% to within normal values for cisgender females (69). A recent systematic review also evaluated evidence to date regarding treatment-related reductions in muscle size, strength, and LBM (70), summarized in Table 8. Although the changes documented in Table 8, along with an increase in fat mass, may contribute to significant reductions in athletic performance, the current lack of data in active or athletic populations makes the magnitude of these changes difficult to assess.

TABLE 8 - LBM, strength, and muscle size of cisgender females and transgender females.
Cisgender Males (Reference) Cisgender Females (Relative to Cisgender Males) Transgender Females (Pretreatment, Relative to Cisgender Males) Reductions in Transgender Females with T Supression (12 mo Posttreatment)
LBM 100 70% 94%–92% −1% to 5.5%*
Muscle CSA 100 94%–88% −1.5% to 12%
Strength 100 64% (handgrip) 90%–86% (handgrip) 1.5% to –7% (handgrip)
The right column shows changes in transgender females after 12 months of testosterone suppression (70).
*One study reported changed from 12 to 31 months posttreatment of −4.7%; summarized in (70).


Androgen signaling at the tissue level occurs primarily genomically through the classical androgen receptor (AR) with multiple levels of integration with other anabolic/catabolic pathways (71). Testosterone, DHT, and other AAS bind to cytoplasmic AR (72). Androgen receptor activity is altered at various sites; phosphorylation may augment androgen/AR transcriptional action (in the presence or absence of androgens) (73). Androgen receptor signaling is activated primarily by ligand binding, but under some circumstances through ligand-independent mechanisms (e.g., insulin like-growth factor-1 [IGF-1] induced mitogen-activated protein kinase-ERK1/2, p38 and c-Jun N-terminal kinase phosphorylation) (74) that may sensitize it to anabolic signals in the presence of low androgens (75). The AR is up-regulated following resistance training and short-term androgen administration (54).

Upon androgen binding to the ligand-binding domain (LBD) of the AR, the liganded AR undergoes phosphorylation, dimerization, and conformational changes, recruits coregulators, and translocates into the nucleus, where it regulates the transcription of androgen response elements (ARE) of the androgen-responsive genes (76). Androgen binding activates and stabilizes the AR, which is selectively induced by T, DHT, and AAS (77). Greater stability is seen with DHT than T (78). Binding affinity for the AR varies between androgens. Nandrolone and metenolone have a higher binding affinity than T, while stanozolol, methandienone, and fluoxymesterone have a lower binding affinity than T; and oxymetholone has a minimal binding affinity (79). Androgen binding to the AR completes the pocket that serves as a recruiting surface for co-activators (80). Some co-activators include BAF57 and 60a, SRC1 and 3, and ARA50 and 74. The activity of these co-regulators and the role of T in ribosome biogenesis may be important in mediating the anabolic effects of AAS on skeletal muscle.

Androgen/AR binding activates signaling through the Wnt-β-catenin pathway. The presence of T (in a dose-dependent manner) increases AR-β-catenin interaction and transcriptional capacity (81). Androgens promote myogenesis via multiple pathways. Satellite cells and myoblasts express AR and androgen binding, increasing satellite cell activation, proliferation, mobilization, differentiation, and incorporation into skeletal muscle (82). Androgens increase myogenesis via increased Notch signaling of satellite cells (83) and increased expression of IGF-1 (84). Androgen binding to AR on pluripotent mesenchymal cells increases their commitment to myogenesis and inhibits adipogenic differentiation via β-catenin signaling (85,86). Testosterone upregulates follistatin expression (which blocks signaling through the TGFβ-SMAD 2/3) and increases myogenic differentiation (82,84,86–88). Androgens may be anticatabolic by decreasing glucocorticoid receptor (GR) expression, interfering with cortisol binding, or the AR-T complex may compete with the cortisol-GR complex for cis-element binding sites on DNA (88–91).

Nongenomic AR signaling is rapid, with short latency periods acting independently of nuclear receptors (92). Nongenomic effects are thought to be mediated by direct binding to a target molecule, through intracellular AR activation (i.e., Src kinase), through a transmembrane AR receptor, or via changes in membrane fluidity (92). Nongenomic signaling involving G-protein 2nd messenger system and may either increase intracellular calcium concentrations via PI3K, phospholipase C, and IP3 signaling (93), stimulate the activation of mitogen-activated protein kinase signaling (94), and mammalian target of rapamycin pathway signaling (95). Cross-talk between IGF-1 signaling and nongenomic AR signaling appears critical to mediating some anabolic effects (96). Nongenomic signaling occurs rapidly within seconds to minutes, much faster than classic genomic signaling, which takes hours and requires the constant presence of androgens to maintain intracellular signaling.


Investigations examining the safety of androgen use in various populations have been largely inadequate as there is tremendous variability in androgen dosages and patterns of use, including stacking of multiple AAS and concurrent use of accessory drugs (5). Figure 4 depicts the variety of adverse physiological and psychological effects associated with AAS use. These include relatively rare effects and those that are commonly expected, particularly with long-term AAS abuse (30).

Potential adverse physiological and psychological effects associated with AAS use. TC, total cholesterol; ApoA1, apolipoprotein A1; LV, left ventricle; ECG, electrocardiogram; T, testosterone.

A survey of 500 AAS users (99% male) who had extensive experience (8 wk to 25 yr with 95% having >1–3 yr of AAS use) with high doses showed that 23% to 64% of respondents reported minor side effects (e.g., testicular atrophy, acne, fluid retention, insomnia, sexual dysfunction, gynecomastia) (97). Other common effects of AAS use include deleterious changes in cardiovascular (CV) risk factors: decreased plasma high-density lipoprotein (HDL) cholesterol (98), changes in clotting factors (99), and mood or psychiatric disturbances (79). Suppression of the hypothalamic-pituitary-testicular axis and spermatogenesis may result in infertility, while elevations in liver enzymes may reflect liver dysfunction (100–102). In one study, competitive athletes who used AAS during their competitive careers were more likely to die prematurely than athletes who did not (103). The use of nonsterile needles and needle sharing practices for intramuscular injections increase the risk for infection, muscle abscess, sepsis, and communicable diseases, such as human immunodeficiency virus (HIV) and hepatitis B and C (5).

Although CV effects are commonly reported with AAS use, based on an extensive review, the FDA concluded that “...the studies have significant limitations that weaken their evidentiary value for confirming a causal relationship between testosterone and adverse cardiovascular outcomes” (104). Part of the difficulty in studying the effects of AAS on CV health is that the impacts of androgens on CV function vary with dose, method of administration, and aromatization potential (5). Parenteral administration of physiologic T replacement doses are associated with CV function and vary with dose, method of administration, and aromatization potential (5) with small decreases in plasma HDL, with little or no effect on total cholesterol, low-density lipoprotein (LDL) or triglycerides (105–107). However, supraphysiologic T doses are associated with significant reductions in HDL (108,109). Orally administered 17-alpha-alkylated, nonaromatizing AAS produce greater reductions in HDL and increases in LDL than when AAS are administered parenterally (110). Angell et al. (111) reported that self-administering AAS (median daily dose = 228 mg) for >2 yr was associated with smaller longitudinal LV strain, right ventricular (RV) ejection fraction, and altered diastolic function compared with nonusers. Others showed impaired RV free wall strain and strain rate associations with AAS abuse in competitive bodybuilders (112). D’Andrea et al. (113) showed associations between AAS use (~31 wk; weekly dose = 525 mg) and left atrial impairment (a marker of diastolic burden) in elite bodybuilders compared with nonusers. An increase in left ventricular (LV) mass occurs during resistance training (114–116); however, potential additional effects from AAS use in humans are unclear. In rats, only high T doses (up to 20 mg per kg body mass) induced cardiac hypertrophy with an impaired contractile process (117).

Deceased men who had used AAS showed greater cardiac mass than nonusers (118). Multivariate analysis indicated that increases in heart size were explained by increased body mass and by AAS use. Risk for adverse cardiac events associated with LV mass is supported by case reports detailing sudden death among power athletes who self-administered AAS (100,119–122). Case reports are largely anecdotal, and a causal relationship between AAS use and risk of sudden death has not been established. Strength/power athletes self-administering AAS have short QT intervals but increased QT dispersion compared with endurance athletes with similar LV mass who have long QT intervals but do not have increased QT dispersion (123). The interval from the peak to the end of the ECG T wave (Tp-e), Tp-e/QT ratio, and Tp-e/QTc ratio increases in AAS users, suggesting a link between AAS and ventricular arrhythmias, which may increase the risk for sudden death (124).

Increases in liver enzymes, cholestatic jaundice, hepatic neoplasms, and peliosis hepatis are associated with the use of oral, 17-alpha alkylated AAS (102,125,126), but not with parenterally administered T or its esters (127). The association between liver toxicity and AAS use is based on increases in AST and ALT. These enzymes are not liver-specific and are often elevated from muscle damage after resistance exercise (101,128); thus, possibly overstating the risk of hepatic dysfunction (128,129).

Endogenous LH and follicle stimulating hormone secretion are suppressed during AAS use, with subsequent effects on testicular T secretion and sperm count (130,131). Depending on the dose and duration of AAS use, endogenous T, LH, and follicle stimulating hormone may take weeks to months to return to homeostatic levels (132), and the long-term effects are not well understood. High-dose androgen administration in men is associated with breast tenderness and enlargement, for example, gynecomastia (5,133), thought to result from peripheral conversion of androgens to estrogens in men administering aromatizable AAS (134). The prevalence of gynecomastia is unknown, but prevalence rates as high as 54% were reported in AAS users (5). The use of nonsterile needles and needle-sharing practices for intramuscular injections increases the risk for infection, muscle abscess, sepsis, and communicable diseases, such as HIV and hepatitis B and C (5).

There is no evidence that T causes prostate cancer, but testosterone replacement therapy (TRT) is associated with a small increase in prostate specific antigen levels in older men with low T, which increases the risk of urological referral for prostate biopsy (5). Because many older men harbor subclinical prostate cancer, a prostate biopsy may lead to subclinical low-grade prostate cancer detection. Notably, however, TRT increases the risk of prostate biopsy.

The psychological effects of AAS use have garnered much publicity, especially on issues of aggression and suicide. However, the evidence is inconclusive due to the lack of sensitivity of the research instruments used to measure aggressive behavior, large variability in RT programs, preexisting personality or psychiatric disorders, and prevalence of multiple high-risk behaviors and use of other substances, such as alcohol, psychoactive drugs, and dietary supplements (5). Interestingly, physiologic T replacement in hypogonadal men may improve mood and attenuate negative aspects of mood (4). Morrison et al. (135) reported that the aggression and anxiety-provoking influences of androgens in animals are likely a developmental phenomenon and that adult exposure may be anxiolytic over the long term. However, underlying psychological dysfunction may cause a greater susceptibility to AAS use, and high doses of AAS may provoke a “rage” reaction in some individuals with preexisting psychopathology (136,137). Self-administration of AAS may increase the risk for mood disorders, such as mania, hypomania and depression (136,138). Resting T concentrations are related to posttraumatic stress (PTSD), in which higher T is associated with a lower risk for PTSD (139). Further, long-term use of AAS in former weightlifters was associated with poor cognitive function and negative changes in brain morphology (140,141). Approximately 30% of illicit AAS users will develop AAS dependence, and there is some overlap between AAS dependence and the mechanisms and risk for opioid dependence (142,143). Sudden discontinuation of exogenous AAS use in those who are dependent or have suppressed endogenous production may result in severe depression and suicidality (142,143). A multidisciplinary and medically supervised treatment program is indicated for individuals with AAS dependence.

Women self-administering AAS may undergo masculinization and experience hirsutism, deepening of the voice, enlargement of the clitoris, widening of the upper torso, decreased breast size, menstrual irregularities, and male pattern baldness (144). Some of these adverse effects may not be reversible (5).

Many of the side effects in adults may be seen in adolescents, but information on use in children is scant. Exogenous AAS exposure in preadolescence triggers pubertal onset and may result in early epiphyseal maturation and closure, leading to loss of ultimate height potential (40). Although mild acne is common during adolescence (40), AAS use may result in severe nodular acne, particularly on the back and shoulders, which is often resistant to treatment.


Although athletes and recreational trainees have reported obtaining AAS from physicians for illicit purposes (26,33,50), several clinically approved uses of T exist. Of concern are potential illicit use stemming from a clinical prescription of T given the increased number of antiaging and wellness clinics. The sale of therapeutic T preparations in the United States quadrupled between 2001 and 2011 (145), and an estimated >2.3 million men received physician-prescribed T therapy as of 2013 (146). In military treatment facilities, the number of androgen prescriptions increased > twofold (23% per year) from 2007 to 2011, mainly in 35- to-44-yr-old men (147). Currently, therapeutic T is mostly used to treat primary (i.e., testicular failure) and secondary (i.e., reduced LH) hypogonadism (148). Androgen therapy has numerous clinical uses outlined in Table 9 (145,146). A substantial fraction of young men receiving T prescriptions are former AAS users trying to restore endogenous T production (149–151). The Endocrine Society Clinical Practice Guideline (148) details decision making regarding androgen therapy and the reader is referred to their specific guidelines on the diagnosis, treatment, and monitoring of hypogonadism in men (134).

TABLE 9 - Indications and contraindications for therapeutic use of testosterone.
 Male hypogonadism
 Examples: Testicular trauma/torsion/irradiation, cryptorchidism, orchiectomy,  Klinefelter syndrome, chromosome abnormalities, LH and follicle stimulating  hormone receptor gene mutations, androgen synthesis disorders, myotonic  dystrophy, hypothyroidism
 Examples: Irradiation/tumor of hypothalamus or pituitary, drugs/medications  (opioids, marijuana, glucocorticoids, AAS), alcoholism, sleep deprivation,  surgery, trauma, eating disorder/relative energy deficiency, Kallman syndrome,  Prader-Willi syndrome
 Mixed primary and secondary
 Examples: diabetes, obesity, HIV infection, chronic obstructive pulmonary disease,  chronic kidney disease, liver disease, aging, cancer
 Hypoactive sexual desire disorder in postmenopausal females
 Constitutional delay of growth and puberty
 Gender-affirming treatment for transgender males
 Cancer: prostate, breast, skin
 High prostate specific antigen
 Sleep apnea
 Venous thromboembolism
 CV disease
 Fertility problems

Testosterone replacement therapy has been shown to improve sexual activity (152–155), vertebral and femoral bone mineral density (BMD) and microarchitecture (156,157), hemoglobin content (158,159), LBM, maximal voluntary strength and physical function (160–164), and reduces body fat and BMI (162,165,166). There have also been reports of TRT reducing neuroinflammation and depressive symptoms (167–169), reducing blood pressure and improving lipid profiles (166), and neuronal regeneration (154,156,170–177), and may not change or improve cognitive function in older men (174,178,179). There is a low frequency of adverse events associated with TRT (2,148,153,180–190). However, all TRT should be accompanied by a structured monitoring plan (148). The Endocrine Society recommends evaluating symptoms, adverse events, lower urinary tract symptoms, and measurements of T levels, hematocrit, and prostate specific antigen at baseline, 3 to 6 months after starting treatment, and annually thereafter (148).

Testosterone and free T levels decline with advancing age after peaking in the second and third decades of life (191–194), leading to increased risk of sexual dysfunction; decreased muscle mass and strength, BMD, mobility; increased falls and fractures, late-life low grade persistent depressive disorder (dysthymia), and CV mortality (148,195). Low T is associated with an increased risk of diabetes, metabolic syndrome, and increased carotid artery intima-media thickness (196,197). Whether older men with age-related T decline should receive TRT remains a matter of debate. The Endocrine Society Guideline for TRT of hypogonadal men recommends against routinely prescribing T to all men, 65 yr or older, with low T levels (148). Decisions regarding TRT should be individualized after discussing potential risks and benefits in men with both symptoms suggestive of consistent T deficiency and burden of symptoms (e.g., low libido, unexplained anemia, osteoporosis) and presence of other co-morbid conditions that increase the risk of T treatment (148). The shared decision making should weigh the patient’s and clinician’s values. In male children, physiologic doses of T are used for brief periods to initiate pubertal development in those with constitutional delay of growth and puberty. Testosterone is needed permanently for children with congenital or acquired hypogonadism.

Recent interest has focused on the role of T in athletic performance in transgender and sexual developmentally distinct athletes. Individuals transitioning to females may require a therapeutic-use exemption for spironolactone, which is often used to block the androgen receptor and lower overall testosterone levels. Currently, trans female athletes subject to WADA testing must document subthreshold T levels for at least 12 months before being allowed to compete as a female. The IOC sets this threshold at <10 nM, and World Athletics (formerly the International Amateur Athletics Federation) at <5 nM. Interested readers can obtain a much deeper discussion of this topic in several reviews (198–200).


Anabolic-androgenic steroids include a wide spectrum of compounds that exert their effects through various mechanisms. Anabolic-androgenic steroid use is advantageous in athletic performance predominantly through enhancements in strength, power, increases in muscle mass, reduced recovery time, and other factors. Major competitive sporting bodies ban the use of AAS; however, the predominant area of AAS usage has now expanded into clinical scenarios, persons undergoing sexual reassignment, and by those interested in AAS for purely aesthetic enhancement. Thus, it is not only athletes who are using AAS to gain performance advantages but also other individuals for various reasons. Use for AAS to enhance athletic performance is banned, and coaches, trainers, and medical staff should monitor for signs of use. The use/abuse of AAS has several notable side effects with various consequences that are, in some cases, reversible. Coaches, parents, trainers, and medical staff need to understand why athletes might use AAS and provide educational programming in a preventive capacity. The position of the ACSM is that the illicit use of AAS for athletic and recreational purposes is, in many cases, illegal, unethical and also poses a substantial health risk. Nonetheless, TRT is used in treating various conditions, and clinicians may elect to use this therapy when medically necessary. The ACSM acknowledges the lawful and ethical use of AAS for clinical purposes and supports the physicians’ ability to provide androgen therapy to patients when deemed medically necessary.

This article is published as an official pronouncement of the American College of Sports Medicine and is an update of the 1987 ACSM position stand on the use of anabolic-androgenic steroids. Click here to download a slide deck that summarizes this ACSM pronouncement on anabolic-androgenic steroid use. This pronouncement was reviewed for the American College of Sports Medicine by members-at-large and the Pronouncements Committee.

Care has been taken to confirm the accuracy of the information present and to describe generally accepted practices. However, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from the application of the information in this publication and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication. The application of this information in a particular situation remains the professional responsibility of the practitioner; the clinical treatments described and recommended may not be considered absolute and universal recommendations.


1. American College of Sports Medicine position stand on the use of anabolic-androgenic steroids in sports. Med Sci Sports Exerc. 1987;19(5):534–9.
2. Shores MM, Matsumoto AM, Sloan KL, Kivlahan DR. Low serum testosterone and mortality in male veterans. Arch Intern Med. 2006;166(15):1660–5.
3. National Heart, Lung, and Blood Institute. Study quality assessment tools. Available at
4. Wang C, Alexander G, Berman N, et al. Testosterone replacement therapy improves mood in hypogonadal men—a clinical research center study. J Clin Endocrinol Metab. 1996;81(10):3578–83.
5. Hoffman JR, Kraemer WJ, Bhasin S, et al. Position stand on androgen and human growth hormone use. J Strength Cond Res. 2009;23(5 Suppl):S1–S59.
6. Kanayama G, Pope HG Jr.History and epidemiology of anabolic androgens in athletes and non-athletes. Mol Cell Endocrinol. 2018;464:4–13.
7. Nieschlag E, Nieschlag S. Endocrine history: the history of discovery, synthesis and development of testosterone for clinical use. Eur J Endocrinol. 2019;180(6):R201–12.
8. Morales A. The long and tortuous history of the discovery of testosterone and its clinical application. J Sex Med. 2013;10(4):1178–83.
9. Christou MA, Christou PA, Markozannes G, Tsatsoulis A, Mastorakos G, Tigas S. Effects of anabolic androgenic steroids on the reproductive system of athletes and recreational users: a systematic review and meta-analysis. Sports Med. 2017;47(9):1869–83.
10. Piacentino D, Kotzalidis GD, Del Casale A, et al. Anabolic-androgenic steroid use and psychopathology in athletes. A systematic review. Curr Neuropharmacol. 2015;13(1):101–21.
11. Frati P, Busardo FP, Cipolloni L, Dominicis ED, Fineschi V. Anabolic androgenic steroid (AAS) related deaths: autoptic, histopathological and toxicological findings. Curr Neuropharmacol. 2015;13(1):146–59.
12. Sessa F, Salerno M, Di Mizio G, et al. Anabolic androgenic steroids: searching new molecular biomarkers. Front Pharmacol. 2018;9:1321.
13. Kochakian CD, Yesalis CE 3rd. Anabolic-androgenic steroids: a historical perspective and definition. In: Yesalis CE 3rd, editor. Anabolic Steroids in Sports and Exercise. Champaign, IL: Human Kinetics; 2000. pp. 17–49.
14. Taylor WN. Anabolic Steroids and the Athlete. 2nd ed. North Carolina: McFarland and Company Inc.; 2002.
15. Kopera H. The history of anabolic steroids and a review of clinical experience with anabolic steroids. Acta Endocrinol Suppl (Copenh). 1985;271:11–8.
16. Pope HG, Brower KJ. Anabolic-androgenic steroid-related disorders. In: Sadock B, Sadock V, editors. Comprehensive Textbook of Psychiatry. Philadelphia, PA: Lippincott Williams & Wilkins; 2009. p. 1419e31.
17. Yesalis CE 3rd, Courson SP, Wright JE. History of anabolic steroid use in sport and exercise. In: Anabolic Steroids in Sports and Exercise. Champaign, IL: Human Kinetics; 2000. pp. 51–71.
18. O’Connor T. America on Steroids: A Time to Heal.; 2017, 177 p.
19. Pope HG Jr, Khalsa JH, Bhasin S. Body image disorders and abuse of anabolic-androgenic steroids among men. JAMA. 2017;317(1):23–4.
20. Pope HG, Kanayama G, Ionescu-Pioggia M, Hudson JI. Anabolic steroid users’ attitudes towards physicians. Addiction. 2004;99(9):1189–94.
21. Morente-Sánchez J, Zabala M. Doping in sport: a review of elite athletes’ attitudes, beliefs, and knowledge. Sports Med. 2013;43(6):395–411.
22. Canavan N.Endocrine society pumped up to raise steroid abuse awareness. 2013. Available at:
23. Pope HG Jr, Wood RI, Rogol A, Nyberg F, Bowers L, Bhasin S. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014;35(3):341–75.
24. Pope HG Jr, Kanayama G, Athey A, Ryan E, Hudson JI, Baggish A. The lifetime prevalence of anabolic-androgenic steroid use and dependence in Americans: current best estimates. Am J Addict. 2014;23(4):371–7.
25. Ganson KT, Cadet TJ. Exploring anabolic-androgenic steroid use and teen dating violence among adolescent males. Subst Use Misuse. 2019;54(5):779–86.
26. Thorlindsson T, Halldorsson V. Sport, and use of anabolic androgenic steroids among Icelandic high school students: a critical test of three perspectives. Subst Abuse Treat Prev Policy. 2010;5:32.
27. Kersey RD, Elliot DL, Goldberg L, et al. National Athletic Trainers’ Association position statement: anabolic-androgenic steroids. J Athl Train. 2012;47(5):567–88.
28. Kutscher EC, Lund BC, Perry PJ. Anabolic steroids: a review for the clinician. Sports Med. 2002;32(5):285–96.
29. Buckley WE, Yesalis CE 3rd, Friedl KE, Anderson WA, Streit AL, Wright JE. Estimated prevalence of anabolic steroid use among male high school seniors. JAMA. 1988;260(23):3441–5.
30. Bracken NM. National study of substance use trends among NCAA college student-athletes. Available at:
31. Perry PJ, Lund BC, Deninger MJ, Kutscher EC, Schneider J. Anabolic steroid use in weightlifters and bodybuilders: an Internet survey of drug utilization. Clin J Sport Med. 2005;15(5):326–30.
32. Wroble RR, Gray M, Rodrigo JA. Anabolic steroids and pre-adolescent athletes: prevalence, knowledge, and attitudes. Sport J. 2008;21:1–12.
33. Santos AM, da Rocha MS, da Silva MF. Illicit use and abuse of anabolic-androgenic steroids among Brazilian bodybuilders. Subst Use Misuse. 2011;46(6):742–8.
34. Ip EJ, Barnett MJ, Tenerowicz MJ, Perry PJ. The anabolic 500 survey: characteristics of male users versus nonusers of anabolic-androgenic steroids for strength training. Pharmacotherapy. 2011;31(8):757–66.
35. Ip EJ, Barnett MJ, Tenerowicz MJ, Kim JA, Wei H, Perry PJ. Women and anabolic steroids: an analysis of a dozen users. Clin J Sport Med. 2010;20(6):475–81.
36. Agency WAD. Available from:
37. The 2017 Testing Figures Report (2017 Report). Lausanne, Switzerland; 2018.
38. Christiansen AV, Vinther AS, Dimitris L. Outline of a typology of men’s use of anabolic androgenic steroids in fitness and strength training environments*. Drugs Educ Prevention Policy. 2017;24(3):295–305.
39. Hildebrandt T, Langenbucher JW, Carr SJ, Sanjuan P. Modeling population heterogeneity in appearance- and performance-enhancing drug (APED) use: applications of mixture modeling in 400 regular APED users. J Abnorm Psychol. 2007;116(4):717–33.
40. Zahnow R, McVeigh J, Bates G, et al. Identifying a typology of men who use anabolic androgenic steroids (AAS). Int J Drug Policy. 2018;55:105–12.
41. Cohen J, Collins R, Darkes J, Gwartney D. A league of their own: demographics, motivations and patterns of use of 1,955 male adult non-medical anabolic steroid users in the United States. J Int Soc Sports Nutr. 2007;4:12.
42. LaBotz M, Griesemer BA; Council on Sports Medicine and Fitness. Use of performance-enhancing substances. Pediatrics. 2016;138(1):e20161300.
43. Johnston LD, O’Malley PM, Miech RA, Bachman JG, Schulenberg JE. Monitoring the Future National Survery Results on Drug Use 2975–2014: Key Findings on Adolescent Drug Use. Ann Arbor Institute for Social Research: The University of Michigan; 2015. Available at: The University of Michigan.
44. Kann L, Kinchen S, Shanklin SL, et al; Centers for Disease Control and Prevention (CDC). Youth risk behavior surveillance—United States, 2013. MMWR Suppl. 2014;63(4):1–168.
45. Kanayama G, Boynes M, Hudson JI, Field AE, Pope HG Jr.Anabolic steroid abuse among teenage girls: an illusory problem?Drug Alcohol Depend. 2007;88(2–3):156–62.
46. Frison E, Vandenbosch L, Eggermont S. Exposure to media predicts use of dietary supplements and anabolic-androgenic steroids among Flemish adolescent boys. Eur J Pediatr. 2013;172(10):1387–92.
47. Sandvik MR, Bakken A, Loland S. Anabolic-androgenic steroid use and correlates in Norwegian adolescents. Eur J Sport Sci. 2018;18(6):903–10.
48. Blashill AJ. A dual pathway model of steroid use among adolescent boys: results from a nationally representative Sample. Psychol Men Masculinity. 2014;15(2):229–33.
49. Jampel JD, Murray SB, Griffiths S, Blashill AJ. Self-perceived weight and anabolic steroid misuse among US adolescent boys. J Adolesc Health. 2016;58(4):397–402.
50. Goldman AL, Pope HG, Bhasin S. The health threat posed by the hidden epidemic of anabolic steroid use and body image disorders among young men. J Clin Endocrinol Metab. 2019;104(4):1069–74.
51. Ratnasabapathy R, Dhillo WS. The effects of kisspeptin in human reproductive function—therapeutic implications. Curr Drug Targets. 2013;14(3):365–71.
52. Enea C, Boisseau N, Fargeas-Gluck MA, Diaz V, Dugue B. Circulating androgens in women: exercise-induced changes. Sports Med. 2011;41(1):1–15.
53. Vingren JL, Kraemer WJ, Hatfield DL, et al. Effect of resistance exercise on muscle steroid receptor protein content in strength-trained men and women. Steroids. 2009;74(13–14):1033–9.
54. Kraemer WJ, Ratamess NA, Nindl BC. Recovery responses of testosterone, growth hormone, and IGF-1 after resistance exercise. J Appl Physiol (1985). 2017;122(3):549–58.
55. Andrews MA, Magee CD, Combest TM, Allard RJ, Douglas KM. Physical effects of anabolic-androgenic steroids in healthy exercising adults: a systematic review and meta-analysis. Curr Sports Med Rep. 2018;17(7):232–41.
56. Lippi G, Franchini M, Banfi G. Biochemistry and physiology of anabolic androgenic steroids doping. Mini-Rev Med Chem. 2011;11(5):362–73.
57. Yu JG, Bonnerud P, Eriksson A, Stål PS, Tegner Y, Malm C. Effects of long term supplementation of anabolic androgen steroids on human skeletal muscle. PLoS One. 2014;9(9):e105330.
58. Huang G, Basaria S. Do anabolic-androgenic steroids have performance-enhancing effects in female athletes?Mol Cell Endocrinol. 2018;464:56–64.
59. Cardinale DA, Horwath O, Elings-Knutsson J, et al. Enhanced skeletal muscle oxidative capacity and capillary-to-Fiber ratio following moderately increased testosterone exposure in young healthy women. Front Physiol. 2020;11:585490.
60. Hartgens F, Kuipers H. Effects of androgenic-anabolic steroids in athletes. Sports Med. 2004;34(8):513–54.
61. Giorgi A, Weatherby RP, Murphy PW. Muscular strength, body composition and health responses to the use of testosterone enanthate: a double blind study. J Sci Med Sport. 1999;2(4):341–55.
62. Alén M, Häkkinen K, Komi PV. Changes in neuromuscular performance and muscle fiber characteristics of elite power athletes self-administering androgenic and anabolic steroids. Acta Physiol Scand. 1984;122(4):535–44.
63. Egner IM, Bruusgaard JC, Eftestøl E, Gundersen K. A cellular memory mechanism aids overload hypertrophy in muscle long after an episodic exposure to anabolic steroids. J Physiol. 2013;591(24):6221–30.
64. Huebner M, Perperoglou A. Sex differences and impact of body mass on performance from childhood to senior athletes in Olympic weightlifting. PLoS One. 2020;15(9):e0238369.
65. Senefeld JW, Clayburn AJ, Baker SE, Carter RE, Johnson PW, Joyner MJ. Sex differences in youth elite swimming. PLoS One. 2019;14(11):e0225724.
66. Tønnessen E, Svendsen IS, Olsen IC, Guttormsen A, Haugen T. Performance development in adolescent track and field athletes according to age, sex and sport discipline. PLoS One. 2015;10(6):e0129014.
67. Ploegmakers JJ, Hepping AM, Geertzen JH, Bulstra SK, Stevens M. Grip strength is strongly associated with height, weight and gender in childhood: a cross sectional study of 2241 children and adolescents providing reference values. Aust J Phys. 2013;59(4):255–61.
68. Winsley RJ, Fulford J, Roberts AC, Welsman JR, Armstrong N. Sex difference in peak oxygen uptake in prepubertal children. J Sci Med Sport. 2009;12(6):647–51.
69. Defreyne J, Vantomme B, Van Caenegem E, et al. Prospective evaluation of hematocrit in gender-affirming hormone treatment: results from European Network for the investigation of gender incongruence. Andrology. 2018;6(3):446–54.
70. Harper J, O’Donnell E, Sorouri Khorashad B, McDermott H, Witcomb GL. How does hormone transition in transgender women change body composition, muscle strength and haemoglobin? Systematic review with a focus on the implications for sport participation. Br J Sports Med. 2021:bjsports-2020-103106. doi:10.1136/bjsports-2020-103106.
71. Kraemer WJ, Ratamess NA, Hymer WC, Nindl BC, Fragala MS. Growth hormone(s), testosterone, insulin-like growth factors, and cortisol: roles and integration for cellular development and growth with exercise. Front Endocrinol. 2020;11. doi:10.3389/fendo.2020.00033.
72. Wilson CM, McPhaul MJ. A and B forms of the androgen receptor are expressed in a variety of human tissues. Mol Cell Endocrinol. 1996;120(1):51–7.
73. Wong HY, Burghoorn JA, Van Leeuwen M, et al. Phosphorylation of androgen receptor isoforms. Biochem J. 2004;383(Pt 2):267–76.
74. Kim HJ, Lee WJ. Ligand-independent activation of the androgen receptor by insulin-like growth factor-I and the role of the MAPK pathway in skeletal muscle cells. Mol Cell. 2009;28(6):589–93.
75. Nicoll JX, Fry AC, Mosier EM. Sex-based differences in resting MAPK, androgen, and glucocorticoid receptor phosphorylation in human skeletal muscle. Steroids. 2019;141:23–9.
76. Eder IE, Culig Z, Putz T, Nessler-Menardi C, Bartsch G, Klocker H. Molecular biology of the androgen receptor: from molecular understanding to the clinic. Eur Urol. 2001;40(3):241–51.
77. Kemppainen JA, Langley E, Wong CI, Bobseine K, Kelce WR, Wilson EM. Distinguishing androgen receptor agonists and antagonists: distinct mechanisms of activation by medroxyprogesterone acetate and dihydrotestosterone. Mol Endocrinol. 1999;13(3):440–54.
78. Zhou ZX, Lane MV, Kemppainen JA, French FS, Wilson EM. Specificity of ligand-dependent androgen receptor stabilization: receptor domain interactions influence ligand dissociation and receptor stability. Mol Endocrinol. 1995;9(2):208–18.
79. Saartok T, Dahlberg E, Gustafsson JA. Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin. Endocrinology. 1984;114(6):2100–6.
80. van de Wijngaart DJ, Dubbink HJ, van Royen ME, Trapman J, Jenster G. Androgen receptor coregulators: recruitment via the coactivator binding groove. Mol Cell Endocrinol. 2012;352(1–2):57–69.
81. Mumford PW, Romero MA, Mao X, et al. Cross talk between androgen and Wnt signaling potentially contributes to age-related skeletal muscle atrophy in rats. J Appl Physiol (1985). 2018;125(2):486–94.
82. Braga M, Bhasin S, Jasuja R, Pervin S, Singh R. Testosterone inhibits transforming growth factor-β signaling during myogenic differentiation and proliferation of mouse satellite cells: potential role of follistatin in mediating testosterone action. Mol Cell Endocrinol. 2012;350(1):39–52.
83. Kovacheva EL, Hikim AP, Shen R, Sinha I, Sinha-Hikim I. Testosterone supplementation reverses sarcopenia in aging through regulation of myostatin, c-Jun NH2-terminal kinase, Notch, and Akt signaling pathways. Endocrinology. 2010;151(2):628–38.
84. Sculthorpe N, Solomon AM, Sinanan AC, Bouloux PM, Grace F, Lewis MP. Androgens affect myogenesis in vitro and increase local IGF-1 expression. Med Sci Sports Exerc. 2012;44(4):610–5.
85. Bhasin S, Taylor WE, Singh R, et al. The mechanisms of androgen effects on body composition: mesenchymal pluripotent cell as the target of androgen action. J Gerontol A Biol Sci Med Sci. 2003;58(12):M1103–10.
86. Singh R, Artaza JN, Taylor WE, Gonzalez-Cadavid NF, Bhasin S. Androgens stimulate myogenic differentiation and inhibit adipogenesis in C3H 10T1/2 pluripotent cells through an androgen receptor-mediated pathway. Endocrinology. 2003;144(11):5081–8.
87. Dubois V, Laurent MR, Sinnesael M, et al. A satellite cell-specific knockout of the androgen receptor reveals myostatin as a direct androgen target in skeletal muscle. FASEB J. 2014;28(7):2979–94.
88. MacKrell JG, Yaden BC, Bullock H, et al. Molecular targets of androgen signaling that characterize skeletal muscle recovery and regeneration. Nucl Recept Signal. 2015;13:e005.
89. Harada N, Inui H, Yamaji R. Competitive and compensatory effects of androgen signaling and glucocorticoid signaling. Recept Clin Invest. 2015;2:e785.
90. White JP, Gao S, Puppa MJ, Sato S, Welle SL, Carson JA. Testosterone regulation of Akt/mTORC1/FoxO3a signaling in skeletal muscle. Mol Cell Endocrinol. 2013;365(2):174–86.
91. Ye F, McCoy SC, Ross HH, et al. Transcriptional regulation of myotrophic actions by testosterone and trenbolone on androgen-responsive muscle. Steroids. 2014;87:59–66.
92. Michels G, Hoppe UC. Rapid actions of androgens. Front Neuroendocrinol. 2008;29(2):182–98.
93. Dent JR, Fletcher DK, McGuigan MR. Evidence for a non-genomic action of testosterone in skeletal muscle which may improve athletic performance: implications for the female athlete. J Sports Sci Med. 2012;11(3):363–70.
94. Hamdi MM, Mutungi G. Dihydrotestosterone activates the MAPK pathway and modulates maximum isometric force through the EGF receptor in isolated intact mouse skeletal muscle fibres. J Physiol. 2010;588(Pt 3):511–25.
95. Basualto-Alarcon C, Jorquera G, Altamirano F, Jaimovich E, Estrada M. Testosterone signals through mTOR and androgen receptor to induce muscle hypertrophy. Med Sci Sports Exerc. 2013;45(9):1712–20.
96. Zeng F, Zhao H, Liao J. Androgen interacts with exercise through the mTOR pathway to induce skeletal muscle hypertrophy. Biol Sport. 2017;34(4):313–21.
97. Parkinson AB, Evans NA. Anabolic androgenic steroids: a survey of 500 users. Med Sci Sports Exerc. 2006;38(4):644–51.
98. Glazer G. Atherogenic effects of anabolic steroids on serum lipid levels. A literature review. Arch Intern Med. 1991;151(10):1925–33.
99. Ansell JE, Tiarks C, Fairchild VK. Coagulation abnormalities associated with the use of anabolic steroids. Am Heart J. 1993;125(2 Pt 1):367–71.
100. Dickerman RD, McConathy WJ, Schaller F, Zachariah NY. Cardiovascular complications and anabolic steroids. Eur Heart J. 1996;17(12):1912.
101. Pertusi R, Dickerman RD, McConathy WJ. Evaluation of aminotransferase elevations in a bodybuilder using anabolic steroids: hepatitis or rhabdomyolysis?J Am Osteopath Assoc. 2001;101(7):391–4.
102. Søe KL, Søe M, Gluud C. Liver pathology associated with the use of anabolic-androgenic steroids. Liver. 1992;12(2):73–9.
103. Parssinen M, Kujala U, Vartiainen E, Sarna S, Seppala T. Increased premature mortality of competitive powerlifters suspected to have used anabolic agents. Int J Sports Med. 2000;21(3):225–7.
104. [Internet]. US FDA; [cited 2019].
105. Bhasin S, Calof OM, Storer TW, et al. Drug insight: testosterone and selective androgen receptor modulators as anabolic therapies for chronic illness and aging. Nat Clin Pract Endocrinol Metab. 2006;2(3):146–59.
106. Snyder PJ, Ellenberg SS, Cunningham GR, et al. The testosterone trials: seven coordinated trials of testosterone treatment in elderly men. Clin Trials. 2014;11(3):362–75.
107. Whitsel EA, Boyko EJ, Matsumoto AM, Anawalt BD, Siscovick DS. Intramuscular testosterone esters and plasma lipids in hypogonadal men: a meta-analysis. Am J Med. 2001;111(4):261–9.
108. Bhasin S, Storer TW, Berman N, et al. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med. 1996;335(1):1–7.
109. Singh AB, Hsia S, Alaupovic P, et al. The effects of varying doses of T on insulin sensitivity, plasma lipids, apolipoproteins, and C-reactive protein in healthy young men. J Clin Endocrinol Metab. 2002;87(1):136–43.
110. Jockenhövel F, Bullmann C, Schubert M, et al. Influence of various modes of androgen substitution on serum lipids and lipoproteins in hypogonadal men. Metabolism. 1999;48(5):590–6.
111. Angell PJ, Ismail TF, Jabbour A, et al. Ventricular structure, function, and focal fibrosis in anabolic steroid users: a CMR study. Eur J Appl Physiol. 2014;114(5):921–8.
112. Alizade E, Avci A, Tabakcı MM, et al. Comparison of right ventricle systolic function between long-term anabolic-androgenic steroid user and nonuser bodybuilder athletes: a study of two-dimensional speckle tracking echocardiography. Echocardiography. 2016;33(8):1178–85.
113. D’Andrea A, Radmilovic J, Caselli S, et al. Left atrial myocardial dysfunction after chronic abuse of anabolic androgenic steroids: a speckle tracking echocardiography analysis. Int J Card Imaging. 2018;34(10):1549–59.
114. Spirito P, Pelliccia A, Proschan MA, et al. Morphology of the “athlete’s heart” assessed by echocardiography in 947 elite athletes representing 27 sports. Am J Cardiol. 1994;74(8):802–6.
115. Utomi V, Oxborough D, Whyte GP, et al. Systematic review and meta-analysis of training mode, imaging modality and body size influences on the morphology and function of the male athlete’s heart. Heart. 2013;99(23):1727–33.
116. Spence AL, Naylor LH, Carter HH, et al. A prospective randomised longitudinal MRI study of left ventricular adaptation to endurance and resistance exercise training in humans. J Physiol. 2011;589(Pt 22):5443–52.
117. Pirompol P, Teekabut V, Weerachatyanukul W, Bupha-Intr T, Wattanapermpool J. Supra-physiological dose of testosterone induces pathological cardiac hypertrophy. J Endocrinol. 2016;229(1):13–23.
118. Far HR, Ågren G, Thiblin I. Cardiac hypertrophy in deceased users of anabolic androgenic steroids: an investigation of autopsy findings. Cardiovasc Pathol. 2012;21(4):312–6.
119. Di Paolo M, Agozzino M, Toni C, et al. Sudden anabolic steroid abuse-related death in athletes. Int J Cardiol. 2007;114(1):114–7.
120. Fineschi V, Riezzo I, Centini F, et al. Sudden cardiac death during anabolic steroid abuse: morphologic and toxicologic findings in two fatal cases of bodybuilders. Int J Legal Med. 2007;121(1):48–53.
121. Hernandez-Guerra AI, Tapia J, Menendez-Quintanal LM, Lucena JS. Sudden cardiac death in anabolic androgenic steroids abuse: case report and literature review. Forensic Sci Res. 2019;4(3):267–73.
122. Lichtenfeld J, Deal BJ, Crawford S. Sudden cardiac arrest following ventricular fibrillation attributed to anabolic steroid use in an adolescent. Cardiol Young. 2016;26(5):996–8.
123. Stolt A, Karila T, Viitasalo M, Mäntysaari M, Kujala UM, Karjalainen J. QT interval and QT dispersion in endurance athletes and in power athletes using large doses of anabolic steroids. Am J Cardiol. 1999;84(3):364–6, a9.
124. Alizade E, Avci A, Fidan S, et al. The effect of chronic anabolic-androgenic steroid use on Tp-E interval, Tp-E/Qt ratio, and Tp-E/Qtc ratio in male bodybuilders. Ann Noninvasive Electrocardiol. 2015;20(6):592–600.
125. Pavlatos AM, Fultz O, Monberg MJ, Vootkur A, Pharmd. Review of oxymetholone: a 17alpha-alkylated anabolic-androgenic steroid. Clin Ther. 2001;23(6):789–801; discussion 771.
126. Socas L, Zumbado M, Pérez-Luzardo O, et al. Hepatocellular adenomas associated with anabolic androgenic steroid abuse in bodybuilders: a report of two cases and a review of the literature. Br J Sports Med. 2005;39(5):e27.
127. Calof OM, Singh AB, Lee ML, et al. Adverse events associated with testosterone replacement in middle-age and older men: a meta-analysis of randomized, placebo-controlled trials. J Gerontol A Biol Sci Med Sci. 2005;60(11):1451–7.
128. Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ. Anabolic steroid-induced hepatotoxicity: is it overstated?Clin J Sport Med. 1999;9(1):34–9.
129. Hoffman JR, Ratamess NA. Medical issues associated with anabolic steroid use: are they exaggerated?J Sports Sci Med. 2006;5(2):182–93.
130. MacIndoe JH, Perry PJ, Yates WR, Holman TL, Ellingrod VL, Scott SD. Testosterone suppression of the HPT axis. J Investig Med. 1997;45(8):441–7.
131. El Osta R, Almont T, Diligent C, Hubert N, Eschwège P, Hubert J. Anabolic steroids abuse and male infertility. Basic Clin Androl. 2016;26:2.
132. McBride JA, Coward RM. Recovery of spermatogenesis following testosterone replacement therapy or anabolic-androgenic steroid use. Asian J Androl. 2016;18(3):373–80.
133. Babigian A, Silverman RT. Management of gynecomastia due to use of anabolic steroids in bodybuilders. Plast Reconstr Surg. 2001;107(1):240–2.
134. Nieschlag E, Vorona E. Doping with anabolic androgenic steroids (AAS): adverse effects on non-reproductive organs and functions. Rev Endocr Metab Disord. 2015;16(3):199–211.
135. Morrison TR, Ricci LA, Melloni RH Jr.Anabolic/androgenic steroid administration during adolescence and adulthood differentially modulates aggression and anxiety. Horm Behav. 2015;69:132–8.
136. Pope HG Jr, Katz DL. Homicide and near-homicide by anabolic steroid users. J Clin Psychiatry. 1990;51(1):28–31.
137. Pope HG Jr, Katz DL. Psychiatric and medical effects of anabolic-androgenic steroid use. A controlled study of 160 athletes. Arch Gen Psychiatry. 1994;51(5):375–82.
138. Malone DA Jr, Dimeff RJ, Lombardo JA, Sample RH. Psychiatric effects and psychoactive substance use in anabolic-androgenic steroid users. Clin J Sport Med. 1995;5(1):25–31.
139. Karlovic D, Serretti A, Marcinko D, Martinac M, Silic A, Katinic K. Serum testosterone concentration in combat-related chronic posttraumatic stress disorder. Neuropsychobiology. 2012;65(2):90–5.
140. Bjornebekk A, Walhovd KB, Jorstad ML, Due-Tonnessen P, Hullstein IR, Fjell AM. Structural brain imaging of long-term anabolic-androgenic steroid users and nonusing weightlifters. Biol Psychiatry. 2017;82(4):294–302.
141. Kaufman MJ, Janes AC, Hudson JI, et al. Brain and cognition abnormalities in long-term anabolic-androgenic steroid users. Drug Alcohol Depend. 2015;152:47–56.
142. Kanayama G, Brower KJ, Wood RI, Hudson JI, Pope HG Jr.Issues for DSM-V: clarifying the diagnostic criteria for anabolic-androgenic steroid dependence. Am J Psychiatry. 2009;166(6):642–5.
143. Kanayama G, Hudson JI, Pope HG Jr.Features of men with anabolic-androgenic steroid dependence: a comparison with nondependent AAS users and with AAS nonusers. Drug Alcohol Depend. 2009;102(1–3):130–7.
144. Derman RJ. Effects of sex steroids on women’s health: implications for practitioners. Am J Med. 1995;98(1A):137S–43S.
145. Tsametis CP, Isidori AM. Testosterone replacement therapy: for whom, when and how?Metabolism. 2018;86:69–78.
146. Petering RC, Brooks NA. Testosterone therapy: review of clinical applications. Am Fam Physician. 2017;96(7):441–9.
147. Canup R, Bogenberger K, Attipoe S, et al. Trends in androgen prescriptions from military treatment facilities: 2007 to 2011. Mil Med. 2015;180(7):728–31.
148. Bhasin S, Brito JP, Cunningham GR, et al. Testosterone therapy in men with Hypogonadism: An Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2018;103(5):1715–44.
149. Kanayama G, Hudson JI, DeLuca J, et al. Prolonged hypogonadism in males following withdrawal from anabolic-androgenic steroids: an under-recognized problem. Addiction. 2015;110(5):823–31.
150. Coward RM, Rajanahally S, Kovac JR, Smith RP, Pastuszak AW, Lipshultz LI. Anabolic steroid induced hypogonadism in young men. J Urol. 2013;190(6):2200–5.
151. Rasmussen JJ, Selmer C, Østergren PB, et al. Former abusers of anabolic androgenic steroids exhibit decreased testosterone levels and Hypogonadal symptoms years after cessation: a case-control study. PLoS One. 2016;11(8):e0161208.
152. Brock G, Heiselman D, Maggi M, et al. Effect of testosterone solution 2% on testosterone concentration, sex drive and energy in Hypogonadal men: results of a placebo controlled study. J Urol. 2016;195(3):699–705.
153. Ponce OJ, Spencer-Bonilla G, Alvarez-Villalobos N, et al. The efficacy and adverse events of testosterone replacement therapy in hypogonadal men: a systematic review and meta-analysis of randomized, placebo-controlled trials. J Clin Endocrinol Metab. 2018. doi:10.1210/jc.2018-00404.
154. Snyder PJ, Bhasin S, Cunningham GR, et al; Testosterone Trials Investigators. Effects of testosterone treatment in older men. N Engl J Med. 2016;374(7):611–24.
155. Steidle C, Schwartz S, Jacoby K, Sebree T, Smith T, Bachand R; North American AA2500 T Gel Study Group. AA2500 testosterone gel normalizes androgen levels in aging males with improvements in body composition and sexual function. J Clin Endocrinol Metab. 2003;88(6):2673–81.
156. Snyder PJ, Kopperdahl DL, Stephens-Shields AJ, et al. Effect of testosterone treatment on volumetric bone density and strength in older men with low testosterone: a controlled clinical trial. JAMA Intern Med. 2017;177(4):471–9.
157. Tracz MJ, Sideras K, Boloña ER, et al. Testosterone use in men and its effects on bone health. A systematic review and meta-analysis of randomized placebo-controlled trials. J Clin Endocrinol Metab. 2006;91(6):2011–6.
158. Coviello AD, Kaplan B, Lakshman KM, Chen T, Singh AB, Bhasin S. Effects of graded doses of testosterone on erythropoiesis in healthy young and older men. J Clin Endocrinol Metab. 2008;93(3):914–9.
159. Roy CN, Snyder PJ, Stephens-Shields AJ, et al. Association of Testosterone Levels with Anemia in older men: a controlled clinical trial. JAMA Intern Med. 2017;177(4):480–90.
160. Bhasin S, Storer TW, Berman N, et al. Testosterone replacement increases fat-free mass and muscle size in hypogonadal men. J Clin Endocrinol Metab. 1997;82(2):407–13.
161. Bhasin S, Woodhouse L, Casaburi R, et al. Testosterone dose-response relationships in healthy young men. Am J Physiol Endocrinol Metab. 2001;281(6):E1172–81.
162. Corona G, Giagulli VA, Maseroli E, et al. Therapy of endocrine disease: testosterone supplementation and body composition: results from a meta-analysis study. Eur J Endocrinol. 2016;174(3):R99–116.
163. Storer TW, Magliano L, Woodhouse L, et al. Testosterone dose-dependently increases maximal voluntary strength and leg power, but does not affect fatigability or specific tension. J Clin Endocrinol Metab. 2003;88(4):1478–85.
164. Wang C, Swerdloff RS, Iranmanesh A, et al; Testosterone Gel Study Group. Transdermal testosterone gel improves sexual function, mood, muscle strength, and body composition parameters in hypogonadal men. J Clin Endocrinol Metab. 2000;85(8):2839–53.
165. Woodhouse LJ, Gupta N, Bhasin M, et al. Dose-dependent effects of testosterone on regional adipose tissue distribution in healthy young men. J Clin Endocrinol Metab. 2004;89(2):718–26.
166. Saad F, Caliber M, Doros G, Haider KS, Haider A. Long-term treatment with testosterone undecanoate injections in men with hypogonadism alleviates erectile dysfunction and reduces risk of major adverse cardiovascular events, prostate cancer, and mortality. Aging Male. 2020;23(1):81–92.
167. Bhasin S, Seidman S. Testosterone treatment of depressive disorders in men: too much smoke, not enough high-quality evidence. JAMA Psychiat. 2019;76(1):9–10.
168. Elliott J, Kelly SE, Millar AC, et al. Testosterone therapy in hypogonadal men: a systematic review and network meta-analysis. BMJ Open. 2017;7(11):e015284.
169. Walther A, Breidenstein J, Miller R. Association of Testosterone Treatment with Alleviation of depressive symptoms in men: a systematic review and meta-analysis. JAMA Psychiatry. 2019;76(1):31–40.
170. Cunningham GR, Stephens-Shields AJ, Rosen RC, et al. Testosterone treatment and sexual function in older men with low testosterone levels. J Clin Endocrinol Metab. 2016;101(8):3096–104.
171. Basaria S, Coviello AD, Travison TG, et al. Adverse events associated with testosterone administration. N Engl J Med. 2010;363(2):109–22.
172. Bhasin S, Ellenberg SS, Storer TW, et al. Effect of testosterone replacement on measures of mobility in older men with mobility limitation and low testosterone concentrations: secondary analyses of the testosterone trials. Lancet Diabetes Endocrinol. 2018;6(11):879–90.
173. Emmelot-Vonk MH, Verhaar HJ, Nakhai Pour HR, et al. Effect of testosterone supplementation on functional mobility, cognition, and other parameters in older men: a randomized controlled trial. JAMA. 2008;299(1):39–52.
174. Huang G, Wharton W, Bhasin S, et al. Effects of long-term testosterone administration on cognition in older men with low or low-to-normal testosterone concentrations: a prespecified secondary analysis of data from the randomised, double-blind, placebo-controlled TEAAM trial. Lancet Diabetes Endocrinol. 2016;4(8):657–65.
175. Nair KS, Rizza RA, O’Brien P, et al. DHEA in elderly women and DHEA or testosterone in elderly men. N Engl J Med. 2006;355(16):1647–59.
176. Page ST, Amory JK, Bowman FD, et al. Exogenous testosterone (T) alone or with finasteride increases physical performance, grip strength, and lean body mass in older men with low serum T. J Clin Endocrinol Metab. 2005;90(3):1502–10.
177. Srinivas-Shankar U, Roberts SA, Connolly MJ, et al. Effects of testosterone on muscle strength, physical function, body composition, and quality of life in intermediate-frail and frail elderly men: a randomized, double-blind, placebo-controlled study. J Clin Endocrinol Metab. 2010;95(2):639–50.
178. Resnick SM, Matsumoto AM, Stephens-Shields AJ, et al. Testosterone treatment and cognitive function in older men with low testosterone and age-associated memory impairment. JAMA. 2017;317(7):717–27.
179. Tan S, Sohrabi HR, Weinborn M, et al. Effects of testosterone supplementation on separate cognitive domains in cognitively healthy older men: a meta-analysis of current randomized clinical trials. Am J Geriatr Psychiatry. 2019;27(11):1232–46.
180. Alexander GC, Iyer G, Lucas E, Lin D, Singh S. Cardiovascular risks of exogenous testosterone use among men: a systematic review and meta-analysis. Am J Med. 2017;130(3):293–305.
181. Baillargeon J, Urban RJ, Morgentaler A, et al. Risk of venous thromboembolism in men receiving testosterone therapy. Mayo Clin Proc. 2015;90(8):1038–45.
182. Cheetham TC, An J, Jacobsen SJ, et al. Association of Testosterone Replacement with Cardiovascular Outcomes among men with Androgen Deficiency. JAMA Intern Med. 2017;177(4):491–9.
183. Corona G, Rastrelli G, Monami M, et al. Hypogonadism as a risk factor for cardiovascular mortality in men: a meta-analytic study. Eur J Endocrinol. 2011;165(5):687–701.
184. Khazai B, Golden SH, Colangelo LA, et al. Association of endogenous testosterone with subclinical atherosclerosis in men: the multi-ethnic study of atherosclerosis. Clin Endocrinol. 2016;84(5):700–7.
185. Martinez C, Suissa S, Rietbrock S, et al. Testosterone treatment and risk of venous thromboembolism: population based case-control study. BMJ. 2016;355:i5968.
186. Muraleedharan V, Marsh H, Kapoor D, Channer KS, Jones TH. Testosterone deficiency is associated with increased risk of mortality and testosterone replacement improves survival in men with type 2 diabetes. Eur J Endocrinol. 2013;169(6):725–33.
187. Sharma R, Oni OA, Gupta K, et al. Normalization of testosterone level is associated with reduced incidence of myocardial infarction and mortality in men. Eur Heart J. 2015;36(40):2706–15.
188. Srinath R, Hill Golden S, Carson KA, Dobs A. Endogenous testosterone and its relationship to preclinical and clinical measures of cardiovascular disease in the atherosclerosis risk in communities study. J Clin Endocrinol Metab. 2015;100(4):1602–8.
189. Vigen R, O’Donnell CI, Barón AE, et al. Association of testosterone therapy with mortality, myocardial infarction, and stroke in men with low testosterone levels. JAMA. 2013;310(17):1829–36.
190. Xu L, Freeman G, Cowling BJ, Schooling CM. Testosterone therapy and cardiovascular events among men: a systematic review and meta-analysis of placebo-controlled randomized trials. BMC Med. 2013;11:108.
191. Bhasin S, Pencina M, Jasuja GK, et al. Reference ranges for testosterone in men generated using liquid chromatography tandem mass spectrometry in a community-based sample of healthy nonobese young men in the Framingham heart study and applied to three geographically distinct cohorts. J Clin Endocrinol Metab. 2011;96(8):2430–9.
192. Harman SM, Metter EJ, Tobin JD, Pearson J, Blackman MR; Baltimore Longitudinal Study of Aging. Longitudinal effects of aging on serum total and free testosterone levels in healthy men. Baltimore longitudinal study of aging. J Clin Endocrinol Metab. 2001;86(2):724–31.
193. Travison TG, Vesper HW, Orwoll E, et al. Harmonized reference ranges for circulating testosterone levels in men of four cohort studies in the United States and Europe. J Clin Endocrinol Metab. 2017;102(4):1161–73.
194. Wu FC, Tajar A, Beynon JM, et al; EMAS Group. Identification of late-onset hypogonadism in middle-age and elderly men. N Engl J Med. 2010;363(2):123–35.
195. Spitzer M, Huang G, Basaria S, Travison TG, Bhasin S. Risks and benefits of testosterone therapy in older men. Nat Rev Endocrinol. 2013;9(7):414–24.
196. Bhasin S, Jasjua GK, Pencina M, et al. Sex hormone-binding globulin, but not testosterone, is associated prospectively and independently with incident metabolic syndrome in men: the Framingham heart study. Diabetes Care. 2011;34(11):2464–70.
197. Lakshman KM, Bhasin S, Araujo AB. Sex hormone-binding globulin as an independent predictor of incident type 2 diabetes mellitus in men. J Gerontol A Biol Sci Med Sci. 2010;65(5):503–9.
198. Handelsman DJ, Hirschberg AL, Bermon S. Circulating testosterone as the hormonal basis of sex differences in athletic performance. Endocr Rev. 2018;39(5):803–29.
199. Ingram BJ, Thomas CL. Transgender policy in sport, a review of current policy and commentary of the challenges of policy creation. Curr Sports Med Rep. 2019;18(6):239–47.
200. Jones BA, Arcelus J, Bouman WP, Haycraft E. Sport and transgender people: a systematic review of the literature relating to sport participation and competitive sport policies. Sports Med. 2017;47(4):701–16.


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