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Medical Issues Associated with Anabolic Steroid Use: Are They Exaggerated?

Jay r hoffman, nicholas a ratamess.

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✉ Department of Health and Exercise Science, The College of New Jersey, PO Box 7718, Ewing, New Jersey 08628, USA.

Received 2006 Feb 10; Accepted 2006 Mar 9; Collection date 2006 Jun.

For the past 50 years anabolic steroids have been at the forefront of the controversy surrounding performance enhancing drugs. For almost half of this time no attempt was made by sports governing bodies to control its use, and only recently have all of the major sports governing bodies in North America agreed to ban from competition and punish athletes who test positive for anabolic steroids. These punitive measures were developed with the primary concern for promotion of fair play and eliminating potential health risks associated with androgenic-anabolic steroids. Yet, controversy exists whether these testing programs deter anabolic steroid use. Although the scope of this paper does not focus on the effectiveness of testing, or the issue of fair play, it is of interest to understand why many athletes underestimate the health risks associated from these drugs. What creates further curiosity is the seemingly well-publicized health hazards that the medical community has depicted concerning anabolic steroidabuse. Is there something that the athletes know, or are they simply naïve regarding the dangers? The focus of this review is to provide a brief history of anabolic steroid use in North America, the prevalence of its use in both athletic and recreational populations and its efficacy. Primary discussion will focus on health issues associated with anabolic steroid use with an examination of the contrasting views held between the medical community and the athletes that are using these ergogenic drugs. Existing data suggest that in certain circumstances the medical risk associated with anabolic steroid use may have been somewhat exaggerated, possibly to dissuade use in athletes.

Key Points.

For many years the scientific and medical communities depicted a lack of efficacy and serious adverse effects from anabolic steroid use.

Clinical case studies continue to link anabolic steroid administration with myocardial infarct, suicide, and cancer, evidence to support a cause and effect relationship is lacking.

It may be other contributing factors (i.e. genetic predisposition, diet, etc.) that play a substantial role and potentiate the harmful effects from anabolic steroids.

Key words: Androgens, ergogenic aids, athletes, sport supplements, performance enhancing drugs

Introduction

Anabolic-androgenic steroids (herein referred to as only anabolic steroids) are the man-made derivatives of the male sex hormone testosterone. Physiologically, elevations in testosterone concentrations stimulate protein synthesis resulting in improvements in muscle size, body mass and strength (Bhasin et al., 1996 ; 2001 ). In addition, testosterone and its synthetic derivatives are responsible for the development and maturation of male secondary sexual characteristics (i.e. increase in body hair, masculine voice, development of male pattern baldness, libido, sperm production and aggressiveness).

Testosterone was isolated in the early 20 th century and its discovery led to studies demonstrating that this substance stimulated a strong positive nitrogen balance in castrated dogs and rats (Kochakian, 1950 ). Testosterone, because of its rapid degradation when given through either oral or parenteral administration, poses some limitations as an ergogenic aid. Although its potency is rapidly observed, the high frequency of administration needed becomes problematic. In addition, testosterone has a therapeutic index of 1 meaning there is similarity in the proportion between the anabolic and androgenic effects. As a result it becomes necessary to chemically modify testosterone to retard the degradation process and reduce some of the negative side effects. This allows for maintenance of effective blood concentrations for longer periods of time, may increase its interaction with the androgen receptor, and achieves the desired anabolic and androgenic changes.

Boje, 1939 was the first to suggest that exogenous testosterone administration may enhance athletic performance. By the late 1940’s and 1950’s testosterone compounds were experimented with by some west coast bodybuilders (Yesalis et al., 2000 ). The first dramatic reports of anabolic steroid use occurred following the 1954 world weightlifting championships (Yesalis et al., 2000 ). Use of these drugs spread quickly through the 1960’s and became popular among athletes in a variety of Olympic sports (Dubin, 1990 ). Wide spread use has also been reported in power lifters (Wagman et al., 1995 ), National Football League players (Yesalis et al., 2000 ), collegiate athletes (Yesalis, 1992 ), and recent claims of wide spread use in many sports including Major League Baseball players has made anabolic steroids the number one sports story of 2005 in some markets (Quinn, 2006 ). The ergogenic effects associated with anabolic steroids are presented in Table 1 .

Ergogenic effects associated with anabolic steroid use.

Athletes typically use anabolic steroids in a “stacking” regimen, in which they administer several different drugs simultaneously. The rationale for stacking is to increase the potency of each drug. That is, the potency of one anabolic agent may be enhanced when consumed simultaneously with another anabolic agent. They will use both oral and parenteral compounds. Most users will take anabolic steroids in a cyclic pattern, meaning the athletes will use the drugs for several weeks or months and alternate these cycles with periods of discontinued use. Often the athletes will administer the drugs in a pyramid (step-up) pattern in which dosages are steadily increased over several weeks. Towards the end of the cycle the athlete will ‘step-down’ to reduce the likelihood of negative side effects. At this point, some athletes will discontinue drug use or perhaps initiate another cycle of different drugs (i.e., drugs that may increase endogenous testosterone production to prevent the undesirable drop in testosterone concentrations that follows the removal of the pharmaceutical agents). A recent study has shown that the typical steroid regimen involved 3.1 agents, with a typical cycle ranging from 5 – 10 weeks (Perry et al., 2005 ). The dose that the athlete administers was reported to vary between 5 - 29 times greater than physiological replacement doses (Perry et al., 2005 ). These higher pharmacological dosages appear necessary to elicit the gains that these athletes desire. In a classic study on the dose-response curve of anabolic steroids, Forbes, 1985 demonstrated that the total dose of anabolic steroids have a logarithmic relationship to increases in lean body mass. These results exacerbate the athlete’s philosophy that if a low dose is effective, then more must be better.

Adverse effects associated with anabolic steroid use are listed in Table 2 . For years, the medical and scientific communities attempted to reduce anabolic steroid use by athletes by underscoring their efficacy and focusing on the unhealthy side effects (Biely, 1987 ; Darden, 1983 ; Fahey and Brown, 1973 ; Fowler et al., 1965 ; Golding et al., 1974 ). For the most part, this may have proved to be ineffective and caused athletes to lose trust in the physician’s knowledge of anabolic steroids thereby forcing them to seek advice from friends, internet sites or drug suppliers (Pope et al., 2004 ). However, recent literature has suggested that the medical issues associated with anabolic steroids may be somewhat overstated (Berning et al., 2004 ; Sturmi and Diorio, 1998 ; Street et al., 1996 ) considering that many of the side effects associated with anabolic steroid abuse are reversible upon cessation. It is important to note that there are differences in the side effects associated with anabolic steroid use (i.e.under medical supervision) versus abuse (i.e. consumption of many drugs at high doses).

Adverse effects associated with anabolic steroid use.

The clinical examination of anabolic steroid use is quite limited. Much of the problem in prospectively examining the effects of anabolic steroids on the athletic population is related to the unwillingness of institutional review boards to approve such studies in a non-clinical population. As a result, most of the investigations concerning medical issues associated with anabolic steroid administration have been performed on athletes self-administering the drugs. Anecdotally, it appears that a disproportionate magnitude of use and incidence of adverse effects are evident in bodybuilders (who are also known for consuming several other drugs that relieve some side effects but potentiate other risk factors as well, i.e. diuretics, thyroid hormones, insulin, anti-estrogens, etc.) compared to strength/power athletes. The mindset and motivation of these two types of athletes can be quite different. The strength/power athlete will typically use anabolic steroids to prepare themselves for a season of competition. They will generally cycle the drug to help them reach peak condition at a specific time of the training year. In contrast, bodybuilders use anabolic steroids to enhance muscle growth and definition. Their success is predicated on their aesthetic appearance. As a result many of these athletes may use anabolic steroids excessively for severalyears without cycling off or perhaps minimizing the length of “off cycles” depending on their competition schedule. Recent research has indicated that those athletes exhibit behavior that are consistent with substance dependence disorder (Perry et al., 2005 ). Although the medical issues associated with anabolic steroids may be quite different between these two types of athletes, the scientific literature generally does not differentiate between the two. The following sections will discuss adverse effects on specific physiological systems associated with anabolic-androgenic steroid use. It is important to note that many athletes consume multiple drugs in addition to anabolic steroids. Thus, the unhealthy side effects could be potentiated by the use of drugs such as human growth hormone or IGF-1.

Cardiovascular System

In both the medical and lay literature one of the principal adverse effects generally associated with anabolic steroid use is the increased risk for myocardial infarction. This is primarily based upon several case reports published over the past 20 years describing the occurrence of myocardial infarctions in young and middle-aged body builders or weight lifters attributed to anabolic steroid use and/or abuse (Bowman, 1989 ; Ferenchick and Adelman, 1992 ; Gunes et al., 2004 ; Kennedy and Lawrence, 1993 ; Luke et al., 1990 ; McNutt et al., 1988 ). However, direct evidence showing cause and effect between anabolic steroid administration and myocardial infarction is limited. Many of the case studies reported normal coronary arterial function in anabolic steroid users that experienced an infarct (Kennedy and Lawrence, 1993 ; Luke et al., 1990 ), while others have shown occluded arteries with thrombus formation (Ferenchick and Adelman, 1992 ; Gunes et al., 2004 ; McNutt et al., 1988 ). Still, some of these studies have reported abnormal lipoprotein concentrations with serum cholesterol levels nearly approaching 600 mg·dl -1 (McNutt et al., 1988 ). Interestingly, in most case studies the effects of diet or genetic predisposition for cardiovascular disease were not disseminated and could not be excluded as contributing factors.

Alterations in serum lipids, elevations in blood pressure and an increased risk of thrombosis are additional cardiovascular changes often associated with anabolic steroid use (Cohen et al., 1986 ; Costill et al., 1984 ; Dhar et al., 2005 ; Kuipers et al., 1991 ; LaRoche, 1990 ). The magnitude of these effects may differ depending upon the type, duration, and volume of anabolic steroids used. Interesting to note is that these effects appear to be reversible upon cessation of the drug (Dhar et al., 2005 , Parssinen and Seppala, 2002 ). In instances where the athlete remains on anabolic steroids for prolonged periods of time (e.g “abuse”), the risk for developing cardiovascular disease may increase. Sader and colleagues ( 2001 ) noted that despite low HDL levels in bodybuilders, anabolic steroid use did not appear to cause significant vascular dysfunction. Interestingly, athletes participating in power sports appear to have a higher incidence of cardiovascular dysfunction than other athletes, regardless of androgen use (Tikkanen et al., 1991 ; 1998 ). Thus, a strength/power athlete with underlying cardiovascular abnormalities that begins using anabolic steroids is at a much higher risk for cardiovascular disease. However, anabolic steroid-induced changes in lipid profiles may not, per se, lead to significant cardiovascular dysfunction.

The risk of sudden death from cardiovascular complications in the athlete consuming anabolic steroids can occur in the absence of atherosclerosis. Thrombus formation has been reported in several case studies of bodybuilders self-administering anabolic steroids (Ferenchick, 1991 ; Fineschi et al., 2001 ; McCarthy et al., 2000 ; Sahraian et al., 2004 ). Melchert and Welder, 1995 have suggested that the use of 17α-alkylated steroids (primarily from oral ingestion) likely present the highest risk for thrombus formation. They hypothesized that anabolic steroid consumption can elevate platelet aggregation, possibly through an increase in platelet production of thromboxane A 2 and/or decreasing platelet production of prostaglandin PgI 2, resulting in a hypercoagulable state.

Left ventricular function and anabolic steroid use/abuse has been examined. Climstein and colleagues ( 2003 ) demonstrated that highly strength-trained athletes, with no history of anabolic steroid use exhibited a higher incidence of wave form abnormalities relative to recreationally-trained or sedentary individuals. However, when these athletes self-administered anabolic steroids, a higher percentage of wave form abnormalities were exhibited. Further evidence suggestive of left ventricular dysfunction has been reported in rodent models. A study on rats has shown that 8 weeks of testosterone administration increased left ventricle stiffness and caused a reduction in stroke volume and cardiac performance (LeGros et al., 2000 ). It was hypothesized that the increased stiffness may have been related to formation of crosslinks between adjacent collagen molecules within the heart. Others have suggested that anabolic steroid use may suppress the increases normally shown in myocardial capillary density following prolonged endurance training (Tagarakis et al., 2000 ). However, there are a number of interpretational issues with this study. The changes reported were not statistically significant. In addition, the exercise stimulus employed (prolonged endurance training) is not the primary mode of exercise frequently used by anabolic steroid users. Resistance training, independent of anabolic steroid administration, has been shown to increase left ventricular wall and septal thickness due to the high magnitude of pressure overload (Fleck et al., 1993 ; Fleck, 2003 ; Hoffman, 2002 ). This is known as concentric hypertrophy and does not occur at the expense of left ventricular diameter. In general, cardiac hypertrophy (resulting from a pressure overload, i.e. hypertension) may not be accompanied by a proportional increase in capillary density (Tomanek, 1986 ). Therefore, the potential for a reduction in coronary vasculature density exists for the resistance- trained athlete. However, it does not appear to pose a significant cardiac risk for these athletes. Recent observations have shown a dose-dependent increase in left ventricular hypertrophy (LVH) in anabolic steroid users (Parssinen and Seppala, 2002 ). This may have the potential to exacerbate the reduction in coronary vasculature density. However, the authors have acknowledged that their results may have been potentiated by a concomitant use of human growth hormone by their subjects. Other studies have failed to show additive effects of anabolic steroid administration and LVH in resistance-trained athletes (Palatini et al., 1996 ; Dickerman et al., 1998 ).

Hepatic System

An elevated risk for liver tumors, damage, hepatocellular adenomas, and peliosis hepatitis are often associated with anabolic steroid use or abuse. This is likely due to the liver being the primary site of steroid clearance. In addition, hepatic cancers have been shown to generally occur with higher frequency in males compared to females (El-Serag, 2004 ). It is thought that high endogenous concentrations of testosterone and low estrogen concentrations increase the risk of hepatic carcinomas (Tanaka et al., 2000 ). However, this appears to be prevalent for men with pre-existing liver disease. In normal, healthy men the relationship between testosterone concentrations and liver cancer has not been firmly established. Additional reports of liver cancer and anabolic steroids have been reported in non- athletic populations being treated with testosterone for aplastic anemia (Nakao et al., 2000 ). In regards to liver cancer and disease in athletes consuming anabolic steroids, many concerns have been raised based primarily on several case studies that have documented liver disease in bodybuilders using anabolic steroids (Cabasso, 1994 ; Socas et al., 2005 ; Soe et al., 1992 ).

A few studies have recently questioned the risk to hepatic dysfunction from anabolic steroid use (Dickerman et al., 1999 ). A recent study examining the blood chemistry of bodybuilders self-administering anabolic steroids reported elevations in aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatine kinase (CK), but no change in the often-regarded more sensitive gamma- glutamyltranspeptidase (GGT) concentration (Dickerman et al., 1999 ). Thus, some experts have questioned these criteria tools because of the difficulty in dissociating the effects of muscle damage resulting from training from potential liver dysfunction. This has prompted some researchers to suggest that steroid-induced hepatotoxicity may be overstated. Another study involved a survey sent to physicians asking them to provide a diagnosis for a 28-year-old anabolic steroid using bodybuilder with abnormal serum chemistry profile (elevations in AST, ALT, CK, but with a normal GGT) (Pertusi et al., 2001 ). The majority of physicians (63%) indicated liver disease as the primary diagnosis as 56% of physicians failed to acknowledge the potential role of muscle damage or disease thereby increasing the likelihood of overemphasized anabolic steroid-induced hepatotoxicity diagnoses. Many case reports involving anabolic steroid administration and hepatic cancers examined individuals who were treated with oral steroids (17α-alkylated) for many years. No cysts or tumors have been reported in athletes using 17β-alkylated steroids. Thus, evidence appears to indicate that the risk for hepatic disease from anabolic steroid use may not be as high as the medical community had originally thought although a risk does exist especially with oral anabolic steroid use or abuse.

Bone and Connective Tissue

The issue of anabolic steroids and bone growth has been examined in both young and adult populations. In both populations, androgens have been successfully used as part of the treatment for growth delay (Albanese et al., 1994 ; Bagatell and Bremner, 1996 ; Doeker et al., 1998 ), and for osteoporosis in women (Geusens et al., 1986 ). Androgens are bi-phasic in that they stimulate endochondral bone formation and induce growth plate closure at the end of puberty. The actions of androgens on the growth plate are mediated to a large extent by aromatization to estrogens (Vanderschueren et al., 2004 ; Hoffman, 2002 ). Anabolic steroid use results in significant elevations in estrogens thought to impact premature closure of the growth plate. The acceleration of growth in adolescents treated with testosterone has raised concern for the premature closure of the epiphyseal plate (NIDA, 1996 ; Sturmi and Diorio, 1998 ). However, there does not appear to be any reports documenting the occurrence of premature stunted growth inadolescents taking anabolic steroids. Interesting, anabolic steroid administration in colts has been reported to delay epiphyseal plate closure (Koskinen and Katila, 1997 ). Although comparisons between humans and animals are difficult to make, suprapharmacological dosages that most athletes use may pose a greater risk than the doses studied to date. Thus, for the adolescent athlete using anabolic steroids the risk of premature epiphyseal plate closure may exist.

Anabolic steroids have been suggested to increase the risk of tendon tears in athletes (David et al., 1994 ; Stannard and Bucknell, 1993 ). Studies in mice have suggested that anabolic steroids may lead to degeneration of collagen (proportional to duration of steroid administration) and potentially lead to a decrease in tensile strength (Michna, 1986 ). In addition, a decrease in collagen synthesis has been reported from anabolic steroid administration in rats (Karpakka et al., 1992 ). The response in humans has been less clear. Mechanical failure has been suggested as a mechanism in anabolic steroid-using athletes. Skeletal muscle adaptations (i.e. hypertrophy and strength increases) take place rather rapidly in comparison to connective tissue. Therefore, tendon injuries in athletes are thought to occur from a rapid increase in training intensity and volume where connective tissue fails to withstand the overload. However, case reports of spontaneous tendon ruptures of weightlifters and athletes are limited.Although experimental data from animal models suggest that anabolic steroids may alter biomechanical properties of tendons, ultrastructural evidence supporting this claim is lacking. One study has shown that high doses of anabolic steroids decrease the degradation and increase the synthesis of type I collagen (Parssinen et al., 2000 ). Evans and colleagues ( 1998 ) performed an ultrastructural analysis on ruptured tendons from anabolic steroid users. They concluded that anabolic steroids did not induce any ultrastructural collagen changes that would increase the risk of tendon ruptures. Although the incidences of tendon rupture in anabolic steroid users should not be discounted, it is important to consider it in relation to the mechanical stress encountered from the rapid increases in muscular performance. Prospective research on anabolic steroid use and connective tissue injury is warranted.

Psychological and Behavioral

An issue that is often raised with anabolic steroid use is the psychological and behavioral effects. Increases in aggressiveness, arousal and irritability have been associated with anabolic steroid use. This has potentially beneficial and harmful implications. Elevations in arousal and self-esteem may be a positive side effect for the athlete. The increase in aggressiveness is a benefit that athletes participating in a contact sport may possess. However, increased aggressiveness may occur outside of the athletic arena thereby posing significant risks for anabolic steroid users and those they come in contact with. Anabolic steroids are associated with mood swings and increases in psychotic episodes. Studies have shown that nearly 60% of anabolic steroid users experience increases in irritability and aggressiveness (Pope and Katz, 1994 ; Silvester, 1995 ). A recent study by Pope and colleagues ( 2000 ) reported that significant elevations in aggressiveness and manic scores were observed following 12 weeks of testosterone cypionate injections in a controlled double-blind cross-over study. Interestingly, the results of this study were not uniform across the subjects. Most subjects showed little psychological effect and few developed prominent effects. A cause and effect relationship has yet to be identified in anabolic steroid users and it does appear that individuals who experience psychological or behavioral changes do recover when steroid use is discontinued (Fudula et al., 2003 ).

Additional Adverse Effects Associated with Anabolic Steroid Use

Other adverse events generally associated with anabolic steroid use include acne, male pattern baldness, gynecomastia, decreased sperm count, testicular atrophy, impotence, and transient infertility. Acne is one of the more common side effects associated with anabolic steroid administration. One study reported that 43% of users experienced acne as a consequence from androgen use (O’Sullivan et al., 2000 ). Few other investigations have been able to prospectively determine the occurrence of side effects associated with androgen administration. Increases in acne are thought to be related to a stimulation of sebaceous glands to produce more oil. The most common sites of acne development are on the face and back. Acne appears to disappear upon cessation of androgen administration.

Male pattern baldness does not appear to be a common adverse effect, but is often discussed as a potential side effect associated with androgen use. This is likely related to the role that androgens have in regulating hair growth (Lee et al., 2005 ). An abnormal expression of a specific cutaneous androgen receptor increases the likelihood of androgenic alopecia (Kaufman and Dawber, 1999 ; Lee et al., 2005 ). Thus, it is likely that androgenic alopecia observed as a result of exogenous androgen use is more prevalent in individuals that have a genetic predisposition to balding.

Gynecomastia is a common adverse effect associated with anabolic steroid use. Research has demonstrated a prevalence rate of 37% in anabolic steroid users (O’Sullivan et al., 2000 ). Gynecomastia isa benign enlargement of the male breast resulting from an altered estrogen-androgen balance, or increased breast sensitivity to a circulating estrogen level. Increases in estrogen production in men are seen primarily through the aromatization of circulating testosterone. Many anabolic steroid users will use anti-estrogens (selective estrogen receptor modulators) such as tamoxifen and clomiphene or anastrozole which is a nonsteroidal aromatase inhibitor to minimize side effects of estrogen and stimulate testosterone production. Once gynecomastia is diagnosed cosmetic surgery is often needed to correct the problem.

Changes in libido appear to be the most common adverse event (approximately 61% of users) reported in a small sample of anabolic steroid users (O’Sullivan et al., 2000 ). Although testosterone is often used in hypogonadal men to restore normal sexual function, increasing testosterone above the normal physiological range does not appear to increase sexual interest or frequency of sexual behavior in healthy men administered anabolic steroids in supraphysiological dosages (up to 500 mg·wk -1 ) for 14 weeks (Yates et al., 1999 ). Other studies confirm unchanged libido following 10 weeks of anabolic steroid administration in dosages ranging up to 200 mg·wk -1 (Schurmeyer, et al., 1984 ). However, reports do indicate that towards the end of an androgen cycle some men may experience loss of libido (O’Sullivan et al., 2000 ). It was thought that the decreased libido was related to the transient hypogonadism which typically occurs during exogenous androgen administration. Decreases in libido as a result of hypogonadism appear to be a function of high baseline levels of sexual functioning and desire (Schmidt et al., 2004 ). This may explain the conflicting reports seen in the literature. Regardless, changes in libido do appear to normalize once baseline endogenous testosterone concentrations return (Schmidt et al., 2004 ).

Another frequent adverse event relating to sexual function in males administering anabolic steroids is reversible azoospermia and oligospermia (Alen and Suominen, 1984 ; Schurmeyer et al., 1984 ). As exogenous androgen use increases, endogenous testosterone production is reduced. As a result, testicular size is reduced within three months of androgen administration (Alen and Suominen, 1984 ). In addition, sperm concentration and the number of spermatozoa in ejaculate may be reduced or eliminated by 7 weeks of administration (Schurmeyer et al., 1984 ). During this time risk for infertility is elevated. However, the changes seen in testicular volume, sperm count and concentration are reversible. Anabolic steroid-induced hypogonadism returns to baseline levels within 4 months following discontinuation of androgen use (Jarow and Lipshultz, 1990 ), and sperm counts and concentration return to normal during this time frame (Alen and Suominen, 1984 ; Schurmeyer et al., 1984 ).

Medical Issues Associated with Female Steroid Use

In female anabolic steroid users the medical issues are quite different than that shown in men. Deepening of the voice, enlargement of the clitoris, decreased breast size, altered menstruation, hirsutism and male pattern baldness are all clinical features common to hyperandrogenism in females (Derman, 1995 ). Androgen excess may occur as the result of polycystic ovary syndrome, congenital adrenal hyperplasia and possibly Cushing’s syndrome (Derman, 1995 ; Redmond, 1995 ). However, these clinical symptoms are seen in young, female athletes that are self-administering anabolic steroids. In contrast to men, many of these adverse events in the female anabolic steroid user may not be transient (Pavlatos et al., 2001 ).

Long Term Health Issues Associated with Anabolic Steroid Administration

The acute health issues associated with anabolic steroid use appear to be transient and more prevalent in individuals with genetic predisposition (e.g. hair loss, heart disease). It is the long-term effects that become a larger issue. However, limited data are available. In one study in mice, anabolic steroids were administered in relative dosages typically used by bodybuilders. However, the duration of the study was 1/5 the life span of the mouse which is relatively greater than that experienced by most athletes self-administering androgens. The results demonstrated a shortened life span of the mice with evidence of liver, kidney and heart pathology (Bronson and Matherne, 1997 ). In a study on Finnish power lifters, investigators examined 62 athletes who finished in the top 5 in various weight classes between the years 1977 and 1982 (Parssinen et al., 2000 ). These investigators reported that during a 12-year follow-up, the mortality rate for the power lifters was 12.1% compared to 3.1% in a control population. They concluded that their study depicted the detrimental long-term health effects from anabolic steroid use. Others have suggested that prolonged anabolic steroid use may increase the risk for premature death, but this may be more relevant in subjects with substance abuse or underlying psychiatric disease (Petersson et al., 2006 ).

The use of anabolic steroids in strength/power athletes has been reported for more than 50 years in North America. As discussed in the beginning of this review, during the 1970’s and 1980’s anecdotal reports on the rampant use of anabolic steroids in professional athletes were prevalent. However, little information is available concerning steroid-related diseases or associated deaths in these former strength/power athletes who are now well into middle age. Regardless, research should focus on these former athletes to ascertain possible long-term effects from androgen use.

Is There a Clinical Role of Androgenic Anabolic Steroids?

The efficacy of anabolic steroids in enhancing muscle strength and lean tissue accruement is no longer an issue for debate. While the issue of medical risks in individuals self-administering anabolic steroids is still being hotly debated, the medical community is no longer denying the potential clinical use of these androgens (Dobs, 1999 ). In recent years clinical treatment with anabolic steroids has increased lean tissue and improved daily functional performance in AIDS patients (Strawford et al., 1999 ) patients receiving dialysis (Johansen et al., 1999 ), patients with chronic obstructive pulmonary disease (Ferreira et al., 1998 ), and patients recovering from a myocardial infarction (Nahrendorf et al., 2003 ). In addition, research has demonstrated a positive effect on healing from muscle contusion injuries (Beiner et al., 1999 ). Although the medical community has generally taken a conservative approach to promoting anabolic steroids as part of a treatment plan in combating diseases involving muscle wasting, the body of knowledge that has developed indicates the potential positive effects of androgen therapy for certain diseased populations.

Conclusions

For many years the scientific and medical communities depicted a lack of efficacy and serious adverse effects from anabolic steroid use. However, competitive athletes continued to experiment with, use, and abuse anabolic steroids on a regular basis to enhance athletic performance despite the potential harmful side effects. The empirical evidence that the athletes viewed may have led to the development of distrust between the athletic and medical communities. Science has been lagging several years behind the experimental practices of athletes. In fact, most athletes consume anabolic steroids on a trial and error approach based on information gained from other athletes, coaches, websites, or gym “gurus.” Science has lacked in its approach to study anabolic steroids because only few studies have examined long-term cyclical patterns, high doses, and the effects of stacking different brands of steroids. These practices are common to the athletic community and not for the medicinal purposes of anabolic steroid therapy. In addition, some athletes (especially bodybuilders) have experimented with drugs unbeknown to the medical community, i.e. insulin, thyroid hormones, and site-specific enhancers such as Synthol and Esiclene to name a few.

When examining the potential medical issues associated with anabolic steroid use, evidence indicates that most known side effects are transient. More so, few studies have been able to directly link anabolic steroids to many of the serious adverse effects listed. Although clinical case studies continue to link anabolic steroid administration with myocardial infarct, suicide, and cancer, the evidence to support a cause and effect relationship is lacking and it may be other contributing factors (i.e. genetic predisposition, diet, etc.) play a substantial role and potentiate the harmful effects from anabolic steroids. Consistent physician monitoring is critical to the athlete who consumes anabolic steroids. However, many athletes may not undergo extensive medical exams prior to androgen administration and few physicians may be willing to provide such monitoring.

The purpose of this review was not to support or condone anabolic steroid use. Rather, the aim was to discuss pertinent medical issues and provide another perspective in light of the fact that many anabolic steroids users do not appear to prioritize the health/safety hazards or potential adverse medical events. In order to maintain credibility with the athlete, it is important to provide accurate information to the athlete in regards to these performance enhancing drugs, and provide education about alternative means and potential risks. Finally, anabolic steroids have been used legitimately for several clinical purposes such as muscle wasting or hypogonadal related diseases.

Biographies

Jay R. HOFFMAN

The College of New Jersey.

Research interests

Sport supplementation, resistance training, eExercise endocrinology.

E-mail: [email protected]

Nicholas A. RATAMESS

Sport supplementation, resistance training, exercise endocrinolgy.

E-mail: [email protected]

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• Published: 01 June 2022

Anabolic–androgenic steroid use is associated with psychopathy, risk-taking, anger, and physical problems

• Bryan S. Nelson 1 ,
• Tom Hildebrandt 2 &
• Pascal Wallisch 1  

Scientific Reports volume  12 , Article number:  9133 ( 2022 ) Cite this article

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• Human behaviour

Previous research has uncovered medical and psychological effects of anabolic–androgenic steroid (AAS) use, but the specific relationship between AAS use and risk-taking behaviors as well as between AAS use and psychopathic tendencies remains understudied. To explore these potential relationships, we anonymously recruited 492 biologically male, self-identified bodybuilders (median age 22; range 18–47 years) from online bodybuilding fora to complete an online survey on Appearance and Performance Enhancing Drug (APED) use, psychological traits, lifestyle choices, and health behaviors. We computed odds ratios and 95% confidence intervals using logistic regression, adjusting for age, race, education, exercise frequency, caloric intake, and lean BMI. Bodybuilders with a prior history of AAS use exhibited heightened odds of psychopathic traits, sexual and substance use risk-taking behaviors, anger problems, and physical problems compared to those with no prior history of AAS use. This study is among the first to directly assess psychopathy within AAS users. Our results on risk-taking, anger problems, and physical problems are consistent with prior AAS research as well as with existing frameworks of AAS use as a risk behavior. Future research should focus on ascertaining causality, specifically whether psychopathy is a risk associated with or a result of AAS use.

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An estimated 6% of males globally 1 (including 2.9–4 million Americans 2 ) have used anabolic–androgenic steroids (AAS) such as methyltestosterone, danazol, and oxandrolone, which are a series of synthetic variants of the male sex hormone testosterone that increase lean muscle protein synthesis without increasing fat mass 3 , 4 . Although there are medical uses such as for AIDS-related wasting syndrome 5 , AAS are commonly used by individuals for the purposes of bodybuilding and appearance modification 2 , 3 , 6 . In these cases, doses are commonly 10 to 100 times higher than clinical doses and are typically “cycled” intermittently (i.e., used for a few months, stopped to minimize the stress that AAS impart on the body, then resumed shortly thereafter) 3 , 7 . AAS have a 30% dependence rate among long-term users, higher than many other prescription or illicit drugs such as cocaine and have been linked to medical issues such as liver and kidney damage, cardiovascular problems, testicular atrophy, infertility, hair loss, and gynecomastia 2 , 3 , 7 , 8 , 9 , 10 . AAS use is strongly associated with other substance abuse 8 , 9 , 11 , 12 , and users often exhibit negative, although idiosyncratic, psychological issues 8 , 13 , 14 , 15 , 16 , 17 . Some users report delusions of grandeur and invincibility, while others experience depression and various mood disturbances 8 , 18 , 19 , 20 . As dosage increases, AAS users may become impulsive, moody, aggressive, or even violent 9 , 18 , 19 , 21 , 22 , 23 , 24 , 25 , 26 , 27 . Recent neurobiological studies have focused on effects of AAS on central nervous system functions such as cognition, anxiety, depression, and aggression 10 , 28 , 29 . In recent imaging studies, AAS use was associated with cortex thinning as well as decreased gray matter and increased right amygdala volume 30 , 31 , 32 . AAS use seems to accelerate brain aging through oxidative stress and apoptosis 33 , 34 , 35 , is associated with lower cognitive function 36 , 37 , and may disrupt normal neuronal function in the forebrain, which can increase anxiety and aggressiveness and diminish inhibitory control 10 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 . Increased depression has been frequently observed during AAS withdrawal 32 , 46 .

One area that remains understudied among AAS users is psychopathy, a personality disorder characterized by shallow emotional affect, lack of empathy, and antisocial behavior 47 , 48 , 49 . Psychopathy research has frequently associated psychopathy with violence, repeated imprisonment, disrespect for authority, and substance misuse/abuse 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 . There is growing evidence that AAS use may be associated with psychopathy, including a direct association between AAS and psychopathy in an Iranian sample 56 as well as numerous reports of associations between AAS use and violent crime or “roid rage” 19 , 21 , 22 , 23 , 25 , 27 , 57 . Prior studies examining AAS use and elements of the “Dark Triad” and “Big Five” personality traits suggest that the relationship between AAS use and both violence and risk-behaviors may be due to self-regulatory deficits and low conscientiousness, and that AAS use is predicted by narcissism, low agreeableness, neuroticism, impulsivity, and inability to delay gratification 56 , 58 . Hauger et al. 28 recently identified significantly lower emotion recognition in AAS dependent users compared to AAS non-using weightlifters, suggesting that this lower emotion recognition may contribute to the higher frequencies of antisocial traits that AAS users have previously reported 59 , 60 . Antisocial personality disorder, which is characterized by the disregard for laws and norms, irritability, and the failure to regard the safety of self and others 61 has been suggested as the mechanism that underlies the link between AAS use and aggression 3 , 9 , 60 , 62 , 63 . Conceptually, there are overlaps between antisocial personality disorder and psychopathy 64 . We therefore argue that psychopathic traits among AAS users are worth exploring.

Thus, the present study assessed whether AAS users were more likely than nonusers to exhibit psychopathic traits, risk-taking behaviors such as sharing needles, anger problems such as getting into altercations, emotional problems such as panic attacks and depression, cognitive problems such as difficulty remembering, and physical problems such as hair loss. We hypothesized that AAS users would display heightened odds of psychopathic traits, substance use risk-taking behaviors, sexual risk-taking behaviors, anger problems, emotional stability problems, cognitive problems, depressive symptoms, anxiety symptoms, impulsivity symptoms, and physical problems, although we recognize that many of these traits are highly idiosyncratic in nature. Finally, we hypothesized there is a dose-dependent relationship between these traits and the variety of substances used as well as the number of cycles.

Participants and procedure

This study was approved by the NYU Committee on Activities Involving Human Subjects and we conducted in accordance with the Declaration of Helsinki principles. We anonymously recruited a large online sample of 492 (Mean age = 22.9, SD age = 4.3) adult biologically male bodybuilders and asked them questions about their Appearance and Performance Enhancing Drug (APED) use (if any), exercise and dietary habits, psychological states, risk-taking behaviors, and any physical problems they might have experienced. The anonymous internet survey was posted to online fitness fora in fall 2015. All participants provided informed consent prior to their participation. Participants had the option to enter an online raffle for one of twenty $50 Amazon gift cards, which were distributed via email.

The following subsections are presented in the same order as the online survey.

Diet and exercise

Participants reported how often they had exercised in the past month (every day, most days, some days, very rarely/never) and rated their caloric intake in the past month on a 5-point ordinal scale (1 = extreme restriction of calories, 5 = extreme over-consumption of calories). We measured caloric intake in terms of restriction, maintenance, or surplus rather than total calories per day because participants likely vary in caloric requirements (i.e., 3000 cal/day may be a surplus for some but a deficit for others).

Appearance and performance enhancing drugs

Each participant indicated whether he had ever used oral, injectable, or topical AAS (“yes, currently,” “yes, formerly,” “no, but considered taking,” “no, never considered taking” for each). Additionally, participants reported how many AAS cycles they had completed and responded whether they had ever used the following APEDs (each with “yes”/”no” options): Testosterone, Dianabol (Methandrostenolone), Deca Durabolin (Nandrolone Decanoate), Winstrol (Stanozolol), Anadrol (Oxymetholone), Human Growth Hormone (Somatropin), Synthol, Anti-Estrogens, Fat Burners (Insulin, Clenbuterol, Cytomel, Cynomel), Trenbolone, or Anavar.

Self-reported events

Participants rated each of the following items as “yes, currently,” “yes, formerly,” or “no, never”.

General events Participants self-reported whether they experienced the following events: depression, increased number of mood swings, getting into altercations, panic attacks, irritability, lack of frustration tolerance, aggression, difficulty focusing, racing thoughts, difficulty making decisions, difficulty remembering, suicidal thoughts, acne, trouble sleeping, water retention, hair loss, changes in appetite, and heart problems.

Risk-taking behavior Participants indicated whether they had engaged in or experienced the following: unprotected sex, sex with multiple partners, sexually transmitted disease or infection (STD), sharing needles, reusing needles, using stimulants without prescription (such as crack, powdered cocaine, methamphetamine, amphetamine, or ecstasy [MDMA]), using opiates without prescription (such as heroin, morphine, codeine, or Oxycontin), using hallucinogens without prescription (such as LSD, mescaline, and psilocybin), using depressants without prescription (such as Valium, Xanax, Librium, and barbiturates), drinking alcohol, smoking tobacco, and smoking marijuana.

Impulsivity

We used the Barratt Impulsiveness Scale to quantify impulsivity (BIS-11) 65 . Participants responded to 30 statements such as “I often have extraneous thoughts” using a 4-point ordinal rating scale (1 = rarely/never, 4 = almost always/always). The BIS-11 displayed strong reliability in this sample (Cronbach’s α = 0.84).

Psychopathic traits

We employed the Levenson Self-Report Psychopathy Scale (LSRP) to assess psychopathy 66 . The scale has 26 items graded on a 5-point Likert scale (1 = strongly disagree, 5 = strongly agree) and was strongly reliable in this sample (Cronbach’s α = 0.88).

We assessed anxiety with the Generalized Anxiety Disorder 7-item Scale (GAD-7) 67 . Participants responded to each of the seven items such as “being so restless it is hard to sit still” on a 4-point ordinal rating scale (0 = not at all, 3 = nearly every day). The GAD-7 displayed excellent internal consistency (Cronbach’s α = 0.89). Possible scores range from 0 to 21.

We included the 10-item Center for Epidemiologic Studies Short Depression Scale (CES-D 10) 68 to measure depression. Participants rated statements such as “I felt lonely” on a 4-point ordinal rating scale (0 = rarely or none of the time, 3 = all the time). The CES-D 10 was highly reliable (Cronbach’s α = 0.82), with possible scores ranging from 0 to 30.

Aggravation

Participants responded to the 7-item aggravation subscale of the State Hostility Scale 69 , 70 . In the subscale, participants rate possible descriptions of their current mood (e.g., “stormy” or “vexed”) on a 5-point Likert scale (1 = strongly disagree, 5 = strongly agree). The aggravation subscale of the State Hostility Scale had strong reliability (Cronbach’s α = 0.90).

Demographic questions

Lastly, participants reported their age (years), height (inches), weight (pounds), body fat percentage, racial background, and level of education.

Statistical analysis

The survey was convenience sampled, with no pre-specified sample size or power calculation. For our primary analysis, we grouped participants who responded “yes, currently” or “yes, formerly” to having used AAS (oral, injectable, or topical) as AAS users (n = 154, 31.3%). We considered those who responded “no, but considered taking” or “no, never considered taking” to be AAS nonusers (n = 338, 68.7%). We also conducted a secondary analysis using all four categories (current AAS users (n = 121, 24.6%); former AAS users (n = 33, 6.7%); AAS nonuser, considered using (n = 200, 40.7%); AAS nonuser, never considered using (n = 138, 28.0%)).

Both AAS cycle experience and APED variety were self-reported. APED variety was the number of different APED types used (the number each participant responded “yes” to taking of Testosterone, Dianabol (Methandrostenolone), Deca Durabolin (Nandrolone Decanoate), Winstrol (Stanozolol), Anadrol (Oxymetholone), Human Growth Hormone (Somatropin), Synthol, Anti-Estrogens, Fat Burners (Insulin, Clenbuterol, Cytomel, Cynomel), Trenbolone, and Anavar). AAS cycle experience was the number of AAS cycles participants reported. If the participant was an AAS nonuser, then both APED variety and AAS cycle experience were scored as 0.

We grouped traits of interest into the following categories: psychopathic traits, substance use risk-taking behavior, sexual risk-taking behavior, anger problems, emotional stability problems, cognitive problems, depressive symptoms, anxiety symptoms, impulsivity symptoms, and physical problems. Following Brinkley et al. 71 , we considered participants in the top third of the LSRP distribution to have psychopathic traits. We considered any participant that reported sharing needles, reusing needles, hallucinogen use, stimulant use, depressant use, or opiate use as engaging in substance use risk-taking. Similarly, any participant that reported an STD, engaging in unprotected sex, or having multiple sexual partners was categorized as having sexual risk-taking behavior. Any participant scoring in the top half of the aggravation subscale of the State Hostility Scale, reporting physical altercations, or reporting increased aggression was categorized as having anger problems. Participants who reported mood swings, lower frustration tolerance, or irritability were considered to have emotional stability problems while participants with difficulty remembering, difficulty focusing, or trouble making decisions were considered to have cognitive problems. We considered participants with depressive symptoms as those that reported suicidal thoughts, reported increased depression, or had a CES-D 10 score greater than 10 (the established cut point 68 ). Those with anxiety symptoms either had a GAD-7 score greater than the established cut point 67 of 8 or reported panic attacks. A participant who reported racing thoughts or who scored in the top half of the Barratt Impulsiveness Scale was considered to have impulsivity symptoms. Finally, we considered participants to have physical problems if they reported heart problems, appetite changes, water retention, acne, or hair loss.

We used logistic regression to assess possible associations between these traits of interest and AAS use, number of AAS cycles, and variety of APEDs used. We computed odds ratios (OR) with 95% confidence intervals (CI). All analyses adjusted for age, race, education, exercise frequency, caloric intake, and lean BMI. Age, race, and education were included as basic demographic variables, while exercise frequency, caloric intake, and lean BMI were included to account for differences in bodybuilding goals, success, and dedication. We chose to calculate lean BMI to assess how muscular participants were. We used the standard (kg/m 2 ) BMI formula but used each participant’s lean bodyweight instead of his total bodyweight. Lean body weight was calculated by using each participant’s self-reported body fat percentage to determine how much he weighed excluding his body fat (weight in kg * (100%-bodyfat%)). Given that both psychopathy and AAS use are associated with illicit drug use 21 , we conducted a post hoc subgroup analysis among participants without history of polysubstance use (3 or more different drug classes) to ensure any association between AAS use and psychopathic traits was not confounded by polysubstance use. All analyses were conducted in R (version 3.5.1).

Ethics approval

This study was performed in line with the principles of the Declaration of Helsinki. Approval was granted by the Ethics Committee of New York University.

Consent to participate

Participants provided informed consent prior to their participation in this anonymous internet survey.

Participant characteristics are listed in Table 1 . Most participants were younger than 25 years old (56.5% of AAS users; 79.0% of AAS nonusers), white (85.7% of AAS users; 77.5% of AAS nonusers), and had education beyond high school (75.3% of AAS users; 59.1% of AAS nonusers). The majority in each group exercised most days of the week (79.2% of AAS users; 74.8% of AAS nonusers) and were attempting to gain weight (51.3% of AAS users; 51.2% of AAS nonusers). For AAS users and nonusers, the median (Q1-Q3) lean BMI was 23.6 (22.3–25.4) and 21.6 (20.3–23.3) kg/m 2 . AAS users began use at a median (Q1-Q3) of 21 (20–24) years, had completed 2 (1–3) AAS cycles, and used 4 (2–5) different APED types; 78.6% (121/154) were current AAS users. Among AAS nonusers, 59.2% (200/338) had considered using AAS.

Tables 2 and 3 summarize traits of interest and specific substance use risk-taking behaviors by AAS use status; 25.8% (39/154) of AAS users and 10.2% (34/338) of AAS nonusers had a history of polysubstance use. AAS users had over twice the odds of exhibiting psychopathic traits (OR = 2.50, 95% CI 1.52–4.15), over three times the odds of engaging in substance use risk-taking behaviors (OR = 3.10, 95% CI 1.97–4.93), nearly twice the odds of engaging in sexual risk-taking behaviors (OR = 1.79, 95% CI 1.01–3.26), nearly twice the odds of experiencing anger problems (OR = 1.71, 95% CI 1.02–2.95), and over twice the odds of exhibiting physical problems (OR = 2.23, 95% CI 1.16–4.51) compared to AAS nonusers (Table 4 ). In a post hoc subgroup analysis, AAS users without history of polysubstance use had higher odds of psychopathic traits compared to nonusers without history of polysubstance use (OR = 2.73, 95% CI 1.54–4.90).

In secondary analyses with four levels of AAS use, AAS nonusers who considered using had higher odds of psychopathic traits (OR = 2.19, 95% CI 1.27–3.87), substance use risk-taking (OR = 3.51, 95% CI 2.06–6.14), sexual risk-taking (OR = 3.38, 95% CI 2.00–5.78), anger problems (OR = 3.16, 95% CI 1.86–5.42), emotional stability problems (OR = 1.87, 95% CI 1.16–3.01), depressive symptoms (OR = 2.12, 95% CI 1.32–3.44), and impulsivity symptoms (OR = 2.17, 95% CI 1.31–3.61) compared to AAS nonusers who never considered using; former AAS users had lower odds of both anxiety symptoms (OR = 0.30, 95% CI 0.08–0.84) and impulsivity symptoms (OR = 0.33, 95% CI 0.14–0.74) compared to AAS nonusers who considered using; and current AAS users had higher odds of both impulsivity symptoms (OR = 2.92, 95% CI 1.27–6.84) and physical problems (OR = 5.86, 95% CI 1.83–19.74) compared to former AAS users.

Lastly, we assessed possible relationships between (i) the number of different APED types used and (ii) the number of AAS cycles with the same traits of interest as before. Each additional type of APED used was associated with a 19% increase in the odds of psychopathic traits (OR = 1.19, 95% CI 1.07–1.33), a 24% increase in the odds of substance use risk-taking (OR = 1.24, 95% CI 1.12–1.38), an 18% increase in the odds of sexual risk-taking (OR = 1.18, 95% CI 1.02–1.38), a 15% increase in the odds of emotional stability problems (OR = 1.15, 95% CI 1.04–1.27), and a 33% increase in the odds of physical problems (OR = 1.33, 95% CI 1.12–1.66). For every one-unit increase in the number of AAS cycles, there was a 26% increase in the odds of substance use risk-taking (OR = 1.26, 95% CI 1.10–1.46) and an 85% increase in the odds of physical problems (OR = 1.85, 95% CI 1.29–3.01).

In our online survey of adult biologically male bodybuilders, we found AAS use was associated with higher odds of psychopathic traits, both for AAS users compared to nonusers as well as for increased APED variety. Importantly, this association was also present among participants with no history of polysubstance use. It is not certain whether AAS use predicts psychopathic traits or if the existence of psychopathic traits may actually be a risk factor for AAS use. We note that AAS nonusers who considered AAS use had over twice the odds of psychopathic traits compared to AAS nonusers who never considered AAS use. A recent study of 285 competitive athletes reported that Machiavellianism and psychopathy explained 29% of the variance in positive attitude toward AAS 72 . This is supported generally by the well-established association between psychopathic traits and risk-taking behaviors such as substance abuse 48 . In that case, a large proportion of bodybuilders willing to make the jump to using AAS may already have pre-existing psychopathic traits. Psychopathy is related to both antisocial personality disorder and conduct disorder, each of which is associated with AAS use 9 , 60 . Conduct disorder in particular is a major risk factor for AAS use 9 that cannot be entirely explained by use of other drugs 59 . The relationship may be dynamic; bodybuilders with psychopathic tendencies may be more willing to begin AAS in the first place. Subsequently, these traits might be amplified either chemically by AAS use or psychologically by the environment; prior work has shown the difference between psychopaths and non-psychopaths in emotional-regulatory activity in the aPFC is modified by endogenous testosterone level 73 . With this in mind, longitudinal research is needed to further explore the causal nature of this relationship.

Our study is one of many to link AAS use substance use risk-taking behaviors 74 , 75 and sexual risk-taking behaviors 59 , 76 . It is difficult to ascertain the specific relationship between AAS use and risk-taking. Unlike physical, psychological, cognitive, and anger problems, which have all had experimental and translational research done to strengthen causal interpretations of such links 16 , 77 , there has not been experimental work to test whether risk-taking behaviors are caused by AAS use. In fact, it is important to consider that AAS use is itself a risk behavior, and another form of substance use, so AAS users may already engage in many other risk-taking behaviors prior to their first use. This may be especially true in light of our findings that AAS nonusers who considered AAS use had over three-times the odds of both substance use and sexual risk-taking behaviors compared to AAS nonusers who never considered AAS use, as well as our results regarding APED variety and AAS cycle experience. AAS users willing to try more types of APEDs or willing to undergo more AAS cycles may be more likely to also engage in risk-taking behaviors. Perhaps the relationship between AAS and risk-taking behaviors is bidirectional and interactive, where athletes that engage in these risk behaviors such as illicit drug use experiment with AAS, which may lower their inhibitions to take further risks.

Our finding that AAS users have higher odds of experiencing anger problems is in line with prior research 16 , 19 , 20 . Notably, anger has been previously reported as both a potential risk factor 78 as well as a potential outcome 27 . We did not observe associations between AAS use and emotional stability problems, cognitive problems, depressive symptoms, anxiety symptoms, or impulsivity symptoms. Prior research has identified various psychological and cognitive traits among AAS users such as depression, impulsivity, and mania 18 , 19 , 20 , but they are generally idiosyncratic in nature 8 , 79 , 80 , 81 . We do note that AAS nonusers who considered AAS use had higher odds of emotional stability problems, depressive symptoms, and impulsivity symptoms compared to AAS nonusers who never considered AAS use, former AAS users had lower odds of anxiety symptoms and impulsivity symptoms compared to AAS nonusers who considered AAS use, and current AAS users had higher odds of impulsivity symptoms compared to former AAS users. These findings comparing AAS nonusers who considered vs. never considered AAS use are consistent with prior research about factors relating to the decision to use AAS, including research on the “Big Five” personality traits 58 . Additionally, we observed increased odds of emotional stability problems with increased APED variety. Lastly, our hypothesis about physical problems was supported for AAS users compared to nonusers as well as the dose dependent response in relation to increased APED variety and increased AAS cycle experience. These findings are consistent with prior studies 3 , 8 , 10 , 32 .

There are several limitations. Although we successfully elicited responses from real-world users of AAS, there remain questions about how representative our sample is. AAS users in our sample were relatively new users (median of 2 prior cycles). Our findings may have been different with a group of more experienced users. It is also possible that our online survey was more likely to attract individuals with psychopathic traits or that AAS users with psychopathic traits are more willing to take an online survey than other users. We note that > 50% of AAS users and nonusers were considered to have substance use risk-taking, sexual risk-taking, anger problems, emotional stability problems, cognitive problems, depressive symptoms, impulsivity symptoms, and physical problems. Lastly, this cross-sectional study is entirely correlational and any attempts to speculate about causality should be made with extreme caution. Further prospective or experimental studies are needed. In light of the findings on Machiavellianism and psychopathy in relation to willingness to use AAS 72 , it would be interesting to also examine the link to narcissism and self-esteem/insecurity 82 . We wonder whether self-esteem or narcissistic traits could play an additional role in the motivation to begin AAS use, given the known downsides.

This study is among the first to directly assess psychopathy within AAS users. Our results on risk-taking, anger problems, and physical problems are consistent with prior AAS research as well as with existing frameworks of AAS use as a risk behavior. Increased psychopathic traits in AAS users may serve as the underlying mechanism to predict increased anger problems (see 60 regarding antisocial personality disorder as a mechanism between AAS and aggression). Although the present study highlights the relationship between AAS use and psychopathic traits, future research should emphasize possible causal explanations and try to elucidate the directionality of this relationship. Additionally, the mechanisms between AAS use and risk and violent behaviors should be further explored.

Data availability

All data generated or analyzed during this study are included in this published article’s supplementary information files. R code used in data analysis can be made available upon reasonable request to the corresponding author.

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Acknowledgements

We thank Ward Pettibone and Andre Nakkab for administrative assistance. This work was supported by the New York University Dean’s Undergraduate Research Fund.

This work was supported by the New York University Dean’s Undergraduate Research Fund.

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Nelson, B.S., Hildebrandt, T. & Wallisch, P. Anabolic–androgenic steroid use is associated with psychopathy, risk-taking, anger, and physical problems. Sci Rep 12 , 9133 (2022). https://doi.org/10.1038/s41598-022-13048-w

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

Affiliations.

• 1 Department of Medicine, Brigham and Women's Hospital, Boston, MA.
• 2 Department of Kinesiology, University of Rhode Island, Kingston, RI.
• 3 Department of Physical Therapy, Ariel University, Ariel, Israel.
• 4 Department of Human Sciences, The Ohio State University, Columbus, OH.
• 5 Department of Kinesiology, McMaster University, Hamilton, ON.
• 6 Department of Health and Exercise Science, The College of New Jersey, Ewing, NJ.
• PMID: 34261998
• 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.

Copyright © 2021 by the American College of Sports Medicine.

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Steroid Hormones and Receptors in Health and Disease

A Research Conference Co-Organized by FASEB and the International Committee on Rapid Responses to Steroid Hormones (RRSH), May 25–27, 2021

Matthias Barton

Daniel e frigo, zeynep madak-erdogan, franck mauvais-jarvis, eric r prossnitz.

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AUTHOR CONTRIBUTIONS

M. Barton conceived and wrote the manuscript; D. E. Frigo, Z. Madak-Erdogan, F. Mauvais-Jarvis, and E. R. Prossnitz contributed and/or edited content.

Correspondence Matthias Barton, University of Zurich, Y44 G22, Winterthurerstrasse 190, 8057 Zürich, Switzerland. [email protected]

Keywords: aldosterone, estrogen, estradiol, VDR, MR, GR, glucocorticoids, androgens, progesterone, vitamin D, thyroid hormone, nuclear receptors

Steroid hormone effects have been reported for almost 140 years 1 – 3 . Research over the past 50 years has led to the discovery of steroid hormone receptors that act via both genomic and nongenomic (“rapid”) mechanisms. Steroids are involved in physiology and disease, mediating endocrine, cardiovascular, and reproductive functions and play a role in cancer, neurological, metabolic, renal, and cardiovascular diseases. 4 – 7 Over the past decades, both the Federation of American Societies for Experimental Biology (FASEB) and the International Committee on Rapid Responses to Steroid Hormones (RRSH) have held meetings presenting the newest science on steroid hormone biology and receptor signaling 8 – 26 ( Tables 1 and 2 ). Previously, both FASEB 8 – 14 and RRSH 15 – 26 organized their own conferences, usually in alternating years, and in 2018, decided to organize their first joint conference to be held in the United States. Initially, the organizers of this joint conference (i.e., authors of this manuscript) had selected West Palm Beach, FL, as the venue for the conference, which was to be held July 12–17, 2020. However, when the COVID-19 pandemic hit earlier that year, plans were put on hold. Hoping for early control of the pandemic, the organizers prepared for a 4-day in-person meeting to be held in Puerto Rico, USA. However, as COVID-19 continued to be a global health concern, challenging societies, scientists, and science around the world, in late 2020, the organizers took the decision to hold the conference as a virtual meeting. The conference was ultimately held online as a 3-day meeting on May 25–27, 2021. It represented the 10th occurrence of the FASEB Science Research Conferences (SRCs) on Steroid Hormones with Daniel E. Frigo (University of Texas M. D. Anderson Cancer Center, Houston, TX, USA), Zeynep Madak-Erdogan (University of Illinois, Urbana, IL, USA) and Franck Mauvais-Jarvis (Tulane University, New Orleans, LA, USA) as chairs, and the 12th International Meeting on Rapid Responses to Steroid Hormones (RRSH 2020) with Matthias Barton (University of Zurich, Zurich, Switzerland) and Eric R. Prossnitz (University of New Mexico, Albuquerque, NM, USA) as chairs.

History of the FASEB Science Research Conferences on Steroid Hormones

Held as a virtual meeting with RRSH in 2021.

History of the International Meetings on Rapid Responses to Steroid Hormones

Held as a virtual meeting with FASEB in 2021.

The FASEB and RRSH conferences are usually well received by the scientific community since many presentations and discussion topics include unpublished, cutting-edge research. The joint conference brought together scientists and clinicians from all areas of biology and medicine, covering a broad range of topics related to steroid hormone and steroid hormone receptor function in physiology and human health. The program included one keynote speaker, 38 scheduled invited speakers, 18 short talks (“lightning presentations”) and 28 virtual poster presentations. The conference drew a record attendance of 110 participants, reflecting an increasing interest in steroid hormone signaling in the scientific community. In terms of diversity, women constituted over 55% of attendees and over 40% of all invited speakers. Early career scientists (defined as faculty with <10 years of experience, postdoctoral associates, and graduate students) were also well represented, comprising 55% of all conference attendees.

The welcome address was given by Daniel E. Frigo on behalf of FASEB, and Eric R. Prossnitz on behalf of RRSH, who, together with other organizers, led the program. Keynote speaker Donald McDonnell (Duke University School of Medicine, Durham, NC, USA) set the stage of the conference with his intriguing lecture “If we knew then what we know now, what would we have done differently to exploit nuclear receptors as drug targets?”. Dr. McDonnell, who discovered several mechanisms that led to drug treatments for hormone-responsive cancers, provided the audience with a lifetime view of his work, also looking back at the beginnings of field, which he and others pioneered. His lecture was followed by the first session of the day on nuclear steroid receptor regulation of metabolism, led by Sayeepriyadarshini Anakk (University of Illinois, Urbana-Champagne, IL, USA). A series of lectures by Adriana Maggi (University of Milan, Milan, Italy), Carolyn Cummins (University of Toronto, Toronto, ON, Canada), Andrea Hevener (University of California, Los Angeles, CA, USA), Sheng Wu (Johns Hopkins University, Baltimore, MD, USA), Brian Feldman (University of California, San Francisco, CA, USA), Wen Xie (University of Pittsburgh, Pittsburgh, PA, USA), and Warren Thomas (Royal College of Surgeons in Ireland, Dublin, Ireland) presented updates on metabolic functions of estrogen, androgen, and glucocorticoid receptors, as well as evidence for functional roles for estrogen sulfotransferase and steroid sulfatase in energy metabolism, and how aldosterone regulates renal Na + reabsorption through novel protein kinase D isoforms. The lectures were followed by lively discussions moderated by the session chairs, even though the meeting was held online. Following the first session, Dr. Yvette Seger, FASEB Director of Science Policy, introduced the science policy of FASEB and moderated a round table discussion on the subject.

The second half of the first day of the conference was dedicated to clinical aspects of therapies targeting steroid hormone receptors. The session was chaired by Jay Gertz (University of Utah, Salt Lake City, USA) and Martin Wehling (University of Heidelberg, Heidelberg, Germany). Lectures addressed many areas of clinical medicine and disease, including mineralocorticoid receptor function in the treatment of cardiovascular disorders, thyroid receptor signaling in cancer, and membrane progesterone receptor function in the uterus, as well as epigenetics and cistromics in cancer and clinical trials. Lectures were presented by Iris Jaffee (Tufts University, Medford, MA, USA), James Pru (University of Wyoming, Laramie, WY, USA), Paul Davis (Albany Medical College, Albany, NY, USA), Wilbert Zwart (Netherlands Cancer Institute. Amsterdam, The Netherlands), and Mathieu Lupien (University of Toronto). Following the clinical session, a number of young investigators (Florian Le Billan, University of Toronto; Alicia Arredondo Eve, University of Illinois; Ximena Calle Chalco, University of Chile, Santiago, Chile; Innocence Harvey, Pennington Biomedical Research Center, Baton Rouge, LA, USA; and Jia Xu Li, University of Toronto), presented 3-minute poster abstract summaries, which were part of the subsequent virtual poster session presented the same afternoon and well received by the online audience.

The second day of the conference began with the morning session focusing on systems biology approaches to interrogate nuclear steroid receptor functions, and was chaired by Andrea Cignarella (University of Padova, Padua, Italy) and Lindsey Trevino (City of Hope, Duarte, CA, USA). Topics presented in this session included glucocorticoid receptor-dependent transcription in single cells and individual genes (Trevor Archer, National Institute of Environmental Health Sciences, Durham, NC, USA), imaging of nuclear receptor actions at the single cell level (Fabio Stossi, Baylor College of Medicine, Houston, TX, USA), subcellular localization of estrogen receptor (ER) and cardiometabolism (Pierre Gourdy, University of Toulouse, Toulouse, France), mechanisms of ER enhancer function (Lee Kraus, University of Texas Southwestern Medical Center, Dallas, TX, USA), and steroid G protein-coupled receptor (GPCR)-mediated renal fibrosis in Drosophila (Marc Tatar, Brown University, Providence, RI, USA). Lectures were again followed by talks given by young investigators (Eriko Katsuta, Roswell Park Comprehensive Cancer Center, Buffalo, NY, USA; Ayca Mogol, University of Illinois; Qianying Zuo, University of Illinois; and Kendall Langsten, Wake Forest School of Medicine, Winston-Salem, NC, USA) and by a career development workshop entitled “Presenting your science to the public,” by Mila Becker, Chief Policy Officer of the Endocrine Society. The afternoon session was chaired by Martin Kelly (Oregon Health and Science University, Portland, OR, USA) and included a number of presentations of different aspects of steroid functions in the brain. Gabriele Rune (University of Hamburg, Hamburg, Germany) presented insights into the sex-dependent effects of neurosteroids in the hippocampus; Charlotte Cornil (University of Liège, Liège, Belgium) discussed nuclear and membrane-actions of neuroestrogens in the control of male sexual behavior, and Margaret Mohr (University of California, Los Angeles) provided an update on estradiol-induced hypothalamic progesterone synthesis during pubertal development. In the second half of the session, Kevin Sinchak (California State University, Long Beach, CA, USA) discussed how neuroprogesterone and progesterone receptor regulate the lutenizing hormone surge, John Meitzen (North Carolina State University, Raleigh, NC, USA) gave a talk on how estradiol rapidly modulates excitatory synapse properties in the nucleus accumbens, and Karyn Frick (University of Wisconsin, Madison, WI, USA) discussed ERβ activation as a potential treatment for alleviating menopausal symptoms, such as hot flashes. The second day ended with a third lightning round, with 4 short talks given by young investigators (Michael Saikali, University of Toronto; Dominik Awad, M. D. Anderson Cancer Center; Ashlie Santaliz Casiano, University of Illinois; and Cameron Leyers (Medical University of South Carolina, Charleston, NC, USA), summarizing their poster presentations.

The last day of the conference was dedicated to novel roles of steroids and steroid receptors in neoplastic and other diseases. The morning session, “Novel functions of steroid receptors in cancer,” was chaired and moderated by Christy Hagan (University of Kansas, Lawrence, KS, USA) and Stephen Hammes (University of Rochester, Rochester, NY, USA). The session was opened by Rosamaria Lappano (University of Calabria, Rende, Italy), who spoke about the role of the membrane receptor G protein-coupled estrogen receptor (GPER) in breast cancer, followed by Carol Lange (University of Minnesota, Minneapolis, MN, USA), who discussed signaling properties of progesterone receptor and glucocorticoid receptors in stemness, and Marina Holz (New York Medical College, Valhalla, NY, USA), who presented new data on estrogen/mTOR crosstalk in lymphangioleiomyomatosis and breast cancer. These lectures were followed by Matt Sikora (University of Colorado, Anschutz, CO, USA) who shared recent progress on the role of ERs in the therapy response and resistance in lobular mammary carcinoma and by Scott Tomlins (Strata Oncology, Ann Arbor, MI, USA), who gave a talk on high-throughput -omics to identify driver mutations and gene fusions in cancer. The session also featured short talks from five young investigators, presenting data from their virtual posters (Anasuya Das Gupta, University of Illinois; Sarah El Kharraz, KU Leuven, Leuven, The Netherlands; Asmaa El-Kenawi, Moffitt Cancer Center, Tampa, FL, USA; Wanting Han, University of Massachusetts Boston, Boston, MA, USA; and Thu Truong (University of Minnesota).

In the first afternoon session of day 3 of the conference, Donald DeFranco (University of Pittsburgh) and Ellis Levin (University of California, Irvine, CA, USA) moderated a series of lectures on new mechanisms and approaches of how to target steroid receptors. Elahe Mostaghel (Fred Hutchinson Cancer Center, Seattle, WA, USA) discussed how prostate cancer and how adrenal androgens and AR axis inhibition may contribute to therapy resistance and serve as predictors of the therapeutic response. Douglas Kojetin (Scripps Research Florida, Jupiter, FL, USA) then presented evidence on how to use nuclear magnetic resonance spectroscopy to visualize ligand-induced peroxisome proliferator-activated receptor γ (PPARγ) repression. Edward Filardo (University of Iowa, Iowa City, IA, USA) discussed dual specificity proteolysis-targeting chimeras (PROTACs) targeting GPER and ERs, and John Katzenellenbogen (University of Illinois) presented recent evidence from his laboratory demonstrating ERβ-mediated effects in response to very low affinity ER ligands. All talks were followed by questions from the online audience, with lively and engaging discussions moderated by the chairs.

The subsequent afternoon session, which concluded the conference, was chaired by Kristy Brown (Weill Cornell Medicine, New York, NY, USA) and Subhamoy Dasgupta (Roswell Park Comprehensive Cancer Center). The session focused on mechanisms of crosstalk between nuclear steroid receptors and metabolic pathways. Ian Mills (Queens University Belfast, Belfast, UK) discussed how androgens regulate metabolism in prostate cancer, and Rebecca Riggins (Georgetown University, Washington, DC, USA) presented evidence for novel functions of ER-related receptor β (ERRβ) in the pathogenesis of glioblastoma. Giorgia Zadra (National Research Council of Italy) reported data on the modulation of intra-tumor lipid metabolism via androgen receptor. Erik Nelson (University of Illinois) then discussed how cholesterol, ER, and liver X receptors (LXRs) modulate the tumor microenvironment in breast cancer, and Philip Shaul (University of Texas Southwestern Medical Center) closed the meeting presentations with data from his and other laboratories on endothelial ER signaling and its effects on cardiometabolic health and disease.

Despite the challenges imposed by COVID-19 and the virtual character of the conference, all sessions saw lively discussions and participation from the online audience. Results from the feedback evaluation were very positive regarding the organization of the meeting and the selection of topics. More than 90% of attendees who provided feedback gave favorable comments regarding the general sessions, poster sessions, and the scientific content of the conference. However, there were a few who noted issues with how quickly attendees could access desired on-demand content. Regardless, essentially all respondents of the feedback evaluation indicated that they plan to attend the next meeting, which will be held next year, and that they recommend attending this meeting to other researchers in the field. Many of the speakers and presenters have agreed to write a contribution on the topic of their talks for the conference proceedings, which, as for the last 20 years, 9 – 15 , 18 – 27 will be published in the journal Steroids as a Virtual Special Issue in 2022.

The organizers express their gratitude to FASEB and to the numerous sponsors of the meeting, which are listed in the Acknowledgments, especially the U.S. National Institutes of Health (NIH) for providing funding to sponsor young investigator travel awards. These awards helped to recognize the contributions of students and postdoctoral trainees in the difficult times of the COVID-19 pandemic, resulting in an increased attendance at the meeting by junior researchers. Indeed, with the support of NIH/National Institute of Diabetes and Digestive Diseases, young investigator travel awards were awarded to every student or postdoc who expressed interest in attending the online conference. The next conference (in the form of the 13th International Meeting on Rapid Responses to Steroid Hormones, RRSH 2022) will be held in September 2022 in Paris, France, at the historic venue of the Sorbonne Université, which reaches back to the year 1257 and is one of the oldest and most prestigious universities in the world. 28 The organizers hope to welcome scientists active in all fields of steroid hormone research and medicine in Paris next year.

Acknowledgments

The authors extend special thanks to FASEB for their assistance throughout the organization of this conference, especially Andrea Bauerfeind for her support with organizing the online conference. The authors also thank Silvy Song, their FASEB conference manager, for her hard work in ensuring a well-organized and smoothly run meeting, as well as Bahara Saleh, who was instrumental in coordinating the meeting’s sponsors and finances. A special thanks also to Paul Mermelstein, who helped to plan initial stages of the meeting. Finally, the authors thank their sponsors for their maintained support throughout the COVID19 pandemic, as well as the U.S. National Institutes of Health (NIH)/National Institute of Diabetes and Digestive Diseases (NIDDK) and National Cancer Institute (NCI) for providing generous support for the conference (R13 DK126171). This conference was supported by generous contributions from FASEB, Dr. Paul J. Davis (Pharmaceutical Research Institute at Albany College of Pharmacy and Health Sciences, Albany, NY, USA), the University of Illinois (Urbana-Champagne, IL, USA), the University of New Mexico (Albuquerque. NM, USA), Tulane University (New Orleans, LA, USA), AbbVie (Lake Bluff, IL, USA), Pfizer (New York, NY, USA), and the journals Science Signaling (American Association for the Advancement of Science, Washington, DC, USA), the Journal of Biological Chemistry (American Society for Biochemistry and Molecular Biology, Rockville, MD, USA), Steroids (Elsevier, Amsterdam, The Netherlands), the Journal of Neuroendocrinology (John Wiley& Sons, Hoboken, NJ, USA), and Endocrine-Related Cancer (Society for Endocrinology, North Bristol, UK). This conference was supported by grant R13 DK126171 from NIH/NIDDK and NCI. M. Barton is supported by the Swiss National Science Foundation (grants 108 258 and 122 504); D. E. Frigo is funded by NIH (grants R01CA184208 and P50CA14038s); Z. Madak-Erdogan is funded by the U.S. Department of Agriculture/National Institute of Food and Agriculture (grants ILLU-698-331 and ILLU-698-924); F. Mauvais-Jarvis is funded by NIH (grants DK107444 and DK074970) and a U.S. Department of Veterans Affairs Merit Award (BX003725); and E. R. Prossnitz is supported by NIH (grants R01 CA163890, R01 CA194496, P30 CA118100, P20 GM121176) and Dialysis Clinic, Inc. (Nashville, TN, USA; grant RF#C3937). The views expressed in written conference materials or publications and by organizers, speakers, and moderators do not necessarily reflect the official policies of the NIH, nor does mention by trade names, commercial practices, or organizations imply endorsement by the U.S. Government.

Abbreviations

estrogen receptor

G protein-coupled estrogen receptor

Federation of American Societies for Experimental Biology

Rapid Responses to Steroid Hormones

Science Research Conference

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