by Jack Darkes, PhD
Assistant Professor, Department of Psychology
Director of Interventions, Alcohol and Substance Use Research Institute, University of South Florida

The following is a brief synopsis of a talk given at the 115th Annual Convention of the American Psychological Association (APA) in San Francisco, CA on August 19, 2007.

Existing research on substance use has had little impact on the public or researchers’ view of anabolic/androgenic steroids (AAS) and their effects. One reason is morality: It is obvious that, standing in San Francisco, AAS are synonymous with “cheating” in the public eye - I will not discuss this today. The other seemingly reflects an assumption; AAS are endogenous testosterone’s bigger twins and if endogenous testosterone (T) causes physical aggression then AAS surely must. This notion was expressed by a “clinical psychologist and media personality” who was asked if AAS caused Chris Benoit’s actions; she noted: “Testosterone is linked to aggression. We know that murderers, we measure their levels of testosterone. They have higher levels (Macari, 2007).”

Actually, human T is linked to dominance and social status (Booth et al., 2006) and challenge (Archer, 2006); aggression is but one strategy employed in those pursuits. Murderers have high T levels; so do trial lawyers and soldiers. All seek dominant status in “competitive” environments in different and more or less socially acceptable ways. Ultimately, “…many investigators…assume that testosterone level is a trait that explains differences between individuals with respect to aggression and violence. However, there is little empirical support for this position (Booth et al., 2006; p. 169)”.

Animal research is oft cited as support for a direct and exclusive physiological link between AAS and aggression. However, indiscriminate aggression is not universally observed in AAS-treated animals (McGinnis, 2004). AAS effects on non-human aggression vary by context (in rodentia; Breuer, McGinnis, Lumia, & Possidente, 2004) and status (in non-human primates; Dixson, 1980; Rejeski, Brubaker, Herb, Kaplan, & Koritnik, 1988). Additionally, animal studies often use adolescent animals and dosing regimens irrelevant to adult human AAS use; for instance, AAS roughly equal to 3 grams/week in a 90 kg human administered to adolescent animals throughout puberty resulted in longer-term aggression (Fischer, Ricci, & Melloni, 2007). Although these findings were highlighted in several APA publications (e.g., http://www.apa.org/releases/steroids0226.html), total weekly doses of over 2 g per week are rarely reported by AAS users (e.g., Cohen, Collins, Darkes, & Gwartney, In Press) and, given T’s role in adolescent brain development and the establishment of social behavior (Sisk, Schulz, & Zehr, 2003), such results are both unsurprising and uninformative regarding AAS effects in human adult non-medical use.

Research on aggression in adult human AAS users has largely relied on case studies and surveys. Although case studies (e.g., Pope & Katz, 1990; Thiblin, Lindquist, & Rajs, 2000), surveys (e.g., Galligani, Renck, & Hansen, 1996; Lefavi, Reeve, & Newland, 1990) and prospective surveys that follow self-selected users (e.g., Fudala, Weinrieb, Calarco, Kampman, & Boardman, 2003; Yates, Perry, & Murray, 1992) may suggest an AAS use/aggression association, results are both inconsistent and unable to determine cause and effect. Additionally, aggression measures do not reliably relate to AAS use periods (e.g., Fudala et al., 2003) or dose (e.g., Lefavi et al, 1990; Yates et al., 1992).

Within-subject experiments that administer AAS and placebos (e.g., Pope, Kouri, & Hudson, 2000, Su et al., 1993) may show subtle effects, but find no relationship between blood steroid levels and symptoms (e.g., Su et al., 1993).  Between-subject experiments that evaluate causation by controlling for individual differences via rigorous inclusion criteria, random assignment and blinding to drug conditions offer little evidence of an AAS/aggression link (e.g., O’Connor et al., 2002; Tricker et al., 1996).

Experimental findings vary depending on the measure of aggression. Validated self-report measures typically do not show meaningful increases (e.g., Tricker et al., 1996). Self and observer ratings rarely reflect increased aggression (e.g., Pope et al., 2000; Tricker et al., 1996). The Point Subtraction Aggression Paradigm (PSAP), a laboratory task which scores punitive responses to a fictitious opponent as aggression, increased slightly within participants given AAS, although “…most participants showed little change and a few showed marked changes (p. 135; Pope et al., 2000)”. Additionally, the PSAP may assess aggression as a competitive strategy (Archer, 2006) which may not reflect the aggressive behavior of interest. In addition, the PSAP levels during AAS administration resembled those of marijuana users during withdrawal (Kouri, Pope, & Lukas, 1999).

Aggression in AAS users is rare and there is no consistent evidence that it is a direct effect of AAS. The designs used offer discrepant pictures. Case studies exaggerate problems (Hartgens & Kuipers, 2004) by highlighting illustrative “failures” and ignoring “non-problem” cases, which could provide useful information (“Who does not become aggressive and why?”). Surveys of AAS-users and non-users are descriptive but confound correlates, consequences, or antecedents. Experiments administer supraphysiological doses, raising testosterone levels 300%, but cannot mimic real-world doses and polypharmacy. [Still, if the initial T/aggression hypothesis were correct and physiological T variations predicted aggression, then levels three times normal should also do so, if increased T levels were the sole cause.] Lastly, while still blinded, participants could retrospectively distinguish AAS from placebo (Su et al., 1993) in within-subject experiments, suggesting that inert placebo comparison treatments are insufficient (see Riem & Hersey, 1995).

The role of individual differences, learning and context in drug use and drug-related behaviors has long been explored in substance use research. Antecedent factors, context and anticipation influence alcohol use and post-consumption behaviors (see Goldman, Darkes, & Del Boca, 1999).  Expectations for alcohol mediate (transmit) the influence of antecedents (e.g., sensation seeking, aggression) on drinking (Darkes, Greenbaum, & Goldman, 2004; Derman & George, 1989) and predict non-consumptive (outcome) behavior after exposure to drug-relevant cues (Bartholow & Heinz, 2006; Friedman, McCarthy, Bartholow, & Hicks, 2007).  Procedures that modify expectancies affect consumption (Darkes & Goldman, 1993; Stein, Goldman, & Del Boca, 2000). Expectancies predict patterns of cocaine use and subjective response (e.g., Lundahl & Lukas, 2007; Schafer & Brown, 1991). Seventy-five percent of the effects of anti-depressant drugs can be attributed to expectancies (a placebo effect; Kirsch & Saperstein, 1998). AAS researchers have largely failed to avail themselves of this literature.

AAS’ effects on strength and muscle mass gain were once considered placebo-mediated, but are now largely unquestioned (e.g., Bhasin et al., 1996). Still, building on work by Ariel and Saville (1972), recent studies found changes in strength among college students (e.g., Kalasountas, Reed, & Fitzpatrick, 2007) and national level power lifters (Maganaris, Sharp, & Collins, 2000) in those expecting to consume AAS. A similar, but un-replicated expectancy effect for aggression was seen in placebo-treated participants in an AAS study (Björkqvist, Nygren, Björklund, & Björkvist, 1994). Higher levels of trait impulsivity were associated with increased aggression levels above and beyond any effect of experimentally-administered AAS (O’Connor, Archer, Hair, & Wu, 2002).

Numerous researchers (Brower et al., 1994; Grogan, Shepherd, Evans, Wright, & Hunter, 2006; Hildebrandt et al., 2006; Olrich & Vasallo, 2006) have highlighted expectations that could motivate AAS use and predict use-related outcomes. Users and non-users expect AAS may lead to aggression (e.g., Schwerin & Corcoran, 1996). These expectations may be valued differently; some users may value aggression and both use AAS as a result of, and subsequently behave in accordance with, that expectation, as has been demonstrated for alcohol (Friedman et al., 2007). Although a role for psychosocial factors in AAS-related aggression was suggested years ago (Riem & Hersey, 1995; Sharp & Collins, 1998), these factors remain largely unexplored in AAS use and its psychological effects, perhaps reflecting a bias toward physiological explanations.

Discussing Benoit, Nancy Grace lamented: “…it would ease my heart to know maybe he was on steroids…I’d rather think that than think that he could do that (Grace, 2007)”. Her sentiments imply that “true” inevitable causes are physiological; otherwise the act is less “real” or more deliberate. That notion is inconsistent with what we know about human behavior, substance use and its behavioral effects. A role for psychosocial processes does not mean a behavior any less real or more volitional. Aggression is rare but real, no matter the cause. None of these processes requires contemplation. However common the desire may be, it is a disservice to seek comforting answers instead of accurate ones.

The good news is that aggression is rare among anabolic-androgenic steroid users and does not appear to be caused by AAS. The discrepant findings in the literature suggest a complex causal picture, including antecedent, cognitive, and contextual factors. Users view the AAS experience positively (e.g., Olrich & Ewing, 1999; Olrich & Vasallo, 2006) and minimize negative side-effects (e.g., Grogan et al., 2006). They consider medical authorities uninformed (e.g., Cohen et al., in press; Pope, Kanayama, Ionescu-Pioggia, & Hudson, 2004) likely because AAS research seems narrowly focused on effects that most users do not experience. This distrust is likely to perpetuate because most prospective users learn from current users within the subculture, often via the internet (Cohen at al., in press). Still, many AAS researchers seem determined to run the same studies using different measures until they find the results they are sure are there rather than learning from obtained results and moving forward with new study designs that might explain the phenomenon; an approach that reinforces users’ mistrust. Science would progress by forgoing sweeping generalizations and dire predictions of rare outcomes and moving toward identifying the factors that put a small minority at risk for AAS-related aggression, as well as those that may protect the vast majority. It should broaden its scope to include both biological and psychosocial processes that might convey that risk and, in so doing, explore approaches that might be used to reduce risk for negative outcomes.

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