Anabolic/Androgenic Steroid Use and Aggression I: A Review of the Evidence
by Jack Darkes, PhD
Department of Psychology
Director of Interventions,
Alcohol and Substance Use Research Institute
University of South Florida
The association between anabolic/androgenic steroid (AAS) use and
aggression ("’roid rage") has been widely accepted in the culture in
general, the mainstream media, and the resistance training subculture. This
view has been bolstered by the use of AAS "induced" rage as a legal defense
(Pope & Katz, 1990). And, although AAS use is not limited to those who
perform resistance exercise, the evidence suggests that lifters using AAS
are likely to use much higher doses than are those engaging in other
athletic endeavors. Therefore, aggression has been both expected and
reported to be more prevalent among weight trainers and this phenomenon has
become part of the culture of bodybuilding, as well. More recently,
naturally occurring androgen precursors have also entered the discussion
(Ueki & Okano, 1999; Yesalis, 1999).
This series will examine the support for and potential strength of the
causal link between AAS use and aggression and discuss putative processes
associated with it. In this installment, representative research on the AAS
use and aggression relationship in humans is briefly reviewed, including
limited coverage of research on endogenous testosterone levels and
aggressive behavior, in order to highlight prevalent themes in the
literature. For a more in-depth analysis, recent reviews by Bahrke, Yesalis,
& Wright (1996) and Sharp and Collins (1998) are suggested. Further
installments will evaluate the evidence for a direct causal relationship
between AAS use and aggressive behavior in humans, and a model in which
aggression in AAS users is moderated by distal antecedent factors, and
partially mediated though proximal psychological variables, will be
This series will not discuss the pharmacology of the potential
AAS/aggression relationship or potential undesirable physical effects of AAS
use. Such issues are addressed in many peer-reviewed and popular
periodicals, including Mesomorphosis. This series is not intended to suggest
a lack of potential psychiatric or medical risk involved in AAS use, nor to
endorse or condemn AAS use.
In general, although there has been tacit acceptance of the direct
relationship between AAS use and aggression in most quarters, a review of
the literature finds that support for this relationship is equivocal. In
fact, in studies that controlled for extraneous factors through rigorous
inclusion criteria and random assignment, there is little evidence to
suggest that moderate AAS use leads to aggressive behavior. However,
experimental research addressing real-world patterns and levels of use is
Testosterone, aggression, and dominance
The association of endogenous testosterone (T) with dominance,
aggression, or aggressive behavior has a long history in the literature (see
Bahrke, Yesalis, & Wright, 1990; 1996 for a
full review). The role of T in dominant behavior among males is largely
uncontested. However, the notion that dominance and aggression are the same
phenomenon is not universally accepted (see Mazur & Booth, 1998). For
instance, similar endogenous T levels have been found in both socially
dominant but nonaggressive prisoners and their aggressive counterparts
(Ehrenkranz, Bliss, & Sheard, 1974). In fact, most studies supporting an
endogenous T and aggression link might also be interpreted as suggesting a T
– dominance link (Mazur, 1976).
Studies unequivocally supporting a direct relationship between endogenous
T and aggression have largely been accomplished with animals. This
hypothesis is more rarely supported in humans. Some studies accomplished
with "pathological" populations, such as prison inmates, have found that
higher T relates to higher probabilities of committing violent crime, being
viewed as dominant, and increased rule breaking while incarcerated (Dabbs,
1996). However, this could also reflect a link between T and dominance.
Should studies support such a link, a major interpretive hurdle remains;
incarcerated individuals are likely to differ from the general populace in
many ways that might relate to aggressive behavior, T levels, or both. The
generality of such findings is limited, providing little information about T
and aggression in the general populace. Indeed, Dabbs (1996) noted that
"Relatively few people out of the entire population engage in criminal
behavior, regardless of their testosterone levels (p. 180)" suggesting
crucial differences between incarcerated subjects and the general population
that are not exclusively related to or a result of endogenous T. Such
studies highlight the difficulty in generalizing from index cases (such as
prisoners or individual "pathological" cases) to the general population.
Also of interest is the fact that the relationship between dominance and
endogenous T is not uni-directional. Endogenous T levels not only predict
dominant behavior, but are also predicted by it. Winning (the act of
dominating) has been associated with an increase in T from pre to
post-competition (see Elias, 1981; Gladue, Boehler, & McCaul, 1989; Mazur &
Booth, 1998). Hence, increased levels of T in dominant samples might be a
result rather than a cause, although this finding has not been universally
supported (see Suay et al., 1999, for instance). In addition, some
researchers have reported pre-contest rises in T, suggesting an anticipation
of future need. This anticipatory rise in endogenous T suggests a system
whereby a classically conditioned expectation exerts its influence, a system
with implications for psychological theories of the AAS/aggression
In summary, the relationship between endogenous T and aggression is
complex. As with most relationships between physiology and complex behavior,
it reflects a "biopsychosocial" process, involving an interaction between
the biological substrate of hormonal action, the psychology of the
individual, and the social environment in which behavior occurs.
Additionally, inconsistent definitions and operationalizations (e.g.,
discriminating dominance from aggression), the bi-directional effects of T
and dominance/aggression, and the lack of longitudinal studies of the
T/aggression link in large representative samples, are a few of the factors
that complicate the examination of this relationship.
AAS and aggression in humans
Even a cursory search of the psychological and psychiatric literature
finds it replete with empirical reports and case studies suggesting that AAS
users score more highly than the norm on personality scales measuring
hostility. Regardless of this seeming consensus, it has recently been
acknowledged that, although AAS use and aggression are correlated, the full
extent and nature of the relationship remains unexplained and a clear
inference of causality cannot be drawn (Beel, Maycock, & McLean, 1998). For
instance, Riem and Hursey (1995) presaged Dabbs’ (1996) sentiments regarding
T and aggression, but in relation to AAS use, commenting that "In sum, not
all AAS users exhibit aggressive behavior, even though all experience
increases in sex steroids (p. 250)." Although AAS use is reportedly
widespread (see Brower, 1992), relatively few AAS users exhibit overtly
aggressive behavior (rage). Factors that might underlie this variability
will be discussed later in this series.
The literature on endogenous T and aggression/hostility provides little
assistance in clarifying the potential AAS/aggression relationship in humans
for a number of reasons. First, in contrast to endogenous T, AAS use is a
behavioral choice. Hence, it is not randomly distributed within the
population and AAS users are likely to differ from nonusers. Secondly, AAS
ingestion and injection are not simply physical or chemical events, but also
behavioral events, part of a sub-culture and a ritual.
The literature on AAS use and aggression encompasses a range of research
methods. As with most drug use literature, it is heavily laden with
descriptive statistics. For example, lifetime prevalence of AAS use has been
reported as 9.1% for males in Great Britain (Korkia & Stimson, 1997).
Between 4% and 11% of males in the U.S. have tried AAS (Brower, 1992). And
6.3% of high school football players in Indiana are current or former AAS
users (Stilger & Yesalis, (1999). [For a full review of the epidemiology of
AAS use see Yesalis, Kennedy, Kopstein, & Bahrke (1993).] An abundance of
anecdotal "personal stories" appear in the popular bodybuilding press (e.g.,
Lefavi, 1998) and case studies are also frequent in the scientific
literature (e.g., Corrigan, 1996; Pope & Katz, 1990; Schulte, Hall, & Boyer,
1993; Wilson-Fearon & Parrott, 1999). These data represent naturalistic
evidence of this relationship. Evidence from such reports, while rich in
individual detail, contributes little to an understanding of the
relationship between AAS use and aggression in the larger population. They
are biased in that any number of characteristics might differentiate such
individuals from the general population besides their use of AAS, again
highlighting the difficulty in attempting to speculate about "normal"
processes, pharmacological or psychological, in "abnormal" cases.
Nonetheless, such cases constitute the majority of the evidence to which the
populace is exposed.
More rigorous studies involve the observation of the concurrent
correlation between variables within large groups (empirical research) or
comparisons between existing groups on concurrent measures (cross-sectional
research). Changes in relationships may be evaluated over time, either
within or between existing groups (longitudinal or prospective studies).
Lastly, treatments (i.e., the administration of AAS/placebo) may be applied
to either pre-existing groups (quasi-experimental designs) or to groups of
randomly assigned subjects (true experimental designs) who are then
evaluated over time.
Empirical and Case Studies.
A substantial amount of empirical research supports the AAS/aggression
relationship. For instance, AAS users report higher levels of anger-arousal
and hostile outlook than a group that never used AAS (Lefavi, Reeve, &
Newland, 1990). Interestingly, data collected from former AAS users was not
reported, so it is uncertain if they differed reliably from either group.
AAS users exhibit increased instances of mood disorder (Pope & Katz, 1994),
higher scores on aggression scales on personality measures (Galligani,
Renck, & Hansen, 1996; Yates, Perry, & Murray, 1992) and measures of mood
(Bond, Choi, & Pope, 1995). Nonetheless, as with the T/aggression
relationship, findings of reliable differences in psychometrically assessed
psychological characteristics between AAS users and non-users are not
universal (e.g., Malone, Dimeff, Lombardo, & Sample, 1995; Swanson, 1989).
Several case studies (e.g., Pope & Katz, 1990) and retrospective
evaluations of forensic records (e.g., Thilbin, Kristiansson, & Rajs, 1997)
have also reported associations between AAS and aggression or other
psychopathology. However, as noted previously, generalizing from case study
data or criminal index cases to the larger population is, at best, a tenuous
The majority of the empirical and case studies suffer from methodological
flaws, such as inconsistent operationalizations of aggression and differing
psychometric measures (Bahrke, Yesalis, & Wright, 1996), making comparisons
across studies difficult. Most rely exclusively on self-report measures of
aggression, a method susceptible to several sources of bias. And, as
mentioned earlier, inferring causation using such data is problematic in
that AAS use is not randomly distributed in the population. The choice to
use AAS, potentially at high doses, is likely to be confounded with a number
of predisposing individual differences. For example, current or past AAS
users might value aggression and consider aggressive responding a desirable
Ultimately, the data are largely inconsistent and inconclusive (Uzych,
1992) and a causal relationship between AAS use and aggression has not been
established (Isacsson & Bergman, 1993).
Prospective and Longitudinal Studies
Choi, Parrott, & Cowan (1990) followed current AAS users and a non-using
control group over a period of several months in a prospective and to some
extent quasi-experimental design. The AAS group was evaluated both when
using and not using AAS (an ABBA design) and non-users where evaluated at
the same times, but never used AAS. A significant group (user/non-user) by
drug phase (on/off) interaction for aggression, assessed by the Buss-Durkee
Hostility Inventory (BDHI) resulted. Subsequent tests found no reliable
effect for drug phase or user status. On the other hand, although there was
no significant interaction for hostility (BDHI), there was a reliable effect
for group: AAS users were more hostile than non-users, regardless of drug
phase. This longitudinal (prospective) quasi-experimental (self-selected
and administered treatments - used or did not use) study suggests that those
who chose to use AAS were more hostile over time, whether using or not. The
assessment of hostility prior to first ever drug use (difficult to
accomplish given the low base rate of AAS use) would be more illuminating.
This study was quasi-experimental; there was no random assignment to
conditions. Users self-selected drug use and had a prior history of use, and
the controls chose not to use AAS and were lifetime nonusers. AAS users and
nonusers have, in other empirical studies, differed in their mean scores on
a variety of self-report and psychometric measures of personality and
aggression (e.g., Galligani, Renck, & Hansen, 1996; Moss, Panzak, & Tarter,
1992). Therefore, any between group effects (as compared to "cycling on or
off" differences) merely replicate the cross-sectional findings and might
represent dispositional factors related to self-selection, rather than AAS
In a within subject, double-blind, prospective design, Su et al., (1993)
examined four within subject drug phases: placebo baseline, low dose (40
mg/day) and high dose (240 mg/day) Methyltestosterone and placebo
withdrawal. Each phase lasted 3 days. Significant increases in positive
mood, negative mood, and cognitive impairment during high dose
administration resulted. One out of twenty-nine (approximately 3.4%)
participants exhibited a hypomanic episode (an atypical, but non-severe
elevation of mood). Although changes in hostility across time showed a dose
response relationship, the only reliable differences were between placebo
and high dose time periods. These authors note that "The increased symptoms
we noted during anabolic steroid administration, while significant, were
subtle, reflecting several factors. First, the response to anabolic steroids
across members of the subject group was highly variable, ranking from
negligible to dramatic (p. 2763)." They acknowledged that marked increases
in a small number of subjects were sufficient to create significant
differences across time periods and, perhaps most interestingly, noted that
"Symptomatic differences did not, however, reflect differences in plasma
anabolic steroid levels (p. 2763)." It must be noted that this dosing
pattern, a single AAS used at relatively low doses for a very short period
of time, does not generalize to typical use in a naturalistic setting. In
fact, as the quote above suggests, any behavioral or psychological response
in this sample had less to do with blood levels of AAS than with other
apparently unmeasured variables.
Gradually increasing doses of testosterone cypionate (150, 300 and 600
mg/week) or placebo were injected, in blocks of two weeks, into eight normal
male volunteers, including both prior AAS users and nonusers (Kouri, Lukas,
Pope, & Oliva, 1995). Aggression was operationalized as the number of button
pushes chosen in order to subtract points from a fictitious opponent. The
fictitious opponents’ subtraction of points from participants represented
provocation. Two participants failed to believe the sham opponent deception
and were dropped, leaving six participants for subsequent within subject
comparisons. Increased "aggressive responding" in response to provocation,
as compared to both placebo administration and baseline measures, followed
testosterone administration. Higher scores were also reported on the
Aggression Questionnaire at post testosterone as compared to baseline,
largely due to increases in the Physical Aggression score. Whether the
participants included (five lifters and 3 non-lifters: 3 with a prior
history of AAS use) and the measure of aggression used provide much insight
into the AAS/aggression relationship is uncertain. It was not clear which
participants were excluded or, in light of the exclusions, how to interpret
the statement "Since many of the subjects could not discriminate the
testosterone treatment from the placebo treatment… (pp. 77-78)" in view of
the small number of participants included in the analyses.
Swanson (1989) examined concurrent differences between current AAS users,
non-AAS using athletes, and non-using non-athletes on aggressive behavior.
Group membership was verified by urinalysis. A sham reaction time
competition was used and the participants’ choice of a noise level to which
their "opponent" was exposed if the opponent were slower on the task
constituted the measure of aggression. Participants also completed the BDHI.
No between group differences were found in behavioral or self-report
indices. This study is subject to the previous caveats regarding
self-selection when using pre-existing groups, as well as issues related to
the operationalization of aggression. Even so, while certain correlations
were significant within the AAS using group, there were no differences
reported between AAS users, non-using athletes, and non-using non-athletes.
Several true experimental studies, incorporating random assignment of
non-using participants to AAS or placebo treatments, have recently appeared.
Although the ability of such studies to generalize to self-initiated and
self-maintained AAS use can be limited, they address a number of the
problems associated with the cross-sectional, prospective, and
quasi-experimental designs reviewed above. They constitute a true test of
the AAS/aggression relationship while controlling for biases associated with
self-selection and the existence of predisposing characteristics.
Bjorkqvist, Nygren, Bjorklund, and Bjorkqvist (1994) randomly assigned
twenty-seven male participants to receive no-treatment control, placebo, or
40 mg/day orally administered testosterone (Panteston) over a seven day
period. Both self-reported and observer-rated mood showed no effect of drug
treatment. In fact, the only reliable differences reported, for
self-reported anger, irritation, frustration, and impulsivity and for
observer ratings of frustration, indicated that the placebo group scored
higher than the no-treatment or testosterone treated groups. While, as in
earlier studies, the low dose level certainly impacts the applicability of
these results to real world AAS use, it is clear that anticipation and
expectation played a part in participants’ observer rated behavior and
self-report. However, as these authors point out "What is surprising and
calls for an explanation, is the absence of a placebo effect in the group
receiving testosterone (p. 24)."
Tricker et al. (1996), reported on mood and behavioral changes in a
sample in which physical performance changes were reported separately by
Bhasin et al., (1996). Testosterone administration (600 mg/week testosterone
enanthate in 3 ml. sesame oil or a placebo of 3 ml. of sesame oil, IM) and
exercise (strength training v. no exercise) were completely crossed to
create four treatment cells. Forty-three males were randomly assigned to the
four conditions and evaluated over a 30-week period in the following order –
4-week control period, 10-week treatment period, and 16-week recovery
period. Forty participants completed the study. Attrition was unrelated to
adverse drug effects. No between group difference in mood or behavior
assessed via psychometric instrument, self-report, or observer (significant
other) ratings were reported. As before, both dose and the use of a single
drug may not accurately reflect naturalistic practice. Nonetheless, the
administration of a supraphysiological dose of AAS over a 10-week period to
randomly assigned participants found no reliable differences in aggression
between those receiving AAS and those receiving placebo.
A recent study (Yates, Perry, MacIndoe, Holman, & Ellingrod, 1999)
reported similar results. Of 42 participants randomly assigned to receive
either 100, 250, or 500 mg/week of testosterone cypionate, 31 completed the
study. The design included a 2-week period of placebo injections for all
participants, followed by 14 weeks of injections at their assigned dose.
Attrition was largely related to failure to attend weekly visits, although
two 100 mg. dose dropouts were excluded due to psychological exclusions
(personality disorder and high BDHI prior to treatment). One 250 mg.
participant dropped out due to gynecomastia and one was lost to follow-up.
One 500 mg. subject dropped out due to worsening acne and another withdrew
due to adverse psychological effects (increased irritability, sleep-onset
insomnia, and concentration problems – but no aggressive behavior). Analyses
indicated no significant differences in attrition across the groups and no
effect of non-completion on the results found with those who completed the
No reliable effects of any dose were found for measures of aggression,
whether self-report or collateral ratings. Several quotes from these authors
are noteworthy. First, they noted "…testosterone cypionate at doses of up to
500 mg/week is associated with minimal psychological effects for the
majority of subjects in the study (p. 258)." However, "…the entry criteria
were extremely rigorous. More than half of the potential subjects were
excluded because of evidence of Axis I or II disorders or elevated
psychometric measures of aggression (p. 259)." Again, the use of a single
AAS and the range of doses administered do not reflect real world use, but
neither do the exclusion criteria. Nonetheless, through the use of random
assignment and rigorous exclusionary criteria, most potentially confounding
variables (self-selection and pre-existing psychological factors) were
controlled for in this study. The results suggest that, when such factors
are controlled for, there is relatively little evidence to link AAS use with
aggression at the doses used.
This brief review of the literature finds no clear, consistent, and
unequivocal support for the hypothesis that AAS use causes
aggression. Does this refute the anecdotal reports and case studies that
depict heavy steroid users as aggressive? No. Not only can such idiographic
results not be generalized to the larger population, but also the normative
data cannot account for all individual cases. In addition, ethical concerns
regarding the use of higher dose levels and multiple AAS in experimental
studies, confounds the pattern of use with the method of data collection
(naturalistic, empirical, or experimental). It certainly does not refute the
existing evidence for the modulation of neurotransmitter systems associated
with aggression by androgens (e.g., Cologer-Clifford, Simon, Richer, Smoluk,
& Lu, 1999). Does the inconsistency call into question the reflexive and
widespread assumption that the use of AAS inevitably leads to aggressive
behavior in humans or that such behavior is a result of purely
pharmacological events? It would seem so, at least to some extent, and
within the limits set by issues of dose and simultaneous use of multiple
AAS. Certainly the null hypothesis, that AAS use is not necessarily causally
related to aggression, cannot be rejected.
In short, as Beel et al. (1996) suggested, the literature reveals a
rather complex relationship between AAS use and aggressive behavior. Perhaps
this complexity has been over-simplified for mass distribution, an
occurrence that is common in such instances. If so, there may be several
reasons for it. The complexities of the relationship may be distilled down
to imprecise bits of information for dissemination to a populace that deals
best and most comfortably with short, easily digestible answers. People
often desire easy to grasp dichotomies, preferring simple and clear-cut
conclusions even when faced with decidedly complicated and uncertain
realities. Perhaps this simplification reflects the desire to curtail the
potential abuse of AAS. Such statements, that a certain drug causes
undesirable behavior, often become an integral part of "scare tactic"
approaches, presenting extreme or worse case scenarios to enhance negative
expectations. Unfortunately, such messages mean little to ongoing users,
whose experiences might disconfirm the assertion. And, conversely, such
statements may heighten the drug’s appeal, should the outcome (e.g.,
increased aggression) be desirable to the individual contemplating use or
lead to negative outcomes, when the taking of the drug facilitates the
Part II of this series will examine the
literature reviewed above and discuss its strengths and weaknesses as
evidence for the inference of causation in the AAS use and aggression
Bahrke, M., Yesalis, C., & Wright, J. (1990).
Psychological and behavioral effects of
endogenous testosterone levels and anabolic-androgenic steroids among
males. Sports Medicine, 10, 303-337.
Bahrke, M., Yesalis, C., & Wright, J. (1996). Psychological
and behavioral effects of endogenous testosterone and anabolic-androgenic
steroids: An update. Sports Medicine, 18, 367-390.
Beel, A., Maycock, B., & McLean, N. (1998). Current
perspectives on anabolic steroids. Drug and Alcohol review, 17,
Bhasin, S., Storer, T.W., Berman, N., Callegari, C.,
Clevenger, B., Phillips, J., Bunnell, T.J., Tricker, R., Shirazi, A., &
Casaburi, R. (1996). The effects of supraphysiologic doses of testosterone
on muscle size and strength in normal men. The New England Journal of
Medicine, 335, 1-7.
Bjorkqvist, K., Nygren, T., Bjorklund, A.C., &
Bjorkqvist, S.E. (1994). Testosterone intake and aggressiveness: Real
effect or anticipation. Aggressive Behavior, 20, 17-26.
Bond, A.J., Choi, P.Y.L., & Pope, H.G. (1995).
Assessment of attentional bias and mood in users and non-users of
anabolic-androgenic steroids. Drug & Alcohol Dependence, 37,
Brower, K.J. (1992). Clinical assessment and treatment
of anabolic steroid users. Psychiatric Annals, 22, 35-40.
Choi, P.Y.L., Parrott, A.C., & Cowan, D. (1990). High
dose anabolic steroids in strength athletes: effects upon hostility and
aggression. Human Psychopharmacology, 5, 349-356.
Cologer-Clifford, A., Simon, N.G., Richer, M.L., Smoluk,
S.A., & Lu, S.F. (1999). Androgens and estrogens modulate 5-HT1A and 5HT1B
agonist effects on aggression. Physiology & Behavior, 65,
Corrigan, B. (1996). Anabolic steroids and the mind.
Medical Journal of Australia, 165, 222.
Dabbs, J. (1996). Testosterone, aggression, and
delinquency. In S. Bhasin et al., (Eds.), Pharmacology, Biology, and
Clinical Applications of Androgens: Current Status and Future Prospects
(pp. 179-189). New York: Wiley-Liss, Inc.
Ehrenkranz, J., Bliss, E., & Sheard, M. (1974). Plasma
testosterone: Correlation with aggressive behavior and social dominance in
men. Psychosomatic Medicine, 36, 469-475.
Elias, M. (1981). Serum cortisol, testosterone, and
testosterone-binding globulin responses to competitive fighting in human
males. Aggressive Behavior, 7, 215-224.
Galligani, N., Renck, A., & Hansen, S. (1996).
Personality profile of men using anabolic androgenic steroids. Hormones
and Behavior, 30, 170-175.
Gladue, B.A., Boehler, M., & McCaul, K.D. (1989).
Hormonal response to competition among human males. Aggressive Behavior,
Isacsson, G., & Bergman, U. (1993). Can anabolic
steroids cause personality changes? Nord Med, 108, 180-181.
Korkia, P., & Stimson, G.V. (1997). Indications of
prevalence, practice and effects of anabolic steroid use in Great Britain.
International Journal of Sports Medicine, 18, 557-562.
Kouri, E.M., Lukas, S.E., Pope, G.G., & Oliva, P.S.
(1995). Increased aggressive responding in male volunteers following the
administration of gradually increasing doses of testosterone cypionate.
Drug and Alcohol Dependence, 40, 73-79.
Lefavi, R. (1998). Cops on ‘roids: The tragedy of Jim
Batsel and the formation of a new anti-steroid movement. All Natural
Muscular Development, 35, 144-.
Lefavi, R.G., Reeve, T.G., & Newland, M.C. (1990).
Relationship between anabolic steroid use and selected psychological
parameters in male bodybuilders. Journal of Sport Behavior, 13,
Malone, D.A., Dimeff, R.J., Lombardo, J.A., & Sample,
R.H. (1995). Psychiatric effects and psychoactive substance use in
anabolic-androgenic steroid users. Clin J Sport Med, 5,
Mazur. A. (1976) Effects of testosterone on status in
primate groups. Folia Primatologica, 26, 214-226.
Mazur, A., & Booth, A. (1998). Testosterone and
dominance in men. Behavior & Brain Sciences, 21, 353-397.
Moss, H.B., Panzak, G.L., & Tarter, R.E. (1992).
Personality, mood, and psychiatric symptoms among anabolic steroid users.
The American Journal on Addictions, 1, 315-324.
Pope, H.G., & Katz, D. (1990). Homicide and near
homicide by anabolic steroid users. Journal of Clinical Psychiatry,
Pope, H.G., & Katz, D. (1994). Psychiatric and medical
effects of AAS: A controlled study of 160 athletes. Archives of General
Psychiatry, 51, 375-382.
Riem, K.E., & Hersey, K.G. (1995). Using
anabolic-androgenic steroids to enhance physique and performance: Effects
on mood and behavior. Clinical Psychology review, 15,
Schulte, H.M., Hall, M.J., & Boyer, M. (1993). Domestic
violence associated with anabolic steroid abuse. American Journal of
Psychiatry, 150, 348.
Sharp, M., & Collins, D. (1998). Exploring the
"inevitability" of the relationship between anabolic-androgenic steroid
use and aggression in human males. Journal of Sport and exercise
Psychology, 20, 379-394.
Stilger, V.G., & Yesalis, C.E. (1999).
Anabolic-androgenic steroid use among high school football players.
Journal of Community Health, 24, 131-145.
Su, T., Pagliaro, M., Schmidt, P..J., Pickar, D.,
Wolkowitz, O., & Rubinow, D.R. (1993). Neuropsychiatric effects of
anabolic steroids in male normal volunteers. Journal of the American
Medical Association, 269, 2760-64
Suay, F., Salvador, A., Gonzalez-Bono, E., Sanchis, C.,
Martinez, M., Martinez-Sanchis, S., Simon, V.M., & Montoro, J.B. (1999).
Effects of competition and its outcome on serum testosterone, cortisol and
prolactin. Psychoneuroendocrinology, 24, 551-566.
Swanson, S.J. (1989). The effects of anabolic androgenic
steroids on aggressive behavior in male athletes. Dissertation
Abstracts International, 50, 5336.
Thilbin, I., Kristiansson, M., & Rajs, J. (1997).
Anabolic androgenic steroids and behavioral patterns among violent
offenders. Journal of Forensic Psychiatry, 8, 299-310.
Tricker, R., Casaburi, R., Storer, T.W., Clevenger, B.,
Berman, N., Shirazi, A., & Bhasin, S. (1996). The effects of
supraphysiological doses of testosterone on angry behavior in healthy
eugonadal men: A clinical research center study. Journal of Clinical
Endocrinology and Metabolism, 16, 3754-3758.
Ueki, M., & Okano, M. (1999). Doping with naturally
occurring androgens. Journal of Toxicology-Toxin Reviews, 18,
Uzych, L. (1992). Anabolic steroids and psychiatric
related effects: A review. Canadian Journal of Psychiatry, 37,
Wilson-Fearon, C., & Parrott, A.C. (1999). Multiple drug
use and dietary restraint in a Mr. Universe competitor: Psychobiological
effects. Perceptual and Motor Skills, 88, 579-580.
Yates, W.R., Perry, P.J., MacIndoe, J., Holman, T., &
Ellingrod, V. (1999). Psychosexual effects of three doses of testosterone
cycling in normal men. Biological Psychiatry, 45, 254-260.
Yates, W.R., Perry, P., & Murray, S. (1992). Aggression
and hostility n anabolic steroids users. Biological Psychiatry,
Yesalis, C.E. (1999). Medical, legal, and societal
implications of androstenedione use. Journal of the American Medical
Association, 281, 2043-2044.
Yesalis, C.E., Kennedy, N.J., Kopstein, A.N., & Bahrke,
M.S. (1993). Anabolic-androgenic steroid use in the United States.
Journal of the American Medical Association, 270, 1217-1221.