Download Psychiatric complications of Anabolic Steroid Abuse.

Review Articles
Psychiatric Complications of Anabolic Steroid Abuse
RYAN C.W. HALL, M.D.
RICHARD C.W. HALL, M.D.
MARCIA J. CHAPMAN
The authors review the literature from human and animal studies on the neurochemical and
pathological psychiatric effects of supraphysiological doses of anabolic-androgenic steroids
(AAS) and discuss the AAS use and abuse patterns, additional drug use patterns, and personality
and behavioral characteristics of AAS abusers.
(Psychosomatics 2005; 46:285–290)
I
n 1889, physiologist Charles E. Brown-Sequard made
the first public claims about the effects of anabolic-androgenic steroids (AAS). He announced that he had extracted a substance from dog and guinea pig testicles,
which, when injected, had increased his strength, improved
his intellect, provided relief from constipation, and increased the arc of his urine.1 Since then, an underground
population of athletes, coaches, and recreational users has
developed complicated AAS regimens to enhance their athletic performance and, in so doing, have unleashed a myriad of psychiatric complications such as addiction, depression, rage, and psychosis on themselves and the public at
large.
Psychiatric Syndromes and the Issue of Violence
Historically, low doses of AAS have been used to treat
depression and melancholia, either as primary agents or as
adjuncts to standard treatment.1 Misuse of these agents has
added a new term to the drug lexicon, “roids rage.”2 Studies comparing steroid abusers with non-steroid-using athletes have shown steroid abusers to have a higher incidence
and prevalence of psychiatric symptoms.3–5 The most
prominent psychiatric features associated with AAS abuse
are manic-like presentations defined by irritability, aggressiveness, euphoria, grandiose beliefs, hyperactivity, and
reckless or dangerous behavior. Other psychiatric presentations include the development of acute psychoses, exacerbation of tics and depression, and the development of
Psychosomatics 46:4, July-August 2005
acute confusional/delirious states.2,6–8 Extreme variability
of symptom presentation exists because of differences in
the dose consumed, agent used, duration of use, personality
type of the abuser, and current or previous use of other
recreational drugs.2,9–11
Studies in which steroid abusers have been used as
their own comparison subjects, in the attempt to eliminate
the variable of personality disorder, have shown differences in the degree of hostility, aggression, and severity of
manic-like symptoms during periods of use and nonuse.4–8
Pope and Katz,6,12 in their reviews of the literature, reported that studies in which steroid use is quantified and
categorized on the basis of total weekly dosing have found
that psychiatric symptoms become more common and severe as the dose increases. Studies that have used Pope and
Katz’s categories of medium steroid use (between 300 and
1000 mg/week of any AAS) and high use (more than 1000
mg/week of any AAS)6 have demonstrated that 23% of
subjects using these doses of steroids met the DSM-III-R
criteria for a major mood syndrome (mania, hypomania,
and major depression) and that 3.4%–12% developed psychotic symptoms.6,8
It is hard to determine whether the unexplained violent
Received March 9, 2004; revisions received June 29 and Aug. 19, 2004;
accepted Sept. 27, 2004. From the Department of Psychiatry and Behavioral Sciences, Johns Hopkins Hospital, Baltimore; and the Department
of Psychiatry, University of Florida, Gainesville. Address correspondence
and reprint requests to Richard C.W. Hall, M.D., 100 East Sybelia Ave.,
Suite 210, Maitland, FL 32751.
Copyright 䉷 2005 The Academy of Psychosomatic Medicine.
http://psy.psychiatryonline.org
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rages that occur with AAS abuse might be better understood as part of a paranoid psychotic state or as instances
of unprovoked rage unassociated with other psychiatric
findings (i.e., as a psychiatric or cognitive disorder or as
an impulse control problem). Psychotic symptoms associated with the use of anabolic steroids generally occur
among individuals consuming more than 1,000 mg of testosterone weekly.6 Classic presentations include grandiose
and paranoid delusional states that often occur in the context of a frank psychotic or manic episode. The symptoms
usually resolve within a few weeks after the individual has
discontinued steroid use, although they may persist for as
long as 1 month, even if adequately treated with antipsychotic medication. Reactions tend to be more agitated, violent, and coordinated than the agitation that occurs as an
adverse reaction to corticosteroids, which can also produce
idiosyncratic manic and psychotic symptoms.9,10
Psychiatric Pathology of AAS Abuse
Pope and Katz13 interviewed 41 bodybuilders and football
players who had used AAS. Applying DSM-III-R criteria,
they found that 22% displayed a full affective syndrome
and 12% developed psychotic symptoms in association
with their steroid use, suggesting that major psychiatric
symptoms are an adverse effect of the misuse of these
drugs. In a subsequent study, Pope and Katz6 used the
Structured Clinical Interview for DSM-III-R to compare
88 athletes who used steroids with 68 nonusers. They
found that 23% of the AAS users reported major mood
syndromes, including mania, hypomania, and major depression, in association with their steroid use. The steroid
abusers experienced mood disorders significantly more frequently when using AAS than when they were steroid free.
Su et al.14 administered 40 mg/day and 240 mg/day of
methyltestosterone in a 2-week, double-blind, fixed-order,
placebo-controlled, crossover inpatient study of healthy
male volunteers. The 20 men in the study were otherwise
medication free and were free of any medical or psychiatric
illness. The researchers noted higher symptom scores
during high-dose methyltestosterone administration, compared with baseline. The changes were either moodelevating effects, such as euphoria (“steroid rush”), increased energy, and increased sexual arousal and drive, or
mood-dysphoric effects, such as irritability, mood swings,
increasingly violent feelings, and increased hostility. The
researchers also noted cognitive impairment, including
distractibility, forgetfulness, and confusion, in subjects taking the higher dose of steroids. Baseline characteristics,
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including family history and history of previous drug
abuse, did not predict the development or the nature of
psychiatric symptoms.
In a randomized, placebo-controlled crossover trial,
Pope et al.15 administered testosterone cypionate for 6
weeks in doses ranging to 600 mg/week, followed by 6
weeks of no treatment and then placebo for 6 weeks to
56 men ages 20–50 years. A variety of outcome measures
were used to assess mania, aggression, and depression. The
results showed that testosterone significantly increased mania, elevating scores on multiple instruments; that the drug
was liked and sought after; and that aggression increased.
The investigators noted that the response to the drug, however, was highly variable. Eighty-four percent of the subjects exhibited minimal to no psychiatric effects, 12%
became mildly hypomanic, and 4% became markedly hypomanic. The investigators were not able to differentiate
the manic responders from the nonresponders on the basis
of demographic characteristics or baseline psychological,
laboratory, or physiological measures.
Yates et al.16 examined the psychosocial effects of
low-dose steroids in men as a possible form of birth control
and found minimal risk of adverse psychosexual effects in
the majority of men receiving less than 500 mg/week of
testosterone cypionate. At a dose of 500 mg/week, however, a minority of subjects began to experience significant
adverse psychological effects, such as dysphoria, irritability, and hypomania.
Hall et al.9–11 and Wyszynski and Wyszynski17 suggested that the adverse effects of testosterone may be similar to those of prednisone and other corticosteroids. Studies
by Hall et al.9–11 and the Boston Collaborative Program18
have shown that adverse psychiatric effects increase with
increasing dosages of corticosteroids, a finding similar to
that of Pope et al.15 for AAS.
Investigative Findings and Anecdotal Reports
on Aggression
Choi and Pope19 noted that increased aggression was associated with the illicit use of AAS by athletes and that the
wives and girlfriends of these athletes often become the
victims of physical abuse. In a controlled study, they interviewed 23 AAS-using strength athletes and 14 non-AAS
using athletes. The AAS users reported significantly more
fights, verbal aggression, and violence toward their significant other and had significantly higher scores on two of
three indicators of violence during periods when they were
taking AAS, compared to periods when they were not takPsychosomatics 46:4, July-August 2005
Hall et al.
ing AAS. When they were not taking AAS, the AAS users
were not distinguishable from nonusers on the aggression
scales.
Bond et al.20 investigated the effects of AAS on attentional bias to aggressive cues in 46 male strength athletes.
The researchers found no difference in attentional bias between AAS users and nonusers but noted that AAS users
who were currently taking AAS had subtle mood changes
and slowed cognitive performance, compared to users who
were not actively taking AAS.
Anecdotal case reports published by Pope and Katz21
highlighted both the psychological and physical dangers of
abusing AAS. They described three men with benign premorbid psychiatric histories and no evidence of antisocial
personality disorder or violence who impulsively committed violent crimes, including murder, while taking AAS.
Pope and Katz suggested that the steroids played a necessary, if not primary, role in the etiology of these violent
behaviors. They concluded that steroid-induced violence
poses a little-recognized public health threat.
We have seen six cases of AAS-induced criminal behavior—three homicides and three violent assaults. Two of
the three lethal assaults were senseless, nonpremeditated,
and occurred during a psychotic episode. In three of the
six cases, there was evidence of significant antisocial behavior, violence, or criminal behavior before the steroidrelated episode. The AAS psychosis in each case was remarkably similar to that in the others, as well as to AAS
psychoses described in the literature, and included stereotypic qualities of irritability, aggressiveness, and grandiosity. In each case, an irrational thought of the patient or a
minor deed of an unknown individual prompted a violent
attack. The mental status of all six perpetrators cleared
within weeks to 2 months, and they had specific memory
of the act and of their delusional thinking at the time the
act was committed.
Other studies have tried to measure aggression and
psychiatric disturbances in AAS abusers by looking at how
they died. An investigational study of 34 deceased male
AAS abusers found that nine were the victims of homicide,
11 had committed suicide, and 12 died of accidental
causes.22 The authors concluded that AAS abusers are at a
higher risk of dying violently because of impulsive/
aggressive behavior and/or depression.
Animal Studies of Neurochemical Changes
Studies examining neurochemical changes in sexually maturing/adolescent animal brains exposed to supraphysioPsychosomatics 46:4, July-August 2005
logical doses of AAS have found complex changes in multiple neurochemical communication pathways long
associated with depression, anger, and sexual behavior in
humans. Studies of neurohormonal receptors in adolescent
rodent brains found that AAS exposure was associated with
a decrease in the inhibitory receptors for c-aminobutyric
acid in the medial amygdala, medial preoptic area, and ventromedial nucleus of the hypothalamus.23,24 Studies in nandrolone-treated guinea pigs showed a significantly greater
density of c-Fos and Fos-related antigen-positive neurons
in the central nucleus of the amygdala and of Fos-related
antigen-positive neurons in the frontal cortex, the shell of
the nucleus accumbens, and the supraoptic nucleus.25
These areas have been shown to correlate with human brain
areas that are involved in stress, behavioral, and reward
responses. Animal studies have also shown that AAS have
effects on serotonin receptors, specifically a significant
down-regulation of 5-HT1B receptor density in the hippocampus CA1 region and the medial globus pallidus and a
significant up-regulation of 5-HT2 receptor density in the
nucleus accumbens shell.26 Alterations in receptor density
were also observed in the lateral globus pallidus, ventromedial hypothalamus, amygdala, and intermediate layers
of various cortical regions. In studies of the anterior hypothalamic-arginine vasopressin (AH-AVP) neural system
in animals treated with anabolic steroids, the treated animals had biting tendencies and less time to provocation to
bite, compared with control animals; these effects could be
reduced or reversed by using AH-AVP antagonists.27
Characteristics of AAS Abusers
The typical AAS abuser is a male polysubstance abuser
who has poor self-esteem, poor school performance, and a
cluster B personality disorder or traits and who may or may
not participate in an organized sport.28–32 Males are two to
three times more likely to abuse AAS, compared with females.29,30 Sixty to 70% of AAS abusers actively participate in organized sports.29 Other factors that correlate with
AAS abuse include higher socioeconomic status, a family
history of drug abuse, higher rates of self-reported violence
and aggression, lower self-esteem, and poor body image
before AAS use.29,32,33 In a study by Kindlundh33 in Sweden, being an immigrant was also found to correlate with
AAS use.
There have been some interesting studies concerning
the relationship of personality disorder to AAS abuse.
Yates et al.34 found a higher prevalence of cluster B personality disorders of the histrionic and antisocial type in
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weightlifters who abused AAS, compared to weightlifters
who did not use AAS.34 Porcerelli and Sandler35 found that
steroid users evidenced higher scores on measures of
pathological narcissistic traits (exhibitionism, entitlement,
and exploitativeness) and lower ratings for empathy, relative to non-AAS-using weightlifting comparison subjects.
Another interesting finding of Porcerelli and Sandler was
that 25% of the AAS abusers in their study, but none of
the nonabusing comparison subjects, had memories of
childhood sexual or physical abuse. In a case control study,
Kanayama et al.32 found that AAS abusing weightlifters
reported poorer relationships with their fathers and a
greater incidence of childhood conduct disorder, relative to
non-AAS-using comparison subjects.
mon for users to take multiple forms of AAS (five different
drugs on average) from multiple classes of steroids to take
advantage of the different pharmacokinetic properties of
these drugs.6,40,42
Stackers generally take supraphysiological doses of
anabolic steroids for 4–18 weeks, followed by a drug-free
period of 1–12 months.41 The purpose of the drug-free period is to minimize side effects, promote recuperation of
various hormonal systems, and avoid detection of AAS use
during athletic competition.2 Some abusers will try to taper
off AAS at the end of a stacking cycle to reduce side effects
and withdrawal, a practice called “pyramiding.”41 Because
of the intricate nature of these stacking regimens, many
users have a “coach” who helps coordinate the schedule
and drugs given.42
AAS Dependence
Polysubstance Abuse and AAS
No evidence is reported in the reviewed literature that AAS
abuse or dependence develops from the therapeutic use of
AAS.36 Conversely, 165 instances of AAS dependence
have been reported among weightlifters and bodybuilders
who chronically administered supraphysiological doses of
anabolic steroids as part of their weight training regimen.36,37 Individuals who use high doses of AAS over prolonged periods may develop depressive symptoms, anhedonia, fatigue, impaired concentration, and even suicidal
thoughts when they stop taking AAS, and these withdrawal
effects may contribute to a syndrome of dependence.
Brower et al.5,38,39 conducted several studies examining the
issue of AAS dependence. In their initial studies, 75% of
the steroid abusers met the DSM-III-R criteria for psychoactive substance dependence and all steroid-abusing subjects met the criteria for psychoactive substance abuse.38
In subsequent larger studies, Brower et al.38 found a 60%
rate of psychoactive substance dependence in anabolic steroid abusers. In general, they found that steroid withdrawal
usually presented with depression, especially in cases of
intense AAS abuse.5 Steroid discontinuation effects were
variable and transient and appeared to be more common
when 17-alpha-alkalated formulations of AAS were discontinued.37
Usage Patterns, Including Stacking and Pyramiding
Recreational AAS users generally develop complicated
multidrug regimens using oral and intramuscular preparations (see Table 1) at progressively higher doses until 40–
100 times the usual physiological levels are reached.28,40,41
This practice is referred to as “stacking.” It is not uncom288
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AAS users are often polysubstance abusers, and their polysubstance abuse may include use of traditional recreational
drugs and misuse of prescription drugs. Even those who
avoid traditional recreational drugs are still enveloped in
the drug culture to obtain steroids (e.g., from suppliers or
pushers), to find ways to administer them (e.g., finding
large-gauge needles), and to develop means to continue
using steroids (e.g., hiding use and paying for AAS).5,42–44
Studies examining AAS use as a gateway to other drugs of
abuse found that 29% of people who abused both steroids
and opioids started with steroids and were later introduced
to opioids by the person who supplied them with the
AAS.36,44 DuRant et al.44 found that 25% of the AAS abusers in their study shared needles to inject drugs and that a
positive correlation existed between AAS abuse and the
use and abuse of cocaine, injectable drugs, and marijuana.
Many dual-substance abusers have reported starting to take
opioids to counteract the side effects of AAS, such as insomnia, irritability, jitteriness, and the depression associated with withdrawal from AAS.43
For those who use steroids to enhance “bodily health,”
the use of additional drugs to further enhance the effects
of AAS or to decrease AAS side effects is common. Other
drugs that are frequently abused as adjuncts include human
growth hormone, which acts synergistically with AAS; human chorionic gonadotropin to reduce the testicular side
effects of the anabolic steroids; diuretics to prevent water
retention and improve visual muscle appearance (rippled
effect); and antiestrogens such as tamoxifen to block gynecomastia.44,45 To help hide the fact that steroids are being
used, some AAS abusers will take antibiotics and antiacne
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Hall et al.
medications to prevent testosterone-induced acne, which
often involves the face, neck, and torso.
of certain cancers (hepatocellular carcinoma), and sudden
death.2,5,6
Summary
Complications and Side Effects of Supraphysiological
Doses of Androgens
Data defining the cumulative effects of stacking remain
speculative and are mostly derived from case reports.41 Reported side effects can be as benign as acne and fluid retention or extend to more distressing effects such as gynecomastia, lower levels of high-density lipoprotein (HDL
cholesterol), and sleep apnea. Extreme side effects can lead
to lethal complications such as hepatic failure, myocardial
infraction, tendon rupture, arrhythmias, the development
TABLE 1.
Current data suggest that AAS abuse can increase aggression and cause rage, delirium, depression, mania, psychosis, and withdrawal symptoms. Psychiatric symptoms are
seen at greater frequency with increasing doses of AAS.
After discontinuation of AAS use, most psychiatric sequelae resolve within 8 weeks. Animal data suggest that
taking anabolic steroids alters multiple neurochemical
pathways. Use of AAS can lead to criminal behavior, such
as drug abuse, as well as to assault and homicide that can
be random and senseless.
Commonly Used Androgenic-Anabolic Steroidsa
Oral Agents
Fluoxymesterone (Halotestin, AndroidF, Ultandren)
Mesterolone (Mestoranum, Proviron)
Methandienone, methandrostenolone
(Dianabol)
Methyltestosterone (Android, Testred,
Virilon)
Mibolerone (Cheque Dropsb)
Oxandrolone (Anavar, Oxandrin)
Oxymetholone (Anadrol-50,
Hemogenin)
Stanozolol (Winstrol)
Striant (buccal delivery of testosterone)
Intramuscular Agents
Transdermal Agents
Boldenone undecylenate (Equipoiseb)
Testosterone (Androderm, AndroGel, Testim, Testoderm,
Testoderm TTS)
Methenolone enanthate (Primobolan depot)
Nandrolone decanoate (Deca-Durabolin)
Nandrolone phenpropionate (Durabolin)
Nandrolone undecanoate (Dynabolan)
Stanozolol (Winstrol-Vb)
Testosterone cypionate (Depo-Testosterone,
Virilon IM)
Testosterone enanthate (Delatestryl)
Testosterone esters blends (Sustanon, Sten)
Testosterone propionate (Testoviron,
Androlan)
Testosterone undecanoate (Andriol,
Restandol)
Trenbolone acetate (Finajet, Finaplixb)
Trenbolone hexahydrobencylcarbonate
(Parabolan)
a
International brand names are included for agents with widespread illicit use in the United States.
Veterinary compound.
b
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