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Chapter 17. Treatment of Anabolic-Androgenic Steroid–Related
Disorders
TREATMENT OF ANABOLIC-ANDROGENIC STEROID–RELATED DISORDERS:
INTRODUCTION
The anabolic-androgenic steroids (AAS) are a family of hormones that includes the natural male
hormone testosterone and more than 100 other synthetic relatives of testosterone (Pope and
Brower 2004). All AAS possess both anabolic (muscle-building) and androgenic (masculinizing)
properties. Data from the National Household Survey on Drug Abuse (1994) suggest that about 1
million American men have used these drugs at some time. Although AAS use was once confined
largely to elite athletes, increasing numbers of young men have now begun to use these drugs to
gain muscle and lose fat, often simply for the sake of personal appearance (Kanayama et al. 2001).
The majority of these men are in their 20s or 30s, with a minority starting AAS use as teenagers
(Kanayama et al. 2007). Girls and women rarely use AAS because they are less likely to want to be
muscular and because AAS use makes women subject to their masculinizing effects, such as beard
growth, deepening voice, and masculinizing of sexual characteristics (Gruber and Pope 2000).
Although some recent anonymous surveys have suggested that substantial numbers of females
have used AAS (CDC, U.S. Department of Health and Human Services 2005), these surveys have
likely produced inflated estimates as a result of false positive responses on questionnaires; the true
number of female AAS users is likely very small (Kanayama et al. 2007). For these reasons, the
following discussion will focus primarily on treatment of male AAS users, although the general
principles expressed would presumably apply to the rare cases of female users as well (Gruber and
Pope 2000).
Although AAS pose important medical and psychiatric risks (described later in this chapter), AAS
users almost never seek treatment. Indeed, one recent study reported that 56% of illicit users had
never disclosed their AAS use to any physician at any time in their lives (Pope et al. 2004). There
are several reasons for this phenomenon. First, many users perceive their use of AAS to be a
positive and healthy activity when it is combined with intensive exercise and optimal diet as part of
a bodybuilding lifestyle. Commercial and societal forces are partly responsible for this
misperception of AAS (Kanayama et al. 2001): muscular male bodies are portrayed as an ideal in
advertising, magazines, television, and movies. Even children’s action toys, such as G.I. Joe, have
grown from ordinary-looking men in the 1960s and 1970s to muscle-bound specimens in the 1990s
(Pope et al. 1999). Makers of cars, electronics, and other products may promote their products as
“on steroids,” but they would never claim that their products were “on marijuana” or “on cocaine.”
Given this societal climate, it is not surprising that AAS users rarely perceive their drug use as a
psychiatric disorder requiring treatment.
Second, AAS are very different from conventional drugs of abuse. Most drugs of abuse described in
this volume deliver an immediate reward in the form of intoxication within minutes or hours of
ingestion. However, with body image drugs such as AAS, the immediate reward is negligible
(except perhaps in Stage 2 AAS dependence; see the section “AAS Dependence” later in this
chapter), and the user is seeking a long-term reward in the form of a more muscular body, athletic
success, or admiration from peers or potential sexual partners. Thus, conventional methods of
treating substance abuse are usually inappropriate unless modified specifically for AAS users
(Brower 2000; Kanayama et al. 2001).
Third, some AAS users have little respect for doctors. Underground guides and Internet sites for
illicit AAS users are replete with derogatory remarks about health professionals (Duchaine 1989);
AAS users may regard physicians as “geeks” or “pencil-necks” who have no understanding of thePrint: Chapter 17. Treatment of Anabolic-Androgenic Steroid-Related … http://www.psychiatryonline.com/popup.aspx?aID=348290&print=yes…
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bodybuilding world. For example, in one recent study, AAS users gave high marks to doctors on
knowledge of tobacco, alcohol, and ordinary drugs of abuse, but much lower marks on knowledge
of AAS. In the same study, 40% of AAS users reported that they trusted information about AAS
from their drug dealers at least as much as information from any physician that they had seen
(Pope et al. 2004). There is some basis for this distrust: for decades, many medical professionals
asserted that AAS were ineffective for gaining muscle mass. This claim, based on two decades of
seriously flawed studies, caused doctors to lose their credibility among many athletes (Pope and
Brower 2004). Now, most professionals finally concede that AAS are effective for gaining muscle
mass, but they still remain largely uninformed about the extent and nature of the AAS-using
subculture. Several recent papers have stressed that clinicians should attempt to become more
familiar with AAS and AAS-associated syndromes (Brown 2005; Dawson 2001; Kutscher et al. 2002;
Pope and Kanayama 2005).
Given the above considerations, it is understandable that AAS users almost never voluntarily
request treatment to stop using these drugs. Nevertheless, there are a number of specific
situations that bring AAS users to the attention of clinicians, at which point some attempt at
treatment may be initiated. These include 1) AAS dependence syndromes; 2) hypomanic and manic
syndromes during AAS exposure; 3) syndromes of depression and anxiety associated with AAS
withdrawal; 4) co-occurring substance use disorders, including progression from AAS use to opioid
abuse and dependence; 5) body image disorders associated with AAS use; and 6) forensic
situations, such as cases of AAS-induced violence or criminality. In the sections below, we begin
with a general discussion of the initial identification and assessment of AAS users and continue
with each of the six clinical issues enumerated above.
IDENTIFICATION AND ASSESSMENT
Identification
AAS use is one of the few types of substance use where a diagnosis is often suggested simply by
looking at the patient as he walks through the door (Pope and Kanayama 2005). As we have
described elsewhere (Kouri et al. 1995), there is a fairly sharp upper limit of muscularity that can
be achieved by a lean individual without the help of drugs. We have published a formula to
calculate muscularity, expressed as the fat-free mass index (FFMI), which clinicians can apply if
they know the height, weight, and approximate percentage of body fat of the patient (Kouri et al.
1995). Men who have low body fat and display an FFMI of greater than approximately 26 kg/m2 are
almost certainly using drugs that help them to achieve their size. We have published photographs
comparing bodybuilders who have used AAS with those who have not to aid the clinician in making
this distinction (Pope and Brower 2004). Clinicians who suspect AAS use in any patient should
follow several guidelines, described in the following section, to take a specific history.
History
The clinician may lead into the topic of AAS by asking about athletic or fitness-related activities.
Young men who lift weights regularly are at greatest risk to use AAS (Brower et al. 1994). Other
lead-in topics include the use of over-the-counter and mail-order dietary supplements such as
vitamins, minerals, amino acids, creatine, and dehydroepiandrosterone (DHEA), because the use of
such legal substances is commonly associated with AAS use. The clinician might also ask whether
the patient knows other people who use AAS—potential users often learn about AAS from other
users. Finally, the clinician could directly ask whether the patient has ever tried AAS or thought
about using them, and if so, why the patient is interested in using and what has prevented the
patient from using to date. Patients thinking about AAS use are good candidates for prevention. In
addressing these questions, it is particularly critical for the clinician to be nonjudgmental, while
still discouraging use.
For patients who admit to having tried AAS, both the perceived benefits and any adverse
consequences of use are important to determine. The dates of first and last use, the names and
doses of AAS used, sources of drugs, and routes of administration should be ascertained. PatientsPrint: Chapter 17. Treatment of Anabolic-Androgenic Steroid-Related … http://www.psychiatryonline.com/popup.aspx?aID=348290&print=yes…
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who inject AAS should be asked about needle sharing. Sources of drugs include prescriptions,
diversion from the legal market (including the veterinary market), and the illicit market. Unlike
many other drugs of abuse such as heroin and cocaine, AAS are legally available without a
prescription in many countries outside of the United States. Thus, potential AAS users can easily
travel to nearby countries and also find Internet sites offering to sell AAS from overseas. Drugs
purchased through these sites and received through the mail are often not intercepted. Patients
and clinicians should remember that drugs obtained from the illicit domestic market and from
overseas sources are frequently adulterated, falsely labeled, and sometimes nonsterile. In short,
the user does not necessarily know what and how much he is taking.
Inquiry into the patterns of use is also important. Illicit AAS users typically combine, or “stack,”
multiple AAS, including both oral and injected intramuscular forms, in order to achieve doses that
are 10–100 times the amounts ordinarily prescribed for therapeutic indications (Perry et al. 2005;
Pope and Brower 2004). AAS are usually taken in courses, or “cycles,” of 4–16 weeks or more,
often characterized by taking small doses at the beginning, building to large doses and
combinations in the middle, and tapering doses at the end—a pattern referred to as a pyramid. The
clinician gains useful information when exploring the role of cycling with an individual AAS user.
Does the patient cycle off AAS to avoid testing positive on drug screening? Does the patient cycle
off AAS to give his body a rest, allowing his endogenous hormonal system a chance to regain
normal functioning? Does the patient experience depression or other withdrawal symptoms during
off periods? Dependent users may eliminate cycling altogether in favor of prolonged, continuous
use in order to avoid withdrawal symptoms.
Finally, a history of other drug abuse should be obtained. Users often combine other drugs with
AAS to augment their effects (e.g., human growth hormone, human chorionic gonadotropin,
clenbuterol), to reduce unpleasant side effects (e.g., clomiphene, tamoxifen), and to mask urine
testing (e.g., probenicid, diuretics). Also, in contradiction to the image of the healthy bodybuilding
lifestyle, a large portion of AAS users display a history of other forms of substance abuse or
dependence. For example, in one study, 25% of men hospitalized for opioid dependence were found
to report a history of AAS use (Kanayma et al. 2003a); in another study, 88% of AAS users reported
past use of other illicit drugs, and 44% met the DSM-IV-TR criteria for a history of abuse of or
dependence on alcohol and/or an illicit drug (American Psychiatric Association 2000; Kanayama et
- 2003b).
Physical Examination
The physical examination is essential to detect the somatic consequences of using AAS. Generalized
muscle hypertrophy with a disproportionately large upper torso (neck, shoulders, arms, and chest)
is readily apparent. The skin is examined for acne (on the face, shoulders, and back) and needle
marks in large muscles (especially the gluteals, but sometimes the thigh and deltoids).
Gynecomastia, caused by metabolic conversion of excess testosterone to estrogen, may be
detectable by palpation or even simple observation in some men. Gynecomastia may occasionally
be sufficiently marked to require surgical intervention (Babigian and Silverman 2001). By contrast,
the testicles become atrophic as they shut down testosterone production when exogenous AAS are
administered in high doses; this may lead to azoospermia and sterility (Torres-Calleja et al. 2001).
Male pattern baldness, hirsutism, hypertension, hepatomegaly, right upper quadrant tenderness,
jaundice, and prostatic hypertrophy are also possible but are not reliably associated with AAS use.
In women, hirsutism, deepening of the voice, and clitoral hypertrophy may be detected.
Mental Status Examination
The clinician should assess the patient’s appearance for excessive muscularity as described above,
sometimes disguised by oversized clothes, especially in patients with muscle dysmorphia who
become preoccupied that they do not look big enough (Pope et al. 1997). The patient’s cooperation
may vary depending on his defensiveness or denial of AAS use. Speech and sensorium are generally
normal. However, if the patient is experiencing hypomanic or manic symptoms from current AAS
use, he may display irritability, agitation, and possibly grandiose beliefs. Patients experiencingPrint: Chapter 17. Treatment of Anabolic-Androgenic Steroid-Related … http://www.psychiatryonline.com/popup.aspx?aID=348290&print=yes…
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depression from AAS withdrawal may exhibit depressed mood, dysphoria, anxiety, psychomotor
retardation, and possible suicidal ideation.
Laboratory Examination
Laboratory abnormalities reported in AAS users are summarized in Table 17–1. Standard urine
screens for drugs of abuse do not include AAS, so urine testing for AAS must be performed at a
reference laboratory. Such testing can detect only recent AAS use; orally active AAS disappear from
the urine within weeks, and most intramuscular preparations disappear within a few months.
However, given the association between AAS use and other illicit drug use, standard urine screens
for illicit drugs should also be ordered.
TABLE 17–1. Laboratory abnormalities in anabolic-androgenic steroid users
Blood work
Muscle enzymes
ALT, AST, LDH and CK
Liver function tests
ALT, AST, LDH, GGT and total bilirubin
Cholesterol levels
HDL-C, LDL-C, or no change in total cholesterol and triglycerides
Hormone levels
Testosterone and estradiol (with use of testosterone esters); testosterone (without
use of testosterone esters or during withdrawal); LH and FSH
Complete blood
count
RBC count, hemoglobin and hematocrit
Urine testing
AAS Positive
Other drugs of
abuse
May be positive
Cardiac testing
Electrocardiogram Left ventricular hypertrophy (seen in intensive weight trainers also)
Echocardiogram Impaired diastolic function
Semen analysis
Sperm count and motility, abnormal morphology
Note. ALT = alanine aminotransferase, AST = aspartate aminotransferase, CK = creatine kinase, FSH =
follicle stimulating hormone, GGT = -glutamyltransferase, HDL-C = high-density lipoprotein cholesterol, LDH
= lactate dehydrogenase, LDL-C = low-density lipoprotein cholesterol, LH = luteinizing hormone, RBC = red
blood cell.
Important blood chemistries include skeletal muscle enzymes, but these can be elevated even in
non-AAS users after intensive weight training. AAS users may occasionally display extreme
elevations of creatine kinase from rhabdomyolysis (Braseth et al. 2001; Pertusi et al. 2001).
Standard liver function tests, such as transaminases and lactic dehydrogenase, are nonspecific,
because these enzymes are also present in muscle and may be elevated from weight training.
Elevation of chemistries specific to the liver, such as bilirubin and -glutamyltransferase, may
suggest true hepatic abnormalities, whereas elevated creatine kinase (an enzyme largely specific
to muscle) may suggest muscle damage (Braseth et al. 2001).
Blood testosterone concentrations may be grossly elevated in patients who are administering
exogenous testosterone, or they may be grossly depressed in patients who are administering other
types of AAS and thereby inhibiting their own endogenous testosterone production. Testosterone
levels may also remain depressed for weeks and sometimes months during AAS withdrawal.
General Considerations
Although many health consequences of using AAS are readily detectable by performing a
comprehensive history, physical examination, and laboratory tests, the long-term healthPrint: Chapter 17. Treatment of Anabolic-Androgenic Steroid-Related … http://www.psychiatryonline.com/popup.aspx?aID=348290&print=yes…
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consequences are poorly studied (Parssinen and Seppala 2002) despite the fact that evidence of
premature mortality among AAS users continues to accumulate (Parssinen et al. 2000; Petersson et
- 2006; Thiblin et al. 2000). Therefore, the clinician should be alert to heretofore undocumented
sequelae of AAS use as the first generation of users advance in age. In the meantime, the following
syndromes resulting from long-term use are most likely to bring AAS users to the attention of
psychiatrists.
AAS dependence
Although the “anabolic steroid addiction hypothesis” (Kashkin and Kleber 1989) remains subject to
debate (Bahrke and Yesalis 1994; Midgley et al. 1999), AAS are included and discussed in
DSM-IV-TR under the category of “Other (or Unknown) Substance-Related Disorders,” and a recent
review of the medical literature has documented at least 165 AAS users who met DSM-III-R or
DSM-IV criteria (American Psychiatric Association 1987, 1994) for AAS dependence (Brower 2002).
We have hypothesized a two-stage model of dependence on AAS (Brower 2002; Pope and Brower
2004). During stage 1, users are primarily interested in developing muscle size and power to
improve their body image or athletic performance. Training and diet at this stage have a
compulsive quality to them that extends to using AAS. The AAS user may appear to meet
DSM-IV-TR criteria for substance dependence at this stage because of the compulsive nature of
drug taking. This stage of dependence, however, can be explained without invoking any
psychoactive properties of AAS because AAS are strongly “myoactive” and they do help users to
achieve their muscle-related goals when combined with proper training and diet.
Addiction-specialized treatment is not likely to be needed at this stage, although treatment for a
body image disorder, such as muscle dysmorphia, may be (Pope et al. 1997).
According to the model, some AAS users will eventually develop stage 2 dependence, perhaps due
in part to genetic vulnerability and in part to cumulative, high-dose exposure to AAS. Chronically
consumed high doses of AAS are postulated to stimulate brain reward systems in humans, as
suggested by the animal literature (Kindlundh et al. 2004; Peters and Wood 2005; Wood 2004), and
to result in neuroadaptations in other brain systems that manifest as withdrawal symptoms upon
discontinuation. Thus, users take AAS for both their psychoactive and myoactive effects at this
stage. Clinically, stage 2 dependence resembles dependence on traditional drugs of abuse, and it
meets formal DSM-IV-TR criteria for substance dependence. In addition, stage 2 dependent users
may have co-occurring dependence on other drugs of abuse, such as opioids, alcohol, and
stimulants.
Stage 2 users have difficulty stopping drug use on their own and are likely to require
addiction-specialized treatment. The first step in such treatment is to initiate and motivate the
patient for abstinence. As with other drugs of abuse, motivational techniques include providing
empathic feedback and encouraging self-efficacy as well as involving family and friends (Brower
and Rootenberg 1999). Feedback, given in a nonjudgmental manner, about findings from the
physical examination and laboratory abnormalities allows for engagement around bodily concerns.
Encouraging self-efficacy takes advantage of the patient’s need to see oneself as big, powerful, and
strong. Initiating abstinence also involves the treatment of withdrawal symptoms, which are
discussed in detail in the section “AAS Withdrawal Depression” later in this chapter.
After initiating abstinence, the principles of relapse prevention may be applied as with other
addicted individuals, but there are also unique therapeutic issues to address in AAS users. One is
the overreliance on physical attributes for self-esteem that resembles the dynamics of patients
with eating disorders and body dysmorphic disorder (Pope et al. 1997). Therefore, the diagnosis of
comorbid mental disorders not ordinarily observed in patients with substance dependence is
important. Another therapeutic issue concerns the psychological response to giving up AAS, which
have likely served the patient to achieve some measure of competitive success. The patient will
likely feel smaller and weaker, both literally and figuratively, without AAS. In helping the patient to
accept the loss of AAS, the clinician appreciates that 1) the patient’s goals were culturally
congruent (the bigger, better, stronger, winner) and 2) AAS are potently myoactive and really canPrint: Chapter 17. Treatment of Anabolic-Androgenic Steroid-Related … http://www.psychiatryonline.com/popup.aspx?aID=348290&print=yes…
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facilitate those goals.
AAS hypomania and mania
A substantial portion of the literature since the mid-1990s has demonstrated that AAS produce
hypomanic or manic syndromes in some individuals, which are sometimes accompanied by
aggressive or violent behavior and, very rarely, psychotic symptoms (Pope and Katz 2003). These
effects are rare in individuals taking the equivalent of 300 mg/week or less of testosterone, but
they appear to become progressively more common with higher dosages, especially above 1,000
mg/week (Pope and Katz 1994). These syndromes were initially noted in field studies of illicit AAS
users, and some investigators questioned whether the effects were actually due to AAS themselves,
as opposed to expectational factors, personality variables, or subcultural influences (Bahrke and
Yesalis 1994; Riem and Hursey 1995). Recently, however, several studies have demonstrated that
such syndromes can develop even in psychiatrically healthy volunteers taking supraphysiological
doses of AAS under placebo-controlled, double-blind laboratory conditions (Pope et al. 2000; Su et
- 1993; Yates et al. 1999). Therefore, the mood-altering effects of AAS almost certainly have a
biological basis, even though they can undoubtedly be modified by contextual factors (Rubinow and
Schmidt 1996).
Little has been written about the treatment of manic or hypomanic episodes beyond anecdotal
reports (Pope and Katz 1988; Stanley 1994). Thus, the best treatment recommendations would
seem to include removal of the offending agent and temporary treatment, if necessary, with
neuroleptics or other anti-manic drugs. In general, it appears that manic or hypomanic episodes
will remit quickly when AAS are stopped and that clinicians should be alert for the onset of
depressive symptoms associated with abrupt AAS withdrawal. If a patient reports a history of mood
disorder prior to AAS use or continues to exhibit manic or psychotic symptoms for more than a
week or two after AAS are stopped, it would seem important to consider the possibility of an
underlying major mood disorder independent of AAS.
AAS withdrawal depression
The withdrawal syndrome from AAS is primarily depressive in nature and includes symptoms of
fatigue, restlessness, anorexia, insomnia, decreased libido, and a desire to take more AAS (craving)
in addition to depressed mood (Brower 2000). The syndrome typically lasts for several weeks and
usually does not require specific pharmacological treatment. However, some individuals may
develop severe or persistent depressive symptoms, sometimes accompanied by suicidal ideation. In
one study, 4% of AAS users reported that they had actually made a suicide attempt during AAS
withdrawal (Malone et al. 1995). Depression accompanying AAS withdrawal appears to respond
well to selective serotonin reuptake inhibitors such as fluoxetine (Malone and Dimeff 1992). These
drugs are also the agents of choice for treating muscle dysmorphia and other forms of body
dysmorphic disorder that may accompany AAS use (Phillips 2000).
The hypothalamic-pituitary-gonadal (HPG) axis can be depressed for many months during the
withdrawal period, resulting in sterility in some cases and contributing to depressive symptoms in
others. In men who continue to exhibit impaired sexual function or persistent depressive symptoms
despite pharmacotherapy, consultation with an endocrinologist should be considered. Endocrine
pharmacotherapy, including injected testosterone esters, human chorionic gonadotropin, and
anti-estrogens, may be indicated to restore functioning of the HPG axis in such cases (Brower
2000; Menon 2003).
Syndromes associated with AAS use
Recent years have seen the appearance of two important syndromes that appear associated with
AAS use. The first, termed muscle dysmorphia or reverse anorexia nervosa, is a form of body
dysmorphic disorder in which the individual perceives himself to be small and frail, even though he
is actually large and muscular (Cole et al. 2003; Kanayama et al. 2006; Olivardia et al. 2000; Pope
et al. 1997). Men with muscle dysmorphia will often engage in compulsive weightlifting and
bodybuilding, even to the exclusion of other activities that they enjoy. They frequently will avoidPrint: Chapter 17. Treatment of Anabolic-Androgenic Steroid-Related … http://www.psychiatryonline.com/popup.aspx?aID=348290&print=yes…
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situations in which their body will be seen by others, such as going to the beach or changing in a
locker room, for fear that they look too small. Not surprisingly, such individuals may use AAS to
“treat” their preoccupation, but paradoxically, many describe even more severe symptoms of
muscle dysmorphia following initiation of AAS use. There are no systematic studies of treatment of
muscle dysmorphia per se, but it seems reasonable to follow general principles of treatment of
other forms of body dysmorphic disorder, relying on cognitive-behavioral and pharmacological
interventions (Neziroglu ad Khemlani-Patel 2002; Phillips 2000; Phillips et al. 1997).
Another ominous syndrome associated with AAS use has been progression from AAS to opioid
abuse and dependence. Specifically, many AAS users learn about opioids from fellow bodybuilders
and often first purchase opioids from the same individual who sold them AAS (Arvary and Pope
2000; Kanayama et al. 2003a; McBride et al. 1996; Wines et al. 1999). AAS users often start by
experimenting with the opioid agonist-antagonist nalbuphine, followed by progression to pure
opioid agonists, including heroin. The authors are personally aware of many deaths among AAS
users who developed opioid abuse or dependence and then inadvertently overdosed on intravenous
opioids. Needless to say, opioid abuse or dependence in current or former AAS users should be
aggressively treated (see Chapters 18, 19, and 20 in this volume regarding opioid use and
treatment).
AAS IN FORENSIC SITUATIONS
AAS users may occasionally come to clinical attention through the courts as the result of violent or
criminal behavior. Specifically, numerous works have described individuals, often with no history of
psychiatric disorder, violence, or criminal behavior, who became uncharacteristically violent, and
sometimes committed murder, while intoxicated with AAS (see Pope and Katz 2003). In some such
cases, the relationship to AAS use may be missed because the possibility is never considered.
However, AAS use should be suspected in any unusually muscular man apprehended for violent
behavior, especially if it appears that this violence is not characteristic of his usual personality. The
clinician’s index of suspicion should be particularly raised when such a man rapidly develops
vegetative symptoms of depression after being incarcerated, but then improves a few weeks or
months later. This pattern may indicate AAS withdrawal, precipitated by the abrupt discontinuation
of AAS following incarceration, with a gradual remission of depressive symptoms as suppressed
HPG function gradually returns to normal. Of course, this pattern of biological depression must be
distinguished from the situational depression associated with incarceration itself.
In cases where AAS use is openly acknowledged by the defendant and appears to have been a clear
precipitant of criminal behavior, forensic clinicians may be asked to offer an opinion that the
defendant exhibited “involuntary intoxication” or “diminished capacity” from AAS. (The legal
aspects of this defense have been discussed in detail elsewhere [Bidwell and Katz 1989].) If an
individual is released and placed on probation after a crime believed to be associated with AAS, it
may be wise to require random, unannounced, observed urine tests for AAS to ensure that he does
not resume these drugs.
CONCLUSION
Of the various forms of substance abuse and dependence described in this volume, AAS abuse and
dependence may be the least likely to come to the attention of the average clinician. However, the
frequency of surreptitious AAS abuse and dependence, together with the various psychiatric
syndromes associated with it, is very likely underestimated, and many cases doubtless go
unrecognized. Greater awareness of this problem among clinicians may lead to the detection of
many more cases as well as a better understanding of how best to treat them.
KEY POINTS
The use of anabolic-androgenic steroid (AAS) must be approached differently from other forms of substance
abuse because AAS do not produce an immediate reward or “high” in the manner of conventional drugs of
abuse and are linked to body dysmorphic disorder.Print: Chapter 17. Treatment of Anabolic-Androgenic Steroid-Related … http://www.psychiatryonline.com/popup.aspx?aID=348290&print=yes…
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AAS users rarely see their drug use as pathological, rarely seek treatment, and may have contempt for
physicians.
AAS users often display a history of abuse of or dependence upon other drugs, especially opioids.
Some individuals experience hypomanic or manic symptoms during AAS exposure and depressive symptoms
during AAS withdrawal.
AAS may produce a well-documented dependence syndrome for which an animal model exists.
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Copyright © 2008 American Psychiatric Publishing, Inc. All Rights Reserved.
Course Content
Introduction to Anabolic-Androgenic Steroids (AAS)
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History and Development of Anabolic-Androgenic Steroids
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Understanding the Chemistry of Anabolic-Androgenic Steroids
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Mechanism of Action of Anabolic-Androgenic Steroids
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Quiz: Basic Concepts of Anabolic-Androgenic Steroids
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Therapeutic Uses of Anabolic-Androgenic Steroids
Mechanisms of Action: How AAS Influence the Body
Clinical Guidelines: Safe and Effective AAS Treatment
Advanced Strategies: Tailoring AAS Regimens for Individual Needs
Ethical Considerations and Future Directions in AAS Therapy
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