Harrison G. Pope Jr, MD

Anabolic steroid use by athletes and body-builders has captured public attention but remains poorly understood by most physicians. This is not surprising because users of anabolic-androgenic steroids (AAS):

• rarely seek treatment or disclose their drug use
• frequently distrust professionals.

If you are a clinician who regularly sees male adolescents and young men, you need to become familiar with—and watch for—this often-secret form of substance abuse. This article provides the groundwork for that understanding, starting with the story of “Aaron”—a composite patient whose case represents experiences and verbatim quotes from AAS users known to the authors.

CASE REPORT: ‘I FEEL INVINCIBLE’

At his first visit, Aaron, age 18, told the psychiatrist he had no complaints but was coming to please his parents. “I have a lot of arguments with my Dad,” he said, “and they keep thinking something’s wrong with me.”

The patient was very muscular and dressed in baggy sweats that masked his body proportions. He was appropriately groomed and darkly tanned but displayed some acne. The clinician guessed he weighed about 175 lbs and stood at about 65 inches, with very low body fat. Although superficially confident, he seemed restless, somewhat anxious, and guarded as the interview progressed.

Aaron admitted he experienced prominent mood swings. During rage outbursts, he had damaged objects and put his fist through the wall. “There’s holes all over the wall of my room,” he joked.

He also had assaulted a motorist in a traffic altercation, then left the scene. “Did you hurt him?” the clinician asked. Somewhat sheepishly, Aaron responded, “Well, I bought the newspaper and kept checking the obituaries for about 2 weeks afterwards.”

He spoke with pride about his weightlifting, which was the focus of his life. He revealed that he was preparing for a body-building contest in 2 months. The psychiatrist asked him about use of supplements—protein shakes, creatine, and “andro” (androstenedione)—all of which Aaron acknowledged. The psychiatrist then gently asked about anabolic steroid use (Box 1).

Initially, Aaron strongly denied using AAS. The psychiatrist persisted, pointing out that no information would be disclosed to his parents, and asked again using colloquial terms from the AAS subculture: “Anybody who is prepping for an untested contest in a couple of months is going to be on a cycle. Come on, what are you taking?”

Box 1

Eventually it emerged that Aaron had taken five 8- to 20-week AAS “cycles” (courses), during which he had “stacked” (combined) various “injectables” such as IM testosterone and “orals” such as methyltestosterone (Table 1). His current cycle included:

• a blend of testosterone esters (Sustanon), 500 mg IM once a week
• boldenone (Equipoise), a veterinary AAS normally used for horses, 200 mg IM per week
• oxymetholone (Anadrol), 50 mg orally per day.

Table 1

Commonly used anabolic-androgenic steroids

His friends had taught him to self-inject AAS at age 15; he admitted that he was also occasionally self-injecting the opioid analgesic nalbuphine intravenously because of “pain in my ‘delts’ from military presses.”

During his cycles, Aaron experienced hypomanic symptoms, including euphoria, prominent irritability, increased libido, decreased need for sleep, and grandiosity. “I feel invincible,” he said. His aggressive outbursts had worsened with increasing AAS doses; in addition to attacking the motorist, he also had been physically violent with his girlfriend. “She’s scared of me when I’m on juice,” he conceded.

During the withdrawal phase after stopping each cycle, Aaron described prominent depression with anhedonia, hypersomnia, loss of libido, and suicidal ideation. “I once almost jumped off a bridge after my fourth cycle,” he admitted. “I couldn’t wait to get on my next cycle to feel good again.” His depressions were also characterized by body-image obsessions; he would regularly spend at least 1 hour a day examining his musculature in a mirror, and sometimes refused to go out in public because he “was getting too small.”

Perhaps most disturbing was his increasing use of opioids. In addition to self-injecting nalbuphine, he also ingested oral opioids such as oxycodone almost daily. He mentioned that several of his friends in the gym had progressed from injecting nalbuphine to injecting morphine or heroin, and he knew two bodybuilders who had died from apparently unintentional opioid overdoses.

Aaron said his parents, teachers, and non-bodybuilding friends were unaware of this history. He claimed his parents were proud that their son had apparently eschewed drugs and alcohol to pursue a healthy athletic lifestyle.

RECOGNIZING AAS USE

In our experience with treating substance abusers, we find that AAS users may be the least likely to disclose their drug use to clinicians. In a recent study,¹ 20 of 36 AAS users (56%) reported they had never revealed their AAS use to any physician. When asked to rate their trust in sources of information about AAS, 17 of 42 AAS users (40%) said they trusted information from their drug dealers at least as much as information from any physician they had seen.

Some expressed contempt for physicians as “geeks” or “pencil-necks” who could not comprehend the body-building lifestyle. They gave doctors high marks on knowledge of tobacco, alcohol, and ordinary “street drugs” but much lower ratings on AAS knowledge. Other investigators have shown that many clinicians are unfamiliar with AAS.^2,3

AAS users embrace these beliefs for two other reasons. First, to admit to AAS use is to admit that one’s muscularity and physical prowess is the result of taking a drug; there is no comparable motivation to withhold information about, say, one’s use of marijuana or cocaine.

Second, AAS users are much less likely than other substance abusers to view their behavior as pathologic. We have argued that our culture is partially to blame.⁴ Americans pay to watch 300-lb football linemen and AAS-using movie stars. Makers of cars, computers, and electronics do not hesitate to advertise their products as “on steroids,” but they would never claim their products were “on cocaine.” In this climate, it is easy to forget that AAS use is an illicit substance abuse.

Box 2

Table 2

Clues to possible AAS use in men

To overcome these treatment obstacles, we recommend that you:

• Become as knowledgeable about AAS use as you are about other forms of substance abuse (see Related resources).
• Approach AAS users as you would any other substance abusers—as individuals at risk for potentially serious medical and psychiatric consequences.
• Maintain a high index of suspicion when evaluating any muscular young male patient, even if he initially denies AAS use.

AAS use can often be suspected by looking at the patient as he walks in the door. Using what we call the “fat-free mass index” (FFMI) to calculate muscularity (Box 2), we have shown that a lean man can achieve only a certain amount of muscularity without using drugs.⁵ Although this finding needs to be replicated elsewhere, in our experience a man is almost certainly lying if he:

• is relatively lean (with approximately 10% body fat)
• displays an FFMI >26
• and claims he has not used drugs.

If a patient has an elevated FFMI and other cues suggesting AAS use (Table 2), gently but persistently question him if he denies using these drugs.

TREATING AAS-ASSOCIATED SYNDROMES

When you have established a history of AAS use, you will be far better prepared to anticipate and possibly treat its associated syndromes. Discussion of these effects is beyond the scope of this paper; for details, see reviews of AAS-associated medical effects,^3,6 psychiatric effects,^6,7 and general treatment principles.⁸ We focus here on the four scenarios clinicians encounter most often in practice and offer some pragmatic suggestions.

Forensic cases. AAS users almost never voluntarily seek help to stop their drug use. Such a request would be somewhat analogous to a girl with anorexia nervosa voluntarily asking for help to gain weight. We are unaware of any rehabilitation centers, clinics, 12-step programs, or the like for AAS users—there is no demand for them.

Thus, an AAS user may first come to clinical attention through legal channels. For example, if an AAS user committed a violent crime while experiencing hypomanic effects from these drugs, he might be required to undergo random urine testing as a condition of probation. This may be reasonable, provided that the tests are unannounced and urine is always collected under direct observation.

Monitoring clinicians may serve as little better than policemen, although sometimes it is possible to forge an alliance with the patient.

Depression. Exogenous AAS administration suppresses endogenous testosterone production through feedback mechanisms involving the hypothalamic-pituitary-testicular axis.^3,6 Thus, during a long cycle, the user’s testes may shrink to half their normal size and stop producing testosterone and spermatozoa.

If the user then stops AAS rapidly, he may plunge into a profoundly hypogonadal state associated with symptoms of major depression. In a field study of 77 steroid users (71 male and 6 female), 6 (7.8%) reported they attempted suicide during AAS withdrawal.⁹ Depression associated with AAS withdrawal may prompt users to resume AAS quickly, triggering a syndrome of AAS dependence.^6,10,11

Fortunately, AAS-withdrawal depression is usually self-limited and responds—in our experience and that of others¹²—to standard antidepressants. We recommend aggressively treating such depressions, as doing so may prevent resumption of AAS use and eventual AAS dependence.

Body-image disorders. AAS users often report body-image disorders, especially muscle dysmorphia—a form of body dysmorphic disorder where individuals become preoccupied with the belief that they are not adequately muscular.^13,14 Anxieties about muscularity are a risk factor for subsequent AAS use¹⁵ and a major contributor to AAS dependence.^8,11

Body dysmorphic disorder responds to pharmacologic and cognitive-behavioral interventions.^3,16 Young men showing pathologic concerns about their muscularity or displaying related body-image pathology may benefit from prompt treatment before they are tempted to use AAS.

Progression to opioid dependence. An ominous development among American¹⁷ and British¹⁸ AAS users is a growing tendency to use opioids. In two studies of individuals with opioid dependence,^19,20 7% to 9% reported beginning as AAS users, then learning about opioids from fellow bodybuilders and often buying their first illicit opioids from the person who had sold them AAS. Most learned as teenagers to use needles to inject AAS intramuscularly, so beginning to using opioids intravenously was only a small step.

In the last 5 years, we have become anecdotally aware of numerous AAS users who developed heroin addiction requiring repeated inpatient detoxification or who died of unintentional opioid overdoses. We suspect this phenomenon is under-recognized and urge clinicians to watch for it.

Related resources

• Pope HG Jr, Brower KJ. Anabolic-androgenic steroid abuse. In: Sadock BJ, Sadock VA (eds). Comprehensive textbook of psychiatry (8th ed). Philadelphia: Lippincott Williams & Wilkins (in press).
• Yesalis CE (ed). Anabolic steroids in sport and exercise (2nd ed). Champaign, IL: Human Kinetics, 2000.
• The Taylor Hooton Foundation. Started by the father of a high school athlete who committed suicide during a depressive episode apparently precipitated by AAS withdrawal. Includes links to related Web sites. http://www.taylorhooton.org/about.asp. Accessed Nov. 10, 2004.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Anabolic steroid use by athletes and body-builders has captured public attention but remains poorly understood by most physicians. This is not surprising because users of anabolic-androgenic steroids (AAS):

• rarely seek treatment or disclose their drug use
• frequently distrust professionals.

If you are a clinician who regularly sees male adolescents and young men, you need to become familiar with—and watch for—this often-secret form of substance abuse. This article provides the groundwork for that understanding, starting with the story of “Aaron”—a composite patient whose case represents experiences and verbatim quotes from AAS users known to the authors.

CASE REPORT: ‘I FEEL INVINCIBLE’

At his first visit, Aaron, age 18, told the psychiatrist he had no complaints but was coming to please his parents. “I have a lot of arguments with my Dad,” he said, “and they keep thinking something’s wrong with me.”

The patient was very muscular and dressed in baggy sweats that masked his body proportions. He was appropriately groomed and darkly tanned but displayed some acne. The clinician guessed he weighed about 175 lbs and stood at about 65 inches, with very low body fat. Although superficially confident, he seemed restless, somewhat anxious, and guarded as the interview progressed.

Aaron admitted he experienced prominent mood swings. During rage outbursts, he had damaged objects and put his fist through the wall. “There’s holes all over the wall of my room,” he joked.

He also had assaulted a motorist in a traffic altercation, then left the scene. “Did you hurt him?” the clinician asked. Somewhat sheepishly, Aaron responded, “Well, I bought the newspaper and kept checking the obituaries for about 2 weeks afterwards.”

He spoke with pride about his weightlifting, which was the focus of his life. He revealed that he was preparing for a body-building contest in 2 months. The psychiatrist asked him about use of supplements—protein shakes, creatine, and “andro” (androstenedione)—all of which Aaron acknowledged. The psychiatrist then gently asked about anabolic steroid use (Box 1).

Initially, Aaron strongly denied using AAS. The psychiatrist persisted, pointing out that no information would be disclosed to his parents, and asked again using colloquial terms from the AAS subculture: “Anybody who is prepping for an untested contest in a couple of months is going to be on a cycle. Come on, what are you taking?”

Box 1

Eventually it emerged that Aaron had taken five 8- to 20-week AAS “cycles” (courses), during which he had “stacked” (combined) various “injectables” such as IM testosterone and “orals” such as methyltestosterone (Table 1). His current cycle included:

• a blend of testosterone esters (Sustanon), 500 mg IM once a week
• boldenone (Equipoise), a veterinary AAS normally used for horses, 200 mg IM per week
• oxymetholone (Anadrol), 50 mg orally per day.

Table 1

Commonly used anabolic-androgenic steroids

His friends had taught him to self-inject AAS at age 15; he admitted that he was also occasionally self-injecting the opioid analgesic nalbuphine intravenously because of “pain in my ‘delts’ from military presses.”

During his cycles, Aaron experienced hypomanic symptoms, including euphoria, prominent irritability, increased libido, decreased need for sleep, and grandiosity. “I feel invincible,” he said. His aggressive outbursts had worsened with increasing AAS doses; in addition to attacking the motorist, he also had been physically violent with his girlfriend. “She’s scared of me when I’m on juice,” he conceded.

During the withdrawal phase after stopping each cycle, Aaron described prominent depression with anhedonia, hypersomnia, loss of libido, and suicidal ideation. “I once almost jumped off a bridge after my fourth cycle,” he admitted. “I couldn’t wait to get on my next cycle to feel good again.” His depressions were also characterized by body-image obsessions; he would regularly spend at least 1 hour a day examining his musculature in a mirror, and sometimes refused to go out in public because he “was getting too small.”

Perhaps most disturbing was his increasing use of opioids. In addition to self-injecting nalbuphine, he also ingested oral opioids such as oxycodone almost daily. He mentioned that several of his friends in the gym had progressed from injecting nalbuphine to injecting morphine or heroin, and he knew two bodybuilders who had died from apparently unintentional opioid overdoses.

Aaron said his parents, teachers, and non-bodybuilding friends were unaware of this history. He claimed his parents were proud that their son had apparently eschewed drugs and alcohol to pursue a healthy athletic lifestyle.

RECOGNIZING AAS USE

In our experience with treating substance abusers, we find that AAS users may be the least likely to disclose their drug use to clinicians. In a recent study,¹ 20 of 36 AAS users (56%) reported they had never revealed their AAS use to any physician. When asked to rate their trust in sources of information about AAS, 17 of 42 AAS users (40%) said they trusted information from their drug dealers at least as much as information from any physician they had seen.

Some expressed contempt for physicians as “geeks” or “pencil-necks” who could not comprehend the body-building lifestyle. They gave doctors high marks on knowledge of tobacco, alcohol, and ordinary “street drugs” but much lower ratings on AAS knowledge. Other investigators have shown that many clinicians are unfamiliar with AAS.^2,3

AAS users embrace these beliefs for two other reasons. First, to admit to AAS use is to admit that one’s muscularity and physical prowess is the result of taking a drug; there is no comparable motivation to withhold information about, say, one’s use of marijuana or cocaine.

Second, AAS users are much less likely than other substance abusers to view their behavior as pathologic. We have argued that our culture is partially to blame.⁴ Americans pay to watch 300-lb football linemen and AAS-using movie stars. Makers of cars, computers, and electronics do not hesitate to advertise their products as “on steroids,” but they would never claim their products were “on cocaine.” In this climate, it is easy to forget that AAS use is an illicit substance abuse.

Box 2

Table 2

Clues to possible AAS use in men

To overcome these treatment obstacles, we recommend that you:

• Become as knowledgeable about AAS use as you are about other forms of substance abuse (see Related resources).
• Approach AAS users as you would any other substance abusers—as individuals at risk for potentially serious medical and psychiatric consequences.
• Maintain a high index of suspicion when evaluating any muscular young male patient, even if he initially denies AAS use.

AAS use can often be suspected by looking at the patient as he walks in the door. Using what we call the “fat-free mass index” (FFMI) to calculate muscularity (Box 2), we have shown that a lean man can achieve only a certain amount of muscularity without using drugs.⁵ Although this finding needs to be replicated elsewhere, in our experience a man is almost certainly lying if he:

• is relatively lean (with approximately 10% body fat)
• displays an FFMI >26
• and claims he has not used drugs.

If a patient has an elevated FFMI and other cues suggesting AAS use (Table 2), gently but persistently question him if he denies using these drugs.

TREATING AAS-ASSOCIATED SYNDROMES

When you have established a history of AAS use, you will be far better prepared to anticipate and possibly treat its associated syndromes. Discussion of these effects is beyond the scope of this paper; for details, see reviews of AAS-associated medical effects,^3,6 psychiatric effects,^6,7 and general treatment principles.⁸ We focus here on the four scenarios clinicians encounter most often in practice and offer some pragmatic suggestions.

Forensic cases. AAS users almost never voluntarily seek help to stop their drug use. Such a request would be somewhat analogous to a girl with anorexia nervosa voluntarily asking for help to gain weight. We are unaware of any rehabilitation centers, clinics, 12-step programs, or the like for AAS users—there is no demand for them.

Thus, an AAS user may first come to clinical attention through legal channels. For example, if an AAS user committed a violent crime while experiencing hypomanic effects from these drugs, he might be required to undergo random urine testing as a condition of probation. This may be reasonable, provided that the tests are unannounced and urine is always collected under direct observation.

Monitoring clinicians may serve as little better than policemen, although sometimes it is possible to forge an alliance with the patient.

Depression. Exogenous AAS administration suppresses endogenous testosterone production through feedback mechanisms involving the hypothalamic-pituitary-testicular axis.^3,6 Thus, during a long cycle, the user’s testes may shrink to half their normal size and stop producing testosterone and spermatozoa.

If the user then stops AAS rapidly, he may plunge into a profoundly hypogonadal state associated with symptoms of major depression. In a field study of 77 steroid users (71 male and 6 female), 6 (7.8%) reported they attempted suicide during AAS withdrawal.⁹ Depression associated with AAS withdrawal may prompt users to resume AAS quickly, triggering a syndrome of AAS dependence.^6,10,11

Fortunately, AAS-withdrawal depression is usually self-limited and responds—in our experience and that of others¹²—to standard antidepressants. We recommend aggressively treating such depressions, as doing so may prevent resumption of AAS use and eventual AAS dependence.

Body-image disorders. AAS users often report body-image disorders, especially muscle dysmorphia—a form of body dysmorphic disorder where individuals become preoccupied with the belief that they are not adequately muscular.^13,14 Anxieties about muscularity are a risk factor for subsequent AAS use¹⁵ and a major contributor to AAS dependence.^8,11

Body dysmorphic disorder responds to pharmacologic and cognitive-behavioral interventions.^3,16 Young men showing pathologic concerns about their muscularity or displaying related body-image pathology may benefit from prompt treatment before they are tempted to use AAS.

Progression to opioid dependence. An ominous development among American¹⁷ and British¹⁸ AAS users is a growing tendency to use opioids. In two studies of individuals with opioid dependence,^19,20 7% to 9% reported beginning as AAS users, then learning about opioids from fellow bodybuilders and often buying their first illicit opioids from the person who had sold them AAS. Most learned as teenagers to use needles to inject AAS intramuscularly, so beginning to using opioids intravenously was only a small step.

In the last 5 years, we have become anecdotally aware of numerous AAS users who developed heroin addiction requiring repeated inpatient detoxification or who died of unintentional opioid overdoses. We suspect this phenomenon is under-recognized and urge clinicians to watch for it.

Related resources

• Pope HG Jr, Brower KJ. Anabolic-androgenic steroid abuse. In: Sadock BJ, Sadock VA (eds). Comprehensive textbook of psychiatry (8th ed). Philadelphia: Lippincott Williams & Wilkins (in press).
• Yesalis CE (ed). Anabolic steroids in sport and exercise (2nd ed). Champaign, IL: Human Kinetics, 2000.
• The Taylor Hooton Foundation. Started by the father of a high school athlete who committed suicide during a depressive episode apparently precipitated by AAS withdrawal. Includes links to related Web sites. http://www.taylorhooton.org/about.asp. Accessed Nov. 10, 2004.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Anabolic steroid use by athletes and body-builders has captured public attention but remains poorly understood by most physicians. This is not surprising because users of anabolic-androgenic steroids (AAS):

• rarely seek treatment or disclose their drug use
• frequently distrust professionals.

If you are a clinician who regularly sees male adolescents and young men, you need to become familiar with—and watch for—this often-secret form of substance abuse. This article provides the groundwork for that understanding, starting with the story of “Aaron”—a composite patient whose case represents experiences and verbatim quotes from AAS users known to the authors.

CASE REPORT: ‘I FEEL INVINCIBLE’

At his first visit, Aaron, age 18, told the psychiatrist he had no complaints but was coming to please his parents. “I have a lot of arguments with my Dad,” he said, “and they keep thinking something’s wrong with me.”

The patient was very muscular and dressed in baggy sweats that masked his body proportions. He was appropriately groomed and darkly tanned but displayed some acne. The clinician guessed he weighed about 175 lbs and stood at about 65 inches, with very low body fat. Although superficially confident, he seemed restless, somewhat anxious, and guarded as the interview progressed.

Aaron admitted he experienced prominent mood swings. During rage outbursts, he had damaged objects and put his fist through the wall. “There’s holes all over the wall of my room,” he joked.

He also had assaulted a motorist in a traffic altercation, then left the scene. “Did you hurt him?” the clinician asked. Somewhat sheepishly, Aaron responded, “Well, I bought the newspaper and kept checking the obituaries for about 2 weeks afterwards.”

He spoke with pride about his weightlifting, which was the focus of his life. He revealed that he was preparing for a body-building contest in 2 months. The psychiatrist asked him about use of supplements—protein shakes, creatine, and “andro” (androstenedione)—all of which Aaron acknowledged. The psychiatrist then gently asked about anabolic steroid use (Box 1).

Initially, Aaron strongly denied using AAS. The psychiatrist persisted, pointing out that no information would be disclosed to his parents, and asked again using colloquial terms from the AAS subculture: “Anybody who is prepping for an untested contest in a couple of months is going to be on a cycle. Come on, what are you taking?”

Box 1

Eventually it emerged that Aaron had taken five 8- to 20-week AAS “cycles” (courses), during which he had “stacked” (combined) various “injectables” such as IM testosterone and “orals” such as methyltestosterone (Table 1). His current cycle included:

• a blend of testosterone esters (Sustanon), 500 mg IM once a week
• boldenone (Equipoise), a veterinary AAS normally used for horses, 200 mg IM per week
• oxymetholone (Anadrol), 50 mg orally per day.

Table 1

Commonly used anabolic-androgenic steroids

His friends had taught him to self-inject AAS at age 15; he admitted that he was also occasionally self-injecting the opioid analgesic nalbuphine intravenously because of “pain in my ‘delts’ from military presses.”

During his cycles, Aaron experienced hypomanic symptoms, including euphoria, prominent irritability, increased libido, decreased need for sleep, and grandiosity. “I feel invincible,” he said. His aggressive outbursts had worsened with increasing AAS doses; in addition to attacking the motorist, he also had been physically violent with his girlfriend. “She’s scared of me when I’m on juice,” he conceded.

During the withdrawal phase after stopping each cycle, Aaron described prominent depression with anhedonia, hypersomnia, loss of libido, and suicidal ideation. “I once almost jumped off a bridge after my fourth cycle,” he admitted. “I couldn’t wait to get on my next cycle to feel good again.” His depressions were also characterized by body-image obsessions; he would regularly spend at least 1 hour a day examining his musculature in a mirror, and sometimes refused to go out in public because he “was getting too small.”

Perhaps most disturbing was his increasing use of opioids. In addition to self-injecting nalbuphine, he also ingested oral opioids such as oxycodone almost daily. He mentioned that several of his friends in the gym had progressed from injecting nalbuphine to injecting morphine or heroin, and he knew two bodybuilders who had died from apparently unintentional opioid overdoses.

Aaron said his parents, teachers, and non-bodybuilding friends were unaware of this history. He claimed his parents were proud that their son had apparently eschewed drugs and alcohol to pursue a healthy athletic lifestyle.

RECOGNIZING AAS USE

In our experience with treating substance abusers, we find that AAS users may be the least likely to disclose their drug use to clinicians. In a recent study,¹ 20 of 36 AAS users (56%) reported they had never revealed their AAS use to any physician. When asked to rate their trust in sources of information about AAS, 17 of 42 AAS users (40%) said they trusted information from their drug dealers at least as much as information from any physician they had seen.

Some expressed contempt for physicians as “geeks” or “pencil-necks” who could not comprehend the body-building lifestyle. They gave doctors high marks on knowledge of tobacco, alcohol, and ordinary “street drugs” but much lower ratings on AAS knowledge. Other investigators have shown that many clinicians are unfamiliar with AAS.^2,3

AAS users embrace these beliefs for two other reasons. First, to admit to AAS use is to admit that one’s muscularity and physical prowess is the result of taking a drug; there is no comparable motivation to withhold information about, say, one’s use of marijuana or cocaine.

Second, AAS users are much less likely than other substance abusers to view their behavior as pathologic. We have argued that our culture is partially to blame.⁴ Americans pay to watch 300-lb football linemen and AAS-using movie stars. Makers of cars, computers, and electronics do not hesitate to advertise their products as “on steroids,” but they would never claim their products were “on cocaine.” In this climate, it is easy to forget that AAS use is an illicit substance abuse.

Box 2

Table 2

Clues to possible AAS use in men

To overcome these treatment obstacles, we recommend that you:

• Become as knowledgeable about AAS use as you are about other forms of substance abuse (see Related resources).
• Approach AAS users as you would any other substance abusers—as individuals at risk for potentially serious medical and psychiatric consequences.
• Maintain a high index of suspicion when evaluating any muscular young male patient, even if he initially denies AAS use.

AAS use can often be suspected by looking at the patient as he walks in the door. Using what we call the “fat-free mass index” (FFMI) to calculate muscularity (Box 2), we have shown that a lean man can achieve only a certain amount of muscularity without using drugs.⁵ Although this finding needs to be replicated elsewhere, in our experience a man is almost certainly lying if he:

• is relatively lean (with approximately 10% body fat)
• displays an FFMI >26
• and claims he has not used drugs.

If a patient has an elevated FFMI and other cues suggesting AAS use (Table 2), gently but persistently question him if he denies using these drugs.

TREATING AAS-ASSOCIATED SYNDROMES

When you have established a history of AAS use, you will be far better prepared to anticipate and possibly treat its associated syndromes. Discussion of these effects is beyond the scope of this paper; for details, see reviews of AAS-associated medical effects,^3,6 psychiatric effects,^6,7 and general treatment principles.⁸ We focus here on the four scenarios clinicians encounter most often in practice and offer some pragmatic suggestions.

Forensic cases. AAS users almost never voluntarily seek help to stop their drug use. Such a request would be somewhat analogous to a girl with anorexia nervosa voluntarily asking for help to gain weight. We are unaware of any rehabilitation centers, clinics, 12-step programs, or the like for AAS users—there is no demand for them.

Thus, an AAS user may first come to clinical attention through legal channels. For example, if an AAS user committed a violent crime while experiencing hypomanic effects from these drugs, he might be required to undergo random urine testing as a condition of probation. This may be reasonable, provided that the tests are unannounced and urine is always collected under direct observation.

Monitoring clinicians may serve as little better than policemen, although sometimes it is possible to forge an alliance with the patient.

Depression. Exogenous AAS administration suppresses endogenous testosterone production through feedback mechanisms involving the hypothalamic-pituitary-testicular axis.^3,6 Thus, during a long cycle, the user’s testes may shrink to half their normal size and stop producing testosterone and spermatozoa.

If the user then stops AAS rapidly, he may plunge into a profoundly hypogonadal state associated with symptoms of major depression. In a field study of 77 steroid users (71 male and 6 female), 6 (7.8%) reported they attempted suicide during AAS withdrawal.⁹ Depression associated with AAS withdrawal may prompt users to resume AAS quickly, triggering a syndrome of AAS dependence.^6,10,11

Fortunately, AAS-withdrawal depression is usually self-limited and responds—in our experience and that of others¹²—to standard antidepressants. We recommend aggressively treating such depressions, as doing so may prevent resumption of AAS use and eventual AAS dependence.

Body-image disorders. AAS users often report body-image disorders, especially muscle dysmorphia—a form of body dysmorphic disorder where individuals become preoccupied with the belief that they are not adequately muscular.^13,14 Anxieties about muscularity are a risk factor for subsequent AAS use¹⁵ and a major contributor to AAS dependence.^8,11

Body dysmorphic disorder responds to pharmacologic and cognitive-behavioral interventions.^3,16 Young men showing pathologic concerns about their muscularity or displaying related body-image pathology may benefit from prompt treatment before they are tempted to use AAS.

Progression to opioid dependence. An ominous development among American¹⁷ and British¹⁸ AAS users is a growing tendency to use opioids. In two studies of individuals with opioid dependence,^19,20 7% to 9% reported beginning as AAS users, then learning about opioids from fellow bodybuilders and often buying their first illicit opioids from the person who had sold them AAS. Most learned as teenagers to use needles to inject AAS intramuscularly, so beginning to using opioids intravenously was only a small step.

In the last 5 years, we have become anecdotally aware of numerous AAS users who developed heroin addiction requiring repeated inpatient detoxification or who died of unintentional opioid overdoses. We suspect this phenomenon is under-recognized and urge clinicians to watch for it.

Related resources

• Pope HG Jr, Brower KJ. Anabolic-androgenic steroid abuse. In: Sadock BJ, Sadock VA (eds). Comprehensive textbook of psychiatry (8th ed). Philadelphia: Lippincott Williams & Wilkins (in press).
• Yesalis CE (ed). Anabolic steroids in sport and exercise (2nd ed). Champaign, IL: Human Kinetics, 2000.
• The Taylor Hooton Foundation. Started by the father of a high school athlete who committed suicide during a depressive episode apparently precipitated by AAS withdrawal. Includes links to related Web sites. http://www.taylorhooton.org/about.asp. Accessed Nov. 10, 2004.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Initial visit: Road rage or ‘roid’ rage?

Mr. A, 25, was arrested after police interrupted an altercation between him and a senior citizen at a stoplight. He had emerged from his car, walked over to the older driver in front of him, ripped open the car door, and pulled the man out of the car and onto the street. He was still yelling at the victim when a passing officer intervened.

Mr. A was charged with assault. After a plea bargain, he was sentenced to probation and fined. He had been seeing his probation officer every 2 weeks, but his parents were worried about his erratic and sometimes defiant behavior and insisted he see a psychiatrist. He reluctantly agreed to one consultation, largely because his parents threatened to withhold financial support if he failed to do so.

The first thing the psychiatrist noticed was Mr. A’s striking muscular appearance. He was approximately 5 feet, 7 inches tall, weighed at least 200 pounds, and had a 30-inch waist and less than 10% body fat.

Dr. Carter’s and Pope’s observations

Mr. A’s diagnosis should be suspected immediately upon his entering the office. Extensive anabolic steroid use produces body changes that can be diagnosed almost at a glance. It is virtually impossible to achieve a level of muscle mass comparable to what Mr. A exhibited without the use of anabolic steroids.¹

Remarkably, however, most people—including Mr. A’s parents, law enforcement personnel, and even some members of the treatment team—failed to diagnose Mr. A’s steroid use. He somehow convinced them that his extreme muscularity was the result of hard work, dedication, and scrupulous attention to diet. This suggests that steroid abuse cases involving serious violence—such as that of Mr. A—frequently go unreported and undiagnosed and are probably more common than we suspect.

Epidemiologic data suggest that clinicians should become familiar with the presentation of patients who are using anabolic steroids (Box).

Evaluation: ‘Stacking’ up

Mr. A at first vehemently denied that he had ever used anabolic steroids. After a more detailed conversation, during which the clinician demonstrated some knowledge of this area, Mr. A eventually conceded that he was taking a substantial weekly dose of the drugs at the time of the assault.

A subsequent clinical evaluation revealed that Mr. A had taken several ‘cycles’ (courses) of anabolic steroids over the last 2 to 3 years. Each cycle lasted 10 to 16 weeks and had been characterized by simultaneous use of two or more steroids, a practice known as ‘stacking.’

Mr. A started his first cycle with a modest ‘stack’ of drugs: testosterone cypionate, 200 mg twice a week, and stanozolol, 10 mg/d. Taken together, these dosages represented roughly 470 mg of testosterone equivalent per week—about 10 times the weekly secretion of testosterone in a normal male. He noticed no change in mood during this initial cycle.

With subsequent cycles, however, Mr. A became increasingly obsessed with his body image and used higher dosages. When the assault occurred, he was taking testosterone cypionate, 800 mg a week, nandrolone decanoate, 400 mg a week, and oxymetholone, 50 mg/d. With this regimen—the weekly equivalent of 1,550 mg of testosterone—Mr. A noticed prominent mood changes that met DSM-IV criteria for a manic episode. He experienced euphoria, dramatic irritability, limitless self-confidence, decreased need for sleep, distractibility, extreme recklessness (driving too fast, spending too freely), and some mildly paranoid ideation (without frank delusions). He admitted that he had twice assaulted his girlfriend and that he invariably became enraged at even the slightest annoyance when driving in traffic. He revealed that although the altercation with the older driver had led to his first arrest for ‘road rage,’ it was his third such incident.

The clinician warned Mr. A that continued steroid use could worsen his behavior—and lead to more serious trouble later on. Mr. A, however, said he was more afraid of losing muscle mass and becoming ‘small again.’ When the clinician mentioned that use of anabolic steroids without a prescription is illegal, Mr. A retorted that several of his friends had used the drugs without legal consequences.

Mr. A left the office showing no inclination to return for further treatment. The clinician could only offer to be available in the future.

Box

What medical sequelae await Mr. A if he continues to abuse steroids? How would you convince him to stay in treatment?

Dr. Carter’s and Pope’s observations

Mr. A’s path to mania has been well demonstrated in the literature. Hypomania or even frank manic syndromes, sometimes associated with violent behavior, are rare at weekly doses of 300 mg of testosterone equivalent. At weekly doses of >1,000 mg, psychiatric syndromes such as hypomania or mania may occur in almost one-half of cases.⁵

If he continues to abuse anabolic steroids, however, Mr. A could experience adverse physical reactions ranging from embarrassing acne and male-pattern baldness (Table 1) to rare and life-threatening hepatic effects such as cholestatic jaundice and peliosis hepatitis (blood-filled cysts in the liver).

Table 1

ANABOLIC STEROID ABUSE: COMMON PHYSICAL FINDINGS

The risk of atherosclerotic disease or prostate cancer later in life may also be greatly increased.

More common laboratory changes include:

• increased red blood cell count, hemoglobin and hematocrit
• elevated liver function readings (although these must not be confused with enzymes that originate from muscle tissue)
• and unfavorable changes in triglycerides, total cholesterol, and HDL:LDL cholesterol ratios (Table 2).

Other potential laboratory changes with steroid abuse include decreased luteinizing hormone and follicle-stimulating hormone due to feedback inhibition. Feedback inhibition will also reduce testosterone and estradiol levels with use of anabolic steroids other than testosterone esters. These levels, however, would both be elevated with use of testosterone esters alone.

In men, testicular atrophy and decreased sperm count are generally reversible manifestations of steroid abuse, whereas gynecomastia may be irreversible and require surgical intervention in advanced cases.^3,6 Women who use anabolic steroids (such as for body-building) are vulnerable to disrupted menstrual cycles, decreased breast size, and masculinizing effects including enlarged clitoris, hirsutism, and deepening of the voice.⁶

In adolescents, anabolic steroid use may cause premature closure of the epiphyses, leading to shortened stature.³

Unfortunately, warnings about these many adverse effects rarely deter anabolic steroid users such as Mr. A or persuade them to continue in treatment of any type. Most young anabolic steroid abusers report that they have never felt significant adverse effects from steroid use and know of no one who has experienced such effects. The dramatic muscle gains they have witnessed in themselves and in other users decisively outweigh what they perceive to be remote threats of adverse consequences.

Follow-up: Return to treatment

We didn’t hear from Mr. A until about 18 months later, when he unexpectedly requested a consultation.

Upon arrival, Mr. A exhibited major depression with prominent anhedonia, hypersomnia of 12 to 14 hours per night, loss of appetite, fatigue, prominent psychomotor retardation, feelings of guilt, difficulty concentrating, and suicidal thoughts (but without a frank plan). He also reported panic attacks that were randomly occurring each day, usually in public.

Mr. A conceded that he had experienced similar depressive episodes after stopping anabolic steroid use, but that they typically ran their course after 2 to 3 weeks. He said the present episode showed no sign of abating after nearly 2 months. He had attempted to ‘treat’ this episode by resuming anabolic steroid use, but he could not get an adequate supply from his dealer.

Mr. A’s total testosterone level, measured in the morning when it should be near its diurnal peak, was 127 ng/dl (normal range is 270 to 1,070 ng/dl). Physical examination revealed that his testicles had shrunk to the size of marbles (each approximately 5 mm in diameter). He was referred to an endocrinologist for evaluation and was simultaneously started on fluoxetine, 20 mg/d.

Table 2

LABORATORY ABNORMALITIES ASSOCIATED WITH ANABOLIC STEROID ABUSE

He returned 2 weeks later, exhibiting little improvement and wanting to resume steroids ‘because it was the only thing that really helped.’ Instead, he agreed to continue on fluoxetine and remain in follow-up. At 4 weeks, he noticed a decrease in panic attacks, return of normal mood, decreased anhedonia, and loss of suicidal ideation. He continued taking fluoxetine for another 3 months but then abruptly disappeared from treatment.

Mr. A resurfaced about 1 year later, revealing to the psychiatrist that he had taken yet another cycle of anabolic steroids, largely because he feared losing his muscle mass. His panic attacks had recurred almost immediately when he began tapering down from the peak of this cycle, and he agreed to resume taking fluoxetine.

A look at Mr. A’s extended history may provide clues to his persistent anabolic steroid abuse problem. He had displayed prominent symptoms of conduct disorder as a child. He had been truant from school, had occasionally run away from home, and had been involved in several misdemeanors. While in high school, he typically drank 10 to 12 beers over a weekend and had experimented with hallucinogenic mushrooms and 3,4-methylenedioxymethamphetamine (‘ecstasy’).

He started weightlifting while in high school and by age 17 was visiting the gym every day. He began college on a football scholarship but dropped out after 1 year. Starting in his early 20s, he competed in several bodybuilding contests.

Despite his impressive muscularity, Mr. A was anxious about his body appearance. He often would not take off his shirt—even when at the beach or a swimming pool—for fear that he would appear too small. He sometimes wore heavy sweatpants in the sweltering heat to conceal his legs. He also admitted spending as much as 2 hours a day examining himself in the mirror. ‘Sometimes when I get a bad (look at) myself, I will refuse to go out for the rest of the day,’ he said.

Mr. A has had a succession of girlfriends, but his rigid commitment to diet and exercise invariably ended these relationships.

At this point, would you first address Mr. A’s apparent substance use problem or the underlying body dysmorphic symptoms?

Dr. Carter’s and Pope’s observations

Two comorbidities noted here—substance abuse and body dysmorphic disorder—are common among anabolic steroid abusers. Addressing these problems, especially the body dysmorphic disorder, may sometimes help patients who are unwilling to address their steroid use directly. Body dysmorphic disorder may respond to selective serotonin reuptake inhibitors⁷ and cognitive-behavioral therapy.⁸

Anabolic steroids are not associated with immediate intoxicating effects, and ICD-10 categorizes them as substances not associated with dependence. After prolonged use at high doses, however, anabolic steroids are often associated with euphoria. Researchers also have found that some steroid abusers do meet DSM-IV criteria for substance dependence.⁶

Beyond the direct psychotropic effects of anabolic steroids, the depressive symptoms commonly seen during their withdrawal may perpetuate the dependence, as was the case with Mr. A. Most depressive symptoms that follow steroid cessation do not require drug therapy,³ but Mr. A developed severe and persistent depressive symptoms, complicated by panic disorder and body image concerns at a level diagnostic of body dysmorphic disorder. Such body image concerns often precipitate relapse into steroid use.

Conclusion: Another setback

As of this writing, Mr. A is again lost to follow-up. After taking fluoxetine and keeping monthly appointments for about 6 months, he failed to arrive for a visit and did not set another appointment. The patient may have once again stopped medication and embarked on yet another cycle of anabolic steroid use. If this is so, we can only hope that he returns to treatment before it is too late.

Related resource

• Lukas SE. Steroids. Hillside, NJ: Enslow Publishers, 1994.

Drug brand names

• Fluoxetine • Prozac
• Nandrolone decanoate • Deca-Durabolin
• Oxymetholone • Anadrol
• Stanozolol • Winstrol

Disclosure

Dr. Carter reports that he receives research/grant support from or is a consultant to Eli Lilly and Co., Pfizer Inc., and Ortho-McNeil Pharmaceutical.

Dr. Pope reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Initial visit: Road rage or ‘roid’ rage?

Mr. A, 25, was arrested after police interrupted an altercation between him and a senior citizen at a stoplight. He had emerged from his car, walked over to the older driver in front of him, ripped open the car door, and pulled the man out of the car and onto the street. He was still yelling at the victim when a passing officer intervened.

Mr. A was charged with assault. After a plea bargain, he was sentenced to probation and fined. He had been seeing his probation officer every 2 weeks, but his parents were worried about his erratic and sometimes defiant behavior and insisted he see a psychiatrist. He reluctantly agreed to one consultation, largely because his parents threatened to withhold financial support if he failed to do so.

The first thing the psychiatrist noticed was Mr. A’s striking muscular appearance. He was approximately 5 feet, 7 inches tall, weighed at least 200 pounds, and had a 30-inch waist and less than 10% body fat.

Dr. Carter’s and Pope’s observations

Mr. A’s diagnosis should be suspected immediately upon his entering the office. Extensive anabolic steroid use produces body changes that can be diagnosed almost at a glance. It is virtually impossible to achieve a level of muscle mass comparable to what Mr. A exhibited without the use of anabolic steroids.¹

Remarkably, however, most people—including Mr. A’s parents, law enforcement personnel, and even some members of the treatment team—failed to diagnose Mr. A’s steroid use. He somehow convinced them that his extreme muscularity was the result of hard work, dedication, and scrupulous attention to diet. This suggests that steroid abuse cases involving serious violence—such as that of Mr. A—frequently go unreported and undiagnosed and are probably more common than we suspect.

Epidemiologic data suggest that clinicians should become familiar with the presentation of patients who are using anabolic steroids (Box).

Evaluation: ‘Stacking’ up

Mr. A at first vehemently denied that he had ever used anabolic steroids. After a more detailed conversation, during which the clinician demonstrated some knowledge of this area, Mr. A eventually conceded that he was taking a substantial weekly dose of the drugs at the time of the assault.

A subsequent clinical evaluation revealed that Mr. A had taken several ‘cycles’ (courses) of anabolic steroids over the last 2 to 3 years. Each cycle lasted 10 to 16 weeks and had been characterized by simultaneous use of two or more steroids, a practice known as ‘stacking.’

Mr. A started his first cycle with a modest ‘stack’ of drugs: testosterone cypionate, 200 mg twice a week, and stanozolol, 10 mg/d. Taken together, these dosages represented roughly 470 mg of testosterone equivalent per week—about 10 times the weekly secretion of testosterone in a normal male. He noticed no change in mood during this initial cycle.

With subsequent cycles, however, Mr. A became increasingly obsessed with his body image and used higher dosages. When the assault occurred, he was taking testosterone cypionate, 800 mg a week, nandrolone decanoate, 400 mg a week, and oxymetholone, 50 mg/d. With this regimen—the weekly equivalent of 1,550 mg of testosterone—Mr. A noticed prominent mood changes that met DSM-IV criteria for a manic episode. He experienced euphoria, dramatic irritability, limitless self-confidence, decreased need for sleep, distractibility, extreme recklessness (driving too fast, spending too freely), and some mildly paranoid ideation (without frank delusions). He admitted that he had twice assaulted his girlfriend and that he invariably became enraged at even the slightest annoyance when driving in traffic. He revealed that although the altercation with the older driver had led to his first arrest for ‘road rage,’ it was his third such incident.

The clinician warned Mr. A that continued steroid use could worsen his behavior—and lead to more serious trouble later on. Mr. A, however, said he was more afraid of losing muscle mass and becoming ‘small again.’ When the clinician mentioned that use of anabolic steroids without a prescription is illegal, Mr. A retorted that several of his friends had used the drugs without legal consequences.

Mr. A left the office showing no inclination to return for further treatment. The clinician could only offer to be available in the future.

Box

What medical sequelae await Mr. A if he continues to abuse steroids? How would you convince him to stay in treatment?

Dr. Carter’s and Pope’s observations

Mr. A’s path to mania has been well demonstrated in the literature. Hypomania or even frank manic syndromes, sometimes associated with violent behavior, are rare at weekly doses of 300 mg of testosterone equivalent. At weekly doses of >1,000 mg, psychiatric syndromes such as hypomania or mania may occur in almost one-half of cases.⁵

If he continues to abuse anabolic steroids, however, Mr. A could experience adverse physical reactions ranging from embarrassing acne and male-pattern baldness (Table 1) to rare and life-threatening hepatic effects such as cholestatic jaundice and peliosis hepatitis (blood-filled cysts in the liver).

Table 1

ANABOLIC STEROID ABUSE: COMMON PHYSICAL FINDINGS

The risk of atherosclerotic disease or prostate cancer later in life may also be greatly increased.

More common laboratory changes include:

• increased red blood cell count, hemoglobin and hematocrit
• elevated liver function readings (although these must not be confused with enzymes that originate from muscle tissue)
• and unfavorable changes in triglycerides, total cholesterol, and HDL:LDL cholesterol ratios (Table 2).

Other potential laboratory changes with steroid abuse include decreased luteinizing hormone and follicle-stimulating hormone due to feedback inhibition. Feedback inhibition will also reduce testosterone and estradiol levels with use of anabolic steroids other than testosterone esters. These levels, however, would both be elevated with use of testosterone esters alone.

In men, testicular atrophy and decreased sperm count are generally reversible manifestations of steroid abuse, whereas gynecomastia may be irreversible and require surgical intervention in advanced cases.^3,6 Women who use anabolic steroids (such as for body-building) are vulnerable to disrupted menstrual cycles, decreased breast size, and masculinizing effects including enlarged clitoris, hirsutism, and deepening of the voice.⁶

In adolescents, anabolic steroid use may cause premature closure of the epiphyses, leading to shortened stature.³

Unfortunately, warnings about these many adverse effects rarely deter anabolic steroid users such as Mr. A or persuade them to continue in treatment of any type. Most young anabolic steroid abusers report that they have never felt significant adverse effects from steroid use and know of no one who has experienced such effects. The dramatic muscle gains they have witnessed in themselves and in other users decisively outweigh what they perceive to be remote threats of adverse consequences.

Follow-up: Return to treatment

We didn’t hear from Mr. A until about 18 months later, when he unexpectedly requested a consultation.

Upon arrival, Mr. A exhibited major depression with prominent anhedonia, hypersomnia of 12 to 14 hours per night, loss of appetite, fatigue, prominent psychomotor retardation, feelings of guilt, difficulty concentrating, and suicidal thoughts (but without a frank plan). He also reported panic attacks that were randomly occurring each day, usually in public.

Mr. A conceded that he had experienced similar depressive episodes after stopping anabolic steroid use, but that they typically ran their course after 2 to 3 weeks. He said the present episode showed no sign of abating after nearly 2 months. He had attempted to ‘treat’ this episode by resuming anabolic steroid use, but he could not get an adequate supply from his dealer.

Mr. A’s total testosterone level, measured in the morning when it should be near its diurnal peak, was 127 ng/dl (normal range is 270 to 1,070 ng/dl). Physical examination revealed that his testicles had shrunk to the size of marbles (each approximately 5 mm in diameter). He was referred to an endocrinologist for evaluation and was simultaneously started on fluoxetine, 20 mg/d.

Table 2

LABORATORY ABNORMALITIES ASSOCIATED WITH ANABOLIC STEROID ABUSE

He returned 2 weeks later, exhibiting little improvement and wanting to resume steroids ‘because it was the only thing that really helped.’ Instead, he agreed to continue on fluoxetine and remain in follow-up. At 4 weeks, he noticed a decrease in panic attacks, return of normal mood, decreased anhedonia, and loss of suicidal ideation. He continued taking fluoxetine for another 3 months but then abruptly disappeared from treatment.

Mr. A resurfaced about 1 year later, revealing to the psychiatrist that he had taken yet another cycle of anabolic steroids, largely because he feared losing his muscle mass. His panic attacks had recurred almost immediately when he began tapering down from the peak of this cycle, and he agreed to resume taking fluoxetine.

A look at Mr. A’s extended history may provide clues to his persistent anabolic steroid abuse problem. He had displayed prominent symptoms of conduct disorder as a child. He had been truant from school, had occasionally run away from home, and had been involved in several misdemeanors. While in high school, he typically drank 10 to 12 beers over a weekend and had experimented with hallucinogenic mushrooms and 3,4-methylenedioxymethamphetamine (‘ecstasy’).

He started weightlifting while in high school and by age 17 was visiting the gym every day. He began college on a football scholarship but dropped out after 1 year. Starting in his early 20s, he competed in several bodybuilding contests.

Despite his impressive muscularity, Mr. A was anxious about his body appearance. He often would not take off his shirt—even when at the beach or a swimming pool—for fear that he would appear too small. He sometimes wore heavy sweatpants in the sweltering heat to conceal his legs. He also admitted spending as much as 2 hours a day examining himself in the mirror. ‘Sometimes when I get a bad (look at) myself, I will refuse to go out for the rest of the day,’ he said.

Mr. A has had a succession of girlfriends, but his rigid commitment to diet and exercise invariably ended these relationships.

At this point, would you first address Mr. A’s apparent substance use problem or the underlying body dysmorphic symptoms?

Dr. Carter’s and Pope’s observations

Two comorbidities noted here—substance abuse and body dysmorphic disorder—are common among anabolic steroid abusers. Addressing these problems, especially the body dysmorphic disorder, may sometimes help patients who are unwilling to address their steroid use directly. Body dysmorphic disorder may respond to selective serotonin reuptake inhibitors⁷ and cognitive-behavioral therapy.⁸

Anabolic steroids are not associated with immediate intoxicating effects, and ICD-10 categorizes them as substances not associated with dependence. After prolonged use at high doses, however, anabolic steroids are often associated with euphoria. Researchers also have found that some steroid abusers do meet DSM-IV criteria for substance dependence.⁶

Beyond the direct psychotropic effects of anabolic steroids, the depressive symptoms commonly seen during their withdrawal may perpetuate the dependence, as was the case with Mr. A. Most depressive symptoms that follow steroid cessation do not require drug therapy,³ but Mr. A developed severe and persistent depressive symptoms, complicated by panic disorder and body image concerns at a level diagnostic of body dysmorphic disorder. Such body image concerns often precipitate relapse into steroid use.

Conclusion: Another setback

As of this writing, Mr. A is again lost to follow-up. After taking fluoxetine and keeping monthly appointments for about 6 months, he failed to arrive for a visit and did not set another appointment. The patient may have once again stopped medication and embarked on yet another cycle of anabolic steroid use. If this is so, we can only hope that he returns to treatment before it is too late.

Related resource

• Lukas SE. Steroids. Hillside, NJ: Enslow Publishers, 1994.

Drug brand names

• Fluoxetine • Prozac
• Nandrolone decanoate • Deca-Durabolin
• Oxymetholone • Anadrol
• Stanozolol • Winstrol

Disclosure

Dr. Carter reports that he receives research/grant support from or is a consultant to Eli Lilly and Co., Pfizer Inc., and Ortho-McNeil Pharmaceutical.

Dr. Pope reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Initial visit: Road rage or ‘roid’ rage?

Mr. A, 25, was arrested after police interrupted an altercation between him and a senior citizen at a stoplight. He had emerged from his car, walked over to the older driver in front of him, ripped open the car door, and pulled the man out of the car and onto the street. He was still yelling at the victim when a passing officer intervened.

Mr. A was charged with assault. After a plea bargain, he was sentenced to probation and fined. He had been seeing his probation officer every 2 weeks, but his parents were worried about his erratic and sometimes defiant behavior and insisted he see a psychiatrist. He reluctantly agreed to one consultation, largely because his parents threatened to withhold financial support if he failed to do so.

The first thing the psychiatrist noticed was Mr. A’s striking muscular appearance. He was approximately 5 feet, 7 inches tall, weighed at least 200 pounds, and had a 30-inch waist and less than 10% body fat.

Dr. Carter’s and Pope’s observations

Mr. A’s diagnosis should be suspected immediately upon his entering the office. Extensive anabolic steroid use produces body changes that can be diagnosed almost at a glance. It is virtually impossible to achieve a level of muscle mass comparable to what Mr. A exhibited without the use of anabolic steroids.¹

Remarkably, however, most people—including Mr. A’s parents, law enforcement personnel, and even some members of the treatment team—failed to diagnose Mr. A’s steroid use. He somehow convinced them that his extreme muscularity was the result of hard work, dedication, and scrupulous attention to diet. This suggests that steroid abuse cases involving serious violence—such as that of Mr. A—frequently go unreported and undiagnosed and are probably more common than we suspect.

Epidemiologic data suggest that clinicians should become familiar with the presentation of patients who are using anabolic steroids (Box).

Evaluation: ‘Stacking’ up

Mr. A at first vehemently denied that he had ever used anabolic steroids. After a more detailed conversation, during which the clinician demonstrated some knowledge of this area, Mr. A eventually conceded that he was taking a substantial weekly dose of the drugs at the time of the assault.

A subsequent clinical evaluation revealed that Mr. A had taken several ‘cycles’ (courses) of anabolic steroids over the last 2 to 3 years. Each cycle lasted 10 to 16 weeks and had been characterized by simultaneous use of two or more steroids, a practice known as ‘stacking.’

Mr. A started his first cycle with a modest ‘stack’ of drugs: testosterone cypionate, 200 mg twice a week, and stanozolol, 10 mg/d. Taken together, these dosages represented roughly 470 mg of testosterone equivalent per week—about 10 times the weekly secretion of testosterone in a normal male. He noticed no change in mood during this initial cycle.

With subsequent cycles, however, Mr. A became increasingly obsessed with his body image and used higher dosages. When the assault occurred, he was taking testosterone cypionate, 800 mg a week, nandrolone decanoate, 400 mg a week, and oxymetholone, 50 mg/d. With this regimen—the weekly equivalent of 1,550 mg of testosterone—Mr. A noticed prominent mood changes that met DSM-IV criteria for a manic episode. He experienced euphoria, dramatic irritability, limitless self-confidence, decreased need for sleep, distractibility, extreme recklessness (driving too fast, spending too freely), and some mildly paranoid ideation (without frank delusions). He admitted that he had twice assaulted his girlfriend and that he invariably became enraged at even the slightest annoyance when driving in traffic. He revealed that although the altercation with the older driver had led to his first arrest for ‘road rage,’ it was his third such incident.

The clinician warned Mr. A that continued steroid use could worsen his behavior—and lead to more serious trouble later on. Mr. A, however, said he was more afraid of losing muscle mass and becoming ‘small again.’ When the clinician mentioned that use of anabolic steroids without a prescription is illegal, Mr. A retorted that several of his friends had used the drugs without legal consequences.

Mr. A left the office showing no inclination to return for further treatment. The clinician could only offer to be available in the future.

Box

What medical sequelae await Mr. A if he continues to abuse steroids? How would you convince him to stay in treatment?

Dr. Carter’s and Pope’s observations

Mr. A’s path to mania has been well demonstrated in the literature. Hypomania or even frank manic syndromes, sometimes associated with violent behavior, are rare at weekly doses of 300 mg of testosterone equivalent. At weekly doses of >1,000 mg, psychiatric syndromes such as hypomania or mania may occur in almost one-half of cases.⁵

If he continues to abuse anabolic steroids, however, Mr. A could experience adverse physical reactions ranging from embarrassing acne and male-pattern baldness (Table 1) to rare and life-threatening hepatic effects such as cholestatic jaundice and peliosis hepatitis (blood-filled cysts in the liver).

Table 1

ANABOLIC STEROID ABUSE: COMMON PHYSICAL FINDINGS

The risk of atherosclerotic disease or prostate cancer later in life may also be greatly increased.

More common laboratory changes include:

• increased red blood cell count, hemoglobin and hematocrit
• elevated liver function readings (although these must not be confused with enzymes that originate from muscle tissue)
• and unfavorable changes in triglycerides, total cholesterol, and HDL:LDL cholesterol ratios (Table 2).

Other potential laboratory changes with steroid abuse include decreased luteinizing hormone and follicle-stimulating hormone due to feedback inhibition. Feedback inhibition will also reduce testosterone and estradiol levels with use of anabolic steroids other than testosterone esters. These levels, however, would both be elevated with use of testosterone esters alone.

In men, testicular atrophy and decreased sperm count are generally reversible manifestations of steroid abuse, whereas gynecomastia may be irreversible and require surgical intervention in advanced cases.^3,6 Women who use anabolic steroids (such as for body-building) are vulnerable to disrupted menstrual cycles, decreased breast size, and masculinizing effects including enlarged clitoris, hirsutism, and deepening of the voice.⁶

In adolescents, anabolic steroid use may cause premature closure of the epiphyses, leading to shortened stature.³

Unfortunately, warnings about these many adverse effects rarely deter anabolic steroid users such as Mr. A or persuade them to continue in treatment of any type. Most young anabolic steroid abusers report that they have never felt significant adverse effects from steroid use and know of no one who has experienced such effects. The dramatic muscle gains they have witnessed in themselves and in other users decisively outweigh what they perceive to be remote threats of adverse consequences.

Follow-up: Return to treatment

We didn’t hear from Mr. A until about 18 months later, when he unexpectedly requested a consultation.

Upon arrival, Mr. A exhibited major depression with prominent anhedonia, hypersomnia of 12 to 14 hours per night, loss of appetite, fatigue, prominent psychomotor retardation, feelings of guilt, difficulty concentrating, and suicidal thoughts (but without a frank plan). He also reported panic attacks that were randomly occurring each day, usually in public.

Mr. A conceded that he had experienced similar depressive episodes after stopping anabolic steroid use, but that they typically ran their course after 2 to 3 weeks. He said the present episode showed no sign of abating after nearly 2 months. He had attempted to ‘treat’ this episode by resuming anabolic steroid use, but he could not get an adequate supply from his dealer.

Mr. A’s total testosterone level, measured in the morning when it should be near its diurnal peak, was 127 ng/dl (normal range is 270 to 1,070 ng/dl). Physical examination revealed that his testicles had shrunk to the size of marbles (each approximately 5 mm in diameter). He was referred to an endocrinologist for evaluation and was simultaneously started on fluoxetine, 20 mg/d.

Table 2

LABORATORY ABNORMALITIES ASSOCIATED WITH ANABOLIC STEROID ABUSE

He returned 2 weeks later, exhibiting little improvement and wanting to resume steroids ‘because it was the only thing that really helped.’ Instead, he agreed to continue on fluoxetine and remain in follow-up. At 4 weeks, he noticed a decrease in panic attacks, return of normal mood, decreased anhedonia, and loss of suicidal ideation. He continued taking fluoxetine for another 3 months but then abruptly disappeared from treatment.

Mr. A resurfaced about 1 year later, revealing to the psychiatrist that he had taken yet another cycle of anabolic steroids, largely because he feared losing his muscle mass. His panic attacks had recurred almost immediately when he began tapering down from the peak of this cycle, and he agreed to resume taking fluoxetine.

A look at Mr. A’s extended history may provide clues to his persistent anabolic steroid abuse problem. He had displayed prominent symptoms of conduct disorder as a child. He had been truant from school, had occasionally run away from home, and had been involved in several misdemeanors. While in high school, he typically drank 10 to 12 beers over a weekend and had experimented with hallucinogenic mushrooms and 3,4-methylenedioxymethamphetamine (‘ecstasy’).

He started weightlifting while in high school and by age 17 was visiting the gym every day. He began college on a football scholarship but dropped out after 1 year. Starting in his early 20s, he competed in several bodybuilding contests.

Despite his impressive muscularity, Mr. A was anxious about his body appearance. He often would not take off his shirt—even when at the beach or a swimming pool—for fear that he would appear too small. He sometimes wore heavy sweatpants in the sweltering heat to conceal his legs. He also admitted spending as much as 2 hours a day examining himself in the mirror. ‘Sometimes when I get a bad (look at) myself, I will refuse to go out for the rest of the day,’ he said.

Mr. A has had a succession of girlfriends, but his rigid commitment to diet and exercise invariably ended these relationships.

At this point, would you first address Mr. A’s apparent substance use problem or the underlying body dysmorphic symptoms?

Dr. Carter’s and Pope’s observations

Two comorbidities noted here—substance abuse and body dysmorphic disorder—are common among anabolic steroid abusers. Addressing these problems, especially the body dysmorphic disorder, may sometimes help patients who are unwilling to address their steroid use directly. Body dysmorphic disorder may respond to selective serotonin reuptake inhibitors⁷ and cognitive-behavioral therapy.⁸

Anabolic steroids are not associated with immediate intoxicating effects, and ICD-10 categorizes them as substances not associated with dependence. After prolonged use at high doses, however, anabolic steroids are often associated with euphoria. Researchers also have found that some steroid abusers do meet DSM-IV criteria for substance dependence.⁶

Beyond the direct psychotropic effects of anabolic steroids, the depressive symptoms commonly seen during their withdrawal may perpetuate the dependence, as was the case with Mr. A. Most depressive symptoms that follow steroid cessation do not require drug therapy,³ but Mr. A developed severe and persistent depressive symptoms, complicated by panic disorder and body image concerns at a level diagnostic of body dysmorphic disorder. Such body image concerns often precipitate relapse into steroid use.

Conclusion: Another setback

As of this writing, Mr. A is again lost to follow-up. After taking fluoxetine and keeping monthly appointments for about 6 months, he failed to arrive for a visit and did not set another appointment. The patient may have once again stopped medication and embarked on yet another cycle of anabolic steroid use. If this is so, we can only hope that he returns to treatment before it is too late.

Related resource

• Lukas SE. Steroids. Hillside, NJ: Enslow Publishers, 1994.

Drug brand names

• Fluoxetine • Prozac
• Nandrolone decanoate • Deca-Durabolin
• Oxymetholone • Anadrol
• Stanozolol • Winstrol

Disclosure

Dr. Carter reports that he receives research/grant support from or is a consultant to Eli Lilly and Co., Pfizer Inc., and Ortho-McNeil Pharmaceutical.

Dr. Pope reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Initial visit: Road rage or ‘roid’ rage?

Mr. A, 25, was arrested after police interrupted an altercation between him and a senior citizen at a stoplight. He had emerged from his car, walked over to the older driver in front of him, ripped open the car door, and pulled the man out of the car and onto the street. He was still yelling at the victim when a passing officer intervened.

Mr. A was charged with assault. After a plea bargain, he was sentenced to probation and fined. He had been seeing his probation officer every 2 weeks, but his parents were worried about his erratic and sometimes defiant behavior and insisted he see a psychiatrist. He reluctantly agreed to one consultation, largely because his parents threatened to withhold financial support if he failed to do so.

The first thing the psychiatrist noticed was Mr. A’s striking muscular appearance. He was approximately 5 feet, 7 inches tall, weighed at least 200 pounds, and had a 30-inch waist and less than 10% body fat.

Dr. Carter’s and Pope’s observations

Mr. A’s diagnosis should be suspected immediately upon his entering the office. Extensive anabolic steroid use produces body changes that can be diagnosed almost at a glance. It is virtually impossible to achieve a level of muscle mass comparable to what Mr. A exhibited without the use of anabolic steroids.¹

Remarkably, however, most people—including Mr. A’s parents, law enforcement personnel, and even some members of the treatment team—failed to diagnose Mr. A’s steroid use. He somehow convinced them that his extreme muscularity was the result of hard work, dedication, and scrupulous attention to diet. This suggests that steroid abuse cases involving serious violence—such as that of Mr. A—frequently go unreported and undiagnosed and are probably more common than we suspect.

Epidemiologic data suggest that clinicians should become familiar with the presentation of patients who are using anabolic steroids (Box).

Evaluation: ‘Stacking’ up

Mr. A at first vehemently denied that he had ever used anabolic steroids. After a more detailed conversation, during which the clinician demonstrated some knowledge of this area, Mr. A eventually conceded that he was taking a substantial weekly dose of the drugs at the time of the assault.

A subsequent clinical evaluation revealed that Mr. A had taken several ‘cycles’ (courses) of anabolic steroids over the last 2 to 3 years. Each cycle lasted 10 to 16 weeks and had been characterized by simultaneous use of two or more steroids, a practice known as ‘stacking.’

Mr. A started his first cycle with a modest ‘stack’ of drugs: testosterone cypionate, 200 mg twice a week, and stanozolol, 10 mg/d. Taken together, these dosages represented roughly 470 mg of testosterone equivalent per week—about 10 times the weekly secretion of testosterone in a normal male. He noticed no change in mood during this initial cycle.

With subsequent cycles, however, Mr. A became increasingly obsessed with his body image and used higher dosages. When the assault occurred, he was taking testosterone cypionate, 800 mg a week, nandrolone decanoate, 400 mg a week, and oxymetholone, 50 mg/d. With this regimen—the weekly equivalent of 1,550 mg of testosterone—Mr. A noticed prominent mood changes that met DSM-IV criteria for a manic episode. He experienced euphoria, dramatic irritability, limitless self-confidence, decreased need for sleep, distractibility, extreme recklessness (driving too fast, spending too freely), and some mildly paranoid ideation (without frank delusions). He admitted that he had twice assaulted his girlfriend and that he invariably became enraged at even the slightest annoyance when driving in traffic. He revealed that although the altercation with the older driver had led to his first arrest for ‘road rage,’ it was his third such incident.

The clinician warned Mr. A that continued steroid use could worsen his behavior—and lead to more serious trouble later on. Mr. A, however, said he was more afraid of losing muscle mass and becoming ‘small again.’ When the clinician mentioned that use of anabolic steroids without a prescription is illegal, Mr. A retorted that several of his friends had used the drugs without legal consequences.

Mr. A left the office showing no inclination to return for further treatment. The clinician could only offer to be available in the future.

Box

What medical sequelae await Mr. A if he continues to abuse steroids? How would you convince him to stay in treatment?

Dr. Carter’s and Pope’s observations

Mr. A’s path to mania has been well demonstrated in the literature. Hypomania or even frank manic syndromes, sometimes associated with violent behavior, are rare at weekly doses of 300 mg of testosterone equivalent. At weekly doses of >1,000 mg, psychiatric syndromes such as hypomania or mania may occur in almost one-half of cases.⁵

If he continues to abuse anabolic steroids, however, Mr. A could experience adverse physical reactions ranging from embarrassing acne and male-pattern baldness (Table 1) to rare and life-threatening hepatic effects such as cholestatic jaundice and peliosis hepatitis (blood-filled cysts in the liver).

Table 1

ANABOLIC STEROID ABUSE: COMMON PHYSICAL FINDINGS

The risk of atherosclerotic disease or prostate cancer later in life may also be greatly increased.

More common laboratory changes include:

• increased red blood cell count, hemoglobin and hematocrit
• elevated liver function readings (although these must not be confused with enzymes that originate from muscle tissue)
• and unfavorable changes in triglycerides, total cholesterol, and HDL:LDL cholesterol ratios (Table 2).

Other potential laboratory changes with steroid abuse include decreased luteinizing hormone and follicle-stimulating hormone due to feedback inhibition. Feedback inhibition will also reduce testosterone and estradiol levels with use of anabolic steroids other than testosterone esters. These levels, however, would both be elevated with use of testosterone esters alone.

In men, testicular atrophy and decreased sperm count are generally reversible manifestations of steroid abuse, whereas gynecomastia may be irreversible and require surgical intervention in advanced cases.^3,6 Women who use anabolic steroids (such as for body-building) are vulnerable to disrupted menstrual cycles, decreased breast size, and masculinizing effects including enlarged clitoris, hirsutism, and deepening of the voice.⁶

In adolescents, anabolic steroid use may cause premature closure of the epiphyses, leading to shortened stature.³

Unfortunately, warnings about these many adverse effects rarely deter anabolic steroid users such as Mr. A or persuade them to continue in treatment of any type. Most young anabolic steroid abusers report that they have never felt significant adverse effects from steroid use and know of no one who has experienced such effects. The dramatic muscle gains they have witnessed in themselves and in other users decisively outweigh what they perceive to be remote threats of adverse consequences.

Follow-up: Return to treatment

We didn’t hear from Mr. A until about 18 months later, when he unexpectedly requested a consultation.

Upon arrival, Mr. A exhibited major depression with prominent anhedonia, hypersomnia of 12 to 14 hours per night, loss of appetite, fatigue, prominent psychomotor retardation, feelings of guilt, difficulty concentrating, and suicidal thoughts (but without a frank plan). He also reported panic attacks that were randomly occurring each day, usually in public.

Mr. A conceded that he had experienced similar depressive episodes after stopping anabolic steroid use, but that they typically ran their course after 2 to 3 weeks. He said the present episode showed no sign of abating after nearly 2 months. He had attempted to ‘treat’ this episode by resuming anabolic steroid use, but he could not get an adequate supply from his dealer.

Mr. A’s total testosterone level, measured in the morning when it should be near its diurnal peak, was 127 ng/dl (normal range is 270 to 1,070 ng/dl). Physical examination revealed that his testicles had shrunk to the size of marbles (each approximately 5 mm in diameter). He was referred to an endocrinologist for evaluation and was simultaneously started on fluoxetine, 20 mg/d.

Table 2

LABORATORY ABNORMALITIES ASSOCIATED WITH ANABOLIC STEROID ABUSE

He returned 2 weeks later, exhibiting little improvement and wanting to resume steroids ‘because it was the only thing that really helped.’ Instead, he agreed to continue on fluoxetine and remain in follow-up. At 4 weeks, he noticed a decrease in panic attacks, return of normal mood, decreased anhedonia, and loss of suicidal ideation. He continued taking fluoxetine for another 3 months but then abruptly disappeared from treatment.

Mr. A resurfaced about 1 year later, revealing to the psychiatrist that he had taken yet another cycle of anabolic steroids, largely because he feared losing his muscle mass. His panic attacks had recurred almost immediately when he began tapering down from the peak of this cycle, and he agreed to resume taking fluoxetine.

A look at Mr. A’s extended history may provide clues to his persistent anabolic steroid abuse problem. He had displayed prominent symptoms of conduct disorder as a child. He had been truant from school, had occasionally run away from home, and had been involved in several misdemeanors. While in high school, he typically drank 10 to 12 beers over a weekend and had experimented with hallucinogenic mushrooms and 3,4-methylenedioxymethamphetamine (‘ecstasy’).

He started weightlifting while in high school and by age 17 was visiting the gym every day. He began college on a football scholarship but dropped out after 1 year. Starting in his early 20s, he competed in several bodybuilding contests.

Despite his impressive muscularity, Mr. A was anxious about his body appearance. He often would not take off his shirt—even when at the beach or a swimming pool—for fear that he would appear too small. He sometimes wore heavy sweatpants in the sweltering heat to conceal his legs. He also admitted spending as much as 2 hours a day examining himself in the mirror. ‘Sometimes when I get a bad (look at) myself, I will refuse to go out for the rest of the day,’ he said.

Mr. A has had a succession of girlfriends, but his rigid commitment to diet and exercise invariably ended these relationships.

At this point, would you first address Mr. A’s apparent substance use problem or the underlying body dysmorphic symptoms?

Dr. Carter’s and Pope’s observations

Two comorbidities noted here—substance abuse and body dysmorphic disorder—are common among anabolic steroid abusers. Addressing these problems, especially the body dysmorphic disorder, may sometimes help patients who are unwilling to address their steroid use directly. Body dysmorphic disorder may respond to selective serotonin reuptake inhibitors⁷ and cognitive-behavioral therapy.⁸

Anabolic steroids are not associated with immediate intoxicating effects, and ICD-10 categorizes them as substances not associated with dependence. After prolonged use at high doses, however, anabolic steroids are often associated with euphoria. Researchers also have found that some steroid abusers do meet DSM-IV criteria for substance dependence.⁶

Beyond the direct psychotropic effects of anabolic steroids, the depressive symptoms commonly seen during their withdrawal may perpetuate the dependence, as was the case with Mr. A. Most depressive symptoms that follow steroid cessation do not require drug therapy,³ but Mr. A developed severe and persistent depressive symptoms, complicated by panic disorder and body image concerns at a level diagnostic of body dysmorphic disorder. Such body image concerns often precipitate relapse into steroid use.

Conclusion: Another setback

As of this writing, Mr. A is again lost to follow-up. After taking fluoxetine and keeping monthly appointments for about 6 months, he failed to arrive for a visit and did not set another appointment. The patient may have once again stopped medication and embarked on yet another cycle of anabolic steroid use. If this is so, we can only hope that he returns to treatment before it is too late.

Related resources

• NIDA Research Report: Anabolic Steroid Abuse. http://www.nida.nih.gov/ResearchReports/Steroids/AnabolicSteroids.html
• Lukas SE. Steroids. Hillside, NJ: Enslow Publishers, 1994.

Drug brand names

• Fluoxetine • Prozac
• Nandrolone decanoate • Deca-Durabolin
• Oxymetholone • Anadrol
• Stanozolol • Winstrol

Disclosure

Dr. Carter reports that he receives research/grant support from or is a consultant to Eli Lilly and Co., Pfizer Inc., and Ortho-McNeil Pharmaceutical.

Dr. Pope reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Initial visit: Road rage or ‘roid’ rage?

Mr. A, 25, was arrested after police interrupted an altercation between him and a senior citizen at a stoplight. He had emerged from his car, walked over to the older driver in front of him, ripped open the car door, and pulled the man out of the car and onto the street. He was still yelling at the victim when a passing officer intervened.

Mr. A was charged with assault. After a plea bargain, he was sentenced to probation and fined. He had been seeing his probation officer every 2 weeks, but his parents were worried about his erratic and sometimes defiant behavior and insisted he see a psychiatrist. He reluctantly agreed to one consultation, largely because his parents threatened to withhold financial support if he failed to do so.

The first thing the psychiatrist noticed was Mr. A’s striking muscular appearance. He was approximately 5 feet, 7 inches tall, weighed at least 200 pounds, and had a 30-inch waist and less than 10% body fat.

Dr. Carter’s and Pope’s observations

Mr. A’s diagnosis should be suspected immediately upon his entering the office. Extensive anabolic steroid use produces body changes that can be diagnosed almost at a glance. It is virtually impossible to achieve a level of muscle mass comparable to what Mr. A exhibited without the use of anabolic steroids.¹

Remarkably, however, most people—including Mr. A’s parents, law enforcement personnel, and even some members of the treatment team—failed to diagnose Mr. A’s steroid use. He somehow convinced them that his extreme muscularity was the result of hard work, dedication, and scrupulous attention to diet. This suggests that steroid abuse cases involving serious violence—such as that of Mr. A—frequently go unreported and undiagnosed and are probably more common than we suspect.

Epidemiologic data suggest that clinicians should become familiar with the presentation of patients who are using anabolic steroids (Box).

Evaluation: ‘Stacking’ up

Mr. A at first vehemently denied that he had ever used anabolic steroids. After a more detailed conversation, during which the clinician demonstrated some knowledge of this area, Mr. A eventually conceded that he was taking a substantial weekly dose of the drugs at the time of the assault.

A subsequent clinical evaluation revealed that Mr. A had taken several ‘cycles’ (courses) of anabolic steroids over the last 2 to 3 years. Each cycle lasted 10 to 16 weeks and had been characterized by simultaneous use of two or more steroids, a practice known as ‘stacking.’

Mr. A started his first cycle with a modest ‘stack’ of drugs: testosterone cypionate, 200 mg twice a week, and stanozolol, 10 mg/d. Taken together, these dosages represented roughly 470 mg of testosterone equivalent per week—about 10 times the weekly secretion of testosterone in a normal male. He noticed no change in mood during this initial cycle.

With subsequent cycles, however, Mr. A became increasingly obsessed with his body image and used higher dosages. When the assault occurred, he was taking testosterone cypionate, 800 mg a week, nandrolone decanoate, 400 mg a week, and oxymetholone, 50 mg/d. With this regimen—the weekly equivalent of 1,550 mg of testosterone—Mr. A noticed prominent mood changes that met DSM-IV criteria for a manic episode. He experienced euphoria, dramatic irritability, limitless self-confidence, decreased need for sleep, distractibility, extreme recklessness (driving too fast, spending too freely), and some mildly paranoid ideation (without frank delusions). He admitted that he had twice assaulted his girlfriend and that he invariably became enraged at even the slightest annoyance when driving in traffic. He revealed that although the altercation with the older driver had led to his first arrest for ‘road rage,’ it was his third such incident.

The clinician warned Mr. A that continued steroid use could worsen his behavior—and lead to more serious trouble later on. Mr. A, however, said he was more afraid of losing muscle mass and becoming ‘small again.’ When the clinician mentioned that use of anabolic steroids without a prescription is illegal, Mr. A retorted that several of his friends had used the drugs without legal consequences.

Mr. A left the office showing no inclination to return for further treatment. The clinician could only offer to be available in the future.

Box

What medical sequelae await Mr. A if he continues to abuse steroids? How would you convince him to stay in treatment?

Dr. Carter’s and Pope’s observations

Mr. A’s path to mania has been well demonstrated in the literature. Hypomania or even frank manic syndromes, sometimes associated with violent behavior, are rare at weekly doses of 300 mg of testosterone equivalent. At weekly doses of >1,000 mg, psychiatric syndromes such as hypomania or mania may occur in almost one-half of cases.⁵

If he continues to abuse anabolic steroids, however, Mr. A could experience adverse physical reactions ranging from embarrassing acne and male-pattern baldness (Table 1) to rare and life-threatening hepatic effects such as cholestatic jaundice and peliosis hepatitis (blood-filled cysts in the liver).

Table 1

ANABOLIC STEROID ABUSE: COMMON PHYSICAL FINDINGS

The risk of atherosclerotic disease or prostate cancer later in life may also be greatly increased.

More common laboratory changes include:

• increased red blood cell count, hemoglobin and hematocrit
• elevated liver function readings (although these must not be confused with enzymes that originate from muscle tissue)
• and unfavorable changes in triglycerides, total cholesterol, and HDL:LDL cholesterol ratios (Table 2).

Other potential laboratory changes with steroid abuse include decreased luteinizing hormone and follicle-stimulating hormone due to feedback inhibition. Feedback inhibition will also reduce testosterone and estradiol levels with use of anabolic steroids other than testosterone esters. These levels, however, would both be elevated with use of testosterone esters alone.

In men, testicular atrophy and decreased sperm count are generally reversible manifestations of steroid abuse, whereas gynecomastia may be irreversible and require surgical intervention in advanced cases.^3,6 Women who use anabolic steroids (such as for body-building) are vulnerable to disrupted menstrual cycles, decreased breast size, and masculinizing effects including enlarged clitoris, hirsutism, and deepening of the voice.⁶

In adolescents, anabolic steroid use may cause premature closure of the epiphyses, leading to shortened stature.³

Unfortunately, warnings about these many adverse effects rarely deter anabolic steroid users such as Mr. A or persuade them to continue in treatment of any type. Most young anabolic steroid abusers report that they have never felt significant adverse effects from steroid use and know of no one who has experienced such effects. The dramatic muscle gains they have witnessed in themselves and in other users decisively outweigh what they perceive to be remote threats of adverse consequences.

Follow-up: Return to treatment

We didn’t hear from Mr. A until about 18 months later, when he unexpectedly requested a consultation.

Upon arrival, Mr. A exhibited major depression with prominent anhedonia, hypersomnia of 12 to 14 hours per night, loss of appetite, fatigue, prominent psychomotor retardation, feelings of guilt, difficulty concentrating, and suicidal thoughts (but without a frank plan). He also reported panic attacks that were randomly occurring each day, usually in public.

Mr. A conceded that he had experienced similar depressive episodes after stopping anabolic steroid use, but that they typically ran their course after 2 to 3 weeks. He said the present episode showed no sign of abating after nearly 2 months. He had attempted to ‘treat’ this episode by resuming anabolic steroid use, but he could not get an adequate supply from his dealer.

Mr. A’s total testosterone level, measured in the morning when it should be near its diurnal peak, was 127 ng/dl (normal range is 270 to 1,070 ng/dl). Physical examination revealed that his testicles had shrunk to the size of marbles (each approximately 5 mm in diameter). He was referred to an endocrinologist for evaluation and was simultaneously started on fluoxetine, 20 mg/d.

Table 2

LABORATORY ABNORMALITIES ASSOCIATED WITH ANABOLIC STEROID ABUSE

He returned 2 weeks later, exhibiting little improvement and wanting to resume steroids ‘because it was the only thing that really helped.’ Instead, he agreed to continue on fluoxetine and remain in follow-up. At 4 weeks, he noticed a decrease in panic attacks, return of normal mood, decreased anhedonia, and loss of suicidal ideation. He continued taking fluoxetine for another 3 months but then abruptly disappeared from treatment.

Mr. A resurfaced about 1 year later, revealing to the psychiatrist that he had taken yet another cycle of anabolic steroids, largely because he feared losing his muscle mass. His panic attacks had recurred almost immediately when he began tapering down from the peak of this cycle, and he agreed to resume taking fluoxetine.

A look at Mr. A’s extended history may provide clues to his persistent anabolic steroid abuse problem. He had displayed prominent symptoms of conduct disorder as a child. He had been truant from school, had occasionally run away from home, and had been involved in several misdemeanors. While in high school, he typically drank 10 to 12 beers over a weekend and had experimented with hallucinogenic mushrooms and 3,4-methylenedioxymethamphetamine (‘ecstasy’).

He started weightlifting while in high school and by age 17 was visiting the gym every day. He began college on a football scholarship but dropped out after 1 year. Starting in his early 20s, he competed in several bodybuilding contests.

Despite his impressive muscularity, Mr. A was anxious about his body appearance. He often would not take off his shirt—even when at the beach or a swimming pool—for fear that he would appear too small. He sometimes wore heavy sweatpants in the sweltering heat to conceal his legs. He also admitted spending as much as 2 hours a day examining himself in the mirror. ‘Sometimes when I get a bad (look at) myself, I will refuse to go out for the rest of the day,’ he said.

Mr. A has had a succession of girlfriends, but his rigid commitment to diet and exercise invariably ended these relationships.

At this point, would you first address Mr. A’s apparent substance use problem or the underlying body dysmorphic symptoms?

Dr. Carter’s and Pope’s observations

Two comorbidities noted here—substance abuse and body dysmorphic disorder—are common among anabolic steroid abusers. Addressing these problems, especially the body dysmorphic disorder, may sometimes help patients who are unwilling to address their steroid use directly. Body dysmorphic disorder may respond to selective serotonin reuptake inhibitors⁷ and cognitive-behavioral therapy.⁸

Anabolic steroids are not associated with immediate intoxicating effects, and ICD-10 categorizes them as substances not associated with dependence. After prolonged use at high doses, however, anabolic steroids are often associated with euphoria. Researchers also have found that some steroid abusers do meet DSM-IV criteria for substance dependence.⁶

Beyond the direct psychotropic effects of anabolic steroids, the depressive symptoms commonly seen during their withdrawal may perpetuate the dependence, as was the case with Mr. A. Most depressive symptoms that follow steroid cessation do not require drug therapy,³ but Mr. A developed severe and persistent depressive symptoms, complicated by panic disorder and body image concerns at a level diagnostic of body dysmorphic disorder. Such body image concerns often precipitate relapse into steroid use.

Conclusion: Another setback

As of this writing, Mr. A is again lost to follow-up. After taking fluoxetine and keeping monthly appointments for about 6 months, he failed to arrive for a visit and did not set another appointment. The patient may have once again stopped medication and embarked on yet another cycle of anabolic steroid use. If this is so, we can only hope that he returns to treatment before it is too late.

Related resources

• NIDA Research Report: Anabolic Steroid Abuse. http://www.nida.nih.gov/ResearchReports/Steroids/AnabolicSteroids.html
• Lukas SE. Steroids. Hillside, NJ: Enslow Publishers, 1994.

Drug brand names

• Fluoxetine • Prozac
• Nandrolone decanoate • Deca-Durabolin
• Oxymetholone • Anadrol
• Stanozolol • Winstrol

Disclosure

Dr. Carter reports that he receives research/grant support from or is a consultant to Eli Lilly and Co., Pfizer Inc., and Ortho-McNeil Pharmaceutical.

Dr. Pope reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Initial visit: Road rage or ‘roid’ rage?

Mr. A, 25, was arrested after police interrupted an altercation between him and a senior citizen at a stoplight. He had emerged from his car, walked over to the older driver in front of him, ripped open the car door, and pulled the man out of the car and onto the street. He was still yelling at the victim when a passing officer intervened.

Mr. A was charged with assault. After a plea bargain, he was sentenced to probation and fined. He had been seeing his probation officer every 2 weeks, but his parents were worried about his erratic and sometimes defiant behavior and insisted he see a psychiatrist. He reluctantly agreed to one consultation, largely because his parents threatened to withhold financial support if he failed to do so.

The first thing the psychiatrist noticed was Mr. A’s striking muscular appearance. He was approximately 5 feet, 7 inches tall, weighed at least 200 pounds, and had a 30-inch waist and less than 10% body fat.

Dr. Carter’s and Pope’s observations

Mr. A’s diagnosis should be suspected immediately upon his entering the office. Extensive anabolic steroid use produces body changes that can be diagnosed almost at a glance. It is virtually impossible to achieve a level of muscle mass comparable to what Mr. A exhibited without the use of anabolic steroids.¹

Remarkably, however, most people—including Mr. A’s parents, law enforcement personnel, and even some members of the treatment team—failed to diagnose Mr. A’s steroid use. He somehow convinced them that his extreme muscularity was the result of hard work, dedication, and scrupulous attention to diet. This suggests that steroid abuse cases involving serious violence—such as that of Mr. A—frequently go unreported and undiagnosed and are probably more common than we suspect.

Epidemiologic data suggest that clinicians should become familiar with the presentation of patients who are using anabolic steroids (Box).

Evaluation: ‘Stacking’ up

Mr. A at first vehemently denied that he had ever used anabolic steroids. After a more detailed conversation, during which the clinician demonstrated some knowledge of this area, Mr. A eventually conceded that he was taking a substantial weekly dose of the drugs at the time of the assault.

A subsequent clinical evaluation revealed that Mr. A had taken several ‘cycles’ (courses) of anabolic steroids over the last 2 to 3 years. Each cycle lasted 10 to 16 weeks and had been characterized by simultaneous use of two or more steroids, a practice known as ‘stacking.’

Mr. A started his first cycle with a modest ‘stack’ of drugs: testosterone cypionate, 200 mg twice a week, and stanozolol, 10 mg/d. Taken together, these dosages represented roughly 470 mg of testosterone equivalent per week—about 10 times the weekly secretion of testosterone in a normal male. He noticed no change in mood during this initial cycle.

With subsequent cycles, however, Mr. A became increasingly obsessed with his body image and used higher dosages. When the assault occurred, he was taking testosterone cypionate, 800 mg a week, nandrolone decanoate, 400 mg a week, and oxymetholone, 50 mg/d. With this regimen—the weekly equivalent of 1,550 mg of testosterone—Mr. A noticed prominent mood changes that met DSM-IV criteria for a manic episode. He experienced euphoria, dramatic irritability, limitless self-confidence, decreased need for sleep, distractibility, extreme recklessness (driving too fast, spending too freely), and some mildly paranoid ideation (without frank delusions). He admitted that he had twice assaulted his girlfriend and that he invariably became enraged at even the slightest annoyance when driving in traffic. He revealed that although the altercation with the older driver had led to his first arrest for ‘road rage,’ it was his third such incident.

The clinician warned Mr. A that continued steroid use could worsen his behavior—and lead to more serious trouble later on. Mr. A, however, said he was more afraid of losing muscle mass and becoming ‘small again.’ When the clinician mentioned that use of anabolic steroids without a prescription is illegal, Mr. A retorted that several of his friends had used the drugs without legal consequences.

Mr. A left the office showing no inclination to return for further treatment. The clinician could only offer to be available in the future.

Box

What medical sequelae await Mr. A if he continues to abuse steroids? How would you convince him to stay in treatment?

Dr. Carter’s and Pope’s observations

Mr. A’s path to mania has been well demonstrated in the literature. Hypomania or even frank manic syndromes, sometimes associated with violent behavior, are rare at weekly doses of 300 mg of testosterone equivalent. At weekly doses of >1,000 mg, psychiatric syndromes such as hypomania or mania may occur in almost one-half of cases.⁵

If he continues to abuse anabolic steroids, however, Mr. A could experience adverse physical reactions ranging from embarrassing acne and male-pattern baldness (Table 1) to rare and life-threatening hepatic effects such as cholestatic jaundice and peliosis hepatitis (blood-filled cysts in the liver).

Table 1

ANABOLIC STEROID ABUSE: COMMON PHYSICAL FINDINGS

The risk of atherosclerotic disease or prostate cancer later in life may also be greatly increased.

More common laboratory changes include:

• increased red blood cell count, hemoglobin and hematocrit
• elevated liver function readings (although these must not be confused with enzymes that originate from muscle tissue)
• and unfavorable changes in triglycerides, total cholesterol, and HDL:LDL cholesterol ratios (Table 2).

Other potential laboratory changes with steroid abuse include decreased luteinizing hormone and follicle-stimulating hormone due to feedback inhibition. Feedback inhibition will also reduce testosterone and estradiol levels with use of anabolic steroids other than testosterone esters. These levels, however, would both be elevated with use of testosterone esters alone.

In men, testicular atrophy and decreased sperm count are generally reversible manifestations of steroid abuse, whereas gynecomastia may be irreversible and require surgical intervention in advanced cases.^3,6 Women who use anabolic steroids (such as for body-building) are vulnerable to disrupted menstrual cycles, decreased breast size, and masculinizing effects including enlarged clitoris, hirsutism, and deepening of the voice.⁶

In adolescents, anabolic steroid use may cause premature closure of the epiphyses, leading to shortened stature.³

Unfortunately, warnings about these many adverse effects rarely deter anabolic steroid users such as Mr. A or persuade them to continue in treatment of any type. Most young anabolic steroid abusers report that they have never felt significant adverse effects from steroid use and know of no one who has experienced such effects. The dramatic muscle gains they have witnessed in themselves and in other users decisively outweigh what they perceive to be remote threats of adverse consequences.

Follow-up: Return to treatment

We didn’t hear from Mr. A until about 18 months later, when he unexpectedly requested a consultation.

Upon arrival, Mr. A exhibited major depression with prominent anhedonia, hypersomnia of 12 to 14 hours per night, loss of appetite, fatigue, prominent psychomotor retardation, feelings of guilt, difficulty concentrating, and suicidal thoughts (but without a frank plan). He also reported panic attacks that were randomly occurring each day, usually in public.

Mr. A conceded that he had experienced similar depressive episodes after stopping anabolic steroid use, but that they typically ran their course after 2 to 3 weeks. He said the present episode showed no sign of abating after nearly 2 months. He had attempted to ‘treat’ this episode by resuming anabolic steroid use, but he could not get an adequate supply from his dealer.

Mr. A’s total testosterone level, measured in the morning when it should be near its diurnal peak, was 127 ng/dl (normal range is 270 to 1,070 ng/dl). Physical examination revealed that his testicles had shrunk to the size of marbles (each approximately 5 mm in diameter). He was referred to an endocrinologist for evaluation and was simultaneously started on fluoxetine, 20 mg/d.

Table 2

LABORATORY ABNORMALITIES ASSOCIATED WITH ANABOLIC STEROID ABUSE

He returned 2 weeks later, exhibiting little improvement and wanting to resume steroids ‘because it was the only thing that really helped.’ Instead, he agreed to continue on fluoxetine and remain in follow-up. At 4 weeks, he noticed a decrease in panic attacks, return of normal mood, decreased anhedonia, and loss of suicidal ideation. He continued taking fluoxetine for another 3 months but then abruptly disappeared from treatment.

Mr. A resurfaced about 1 year later, revealing to the psychiatrist that he had taken yet another cycle of anabolic steroids, largely because he feared losing his muscle mass. His panic attacks had recurred almost immediately when he began tapering down from the peak of this cycle, and he agreed to resume taking fluoxetine.

A look at Mr. A’s extended history may provide clues to his persistent anabolic steroid abuse problem. He had displayed prominent symptoms of conduct disorder as a child. He had been truant from school, had occasionally run away from home, and had been involved in several misdemeanors. While in high school, he typically drank 10 to 12 beers over a weekend and had experimented with hallucinogenic mushrooms and 3,4-methylenedioxymethamphetamine (‘ecstasy’).

He started weightlifting while in high school and by age 17 was visiting the gym every day. He began college on a football scholarship but dropped out after 1 year. Starting in his early 20s, he competed in several bodybuilding contests.

Despite his impressive muscularity, Mr. A was anxious about his body appearance. He often would not take off his shirt—even when at the beach or a swimming pool—for fear that he would appear too small. He sometimes wore heavy sweatpants in the sweltering heat to conceal his legs. He also admitted spending as much as 2 hours a day examining himself in the mirror. ‘Sometimes when I get a bad (look at) myself, I will refuse to go out for the rest of the day,’ he said.

Mr. A has had a succession of girlfriends, but his rigid commitment to diet and exercise invariably ended these relationships.

At this point, would you first address Mr. A’s apparent substance use problem or the underlying body dysmorphic symptoms?

Dr. Carter’s and Pope’s observations

Two comorbidities noted here—substance abuse and body dysmorphic disorder—are common among anabolic steroid abusers. Addressing these problems, especially the body dysmorphic disorder, may sometimes help patients who are unwilling to address their steroid use directly. Body dysmorphic disorder may respond to selective serotonin reuptake inhibitors⁷ and cognitive-behavioral therapy.⁸

Anabolic steroids are not associated with immediate intoxicating effects, and ICD-10 categorizes them as substances not associated with dependence. After prolonged use at high doses, however, anabolic steroids are often associated with euphoria. Researchers also have found that some steroid abusers do meet DSM-IV criteria for substance dependence.⁶

Beyond the direct psychotropic effects of anabolic steroids, the depressive symptoms commonly seen during their withdrawal may perpetuate the dependence, as was the case with Mr. A. Most depressive symptoms that follow steroid cessation do not require drug therapy,³ but Mr. A developed severe and persistent depressive symptoms, complicated by panic disorder and body image concerns at a level diagnostic of body dysmorphic disorder. Such body image concerns often precipitate relapse into steroid use.

Conclusion: Another setback

As of this writing, Mr. A is again lost to follow-up. After taking fluoxetine and keeping monthly appointments for about 6 months, he failed to arrive for a visit and did not set another appointment. The patient may have once again stopped medication and embarked on yet another cycle of anabolic steroid use. If this is so, we can only hope that he returns to treatment before it is too late.

Related resources

• NIDA Research Report: Anabolic Steroid Abuse. http://www.nida.nih.gov/ResearchReports/Steroids/AnabolicSteroids.html
• Lukas SE. Steroids. Hillside, NJ: Enslow Publishers, 1994.

Drug brand names

• Fluoxetine • Prozac
• Nandrolone decanoate • Deca-Durabolin
• Oxymetholone • Anadrol
• Stanozolol • Winstrol

Disclosure

Dr. Carter reports that he receives research/grant support from or is a consultant to Eli Lilly and Co., Pfizer Inc., and Ortho-McNeil Pharmaceutical.

Dr. Pope reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.