Anabolic-Androgenic Steroids (AAS): Misuse and Psychiatric Aspects

1. What Are Anabolic-Androgenic Steroids?

• Anabolic - muscle-building
• Androgenic - masculinizing

2. Epidemiology and Patterns of Misuse

• AAS misuse occurs almost entirely in males, despite misconceptions that females commonly use them.
• Use is most widespread in Western cultures - Scandinavian countries show perhaps the highest prevalence, followed by the USA, British Commonwealth countries, and Brazil.
• AAS use is rare in East Asian countries (China, Korea, Japan), likely because masculinity in Confucian tradition is defined by intellect and character rather than physical size.
• A key misconception: the majority of AAS users are NOT competitive athletes. Most are ordinary men lifting weights for personal appearance, not sport.
• AAS are listed under Schedule III controlled substances in the USA (Steroid Trafficking Act, 1991).
• In DSM-5, AAS do not have their own diagnostic category - they are coded as "other or unknown substance-related disorders." ICD-10 classifies them under "Abuse of non-dependence-producing substances."

Doses Used in Misuse

"Cycling" Pattern

3. Risk Factors for AAS Misuse

1. Conduct disorder - Men reporting adolescent conduct disorder were significantly more likely to subsequently develop AAS use.
2. Body image concerns / Muscle dysmorphia - A strong association exists between muscle dysmorphia (a form of body dysmorphic disorder characterized by preoccupations that one is not muscular enough) and AAS use. Paradoxically, muscle dysmorphia may worsen after initiating AAS use, as the individual becomes more embedded in the AAS-using culture.

4. Neurobiological Mechanisms Underlying Psychiatric Effects

• Target sites: limbic system (amygdala, hippocampus, nucleus accumbens), hypothalamus, and cerebral cortex (androgen receptors expressed here)
• Neurotransmitter effects:
  • AAS-induced increases in vasopressin, substance P, and glutamate - associated with aggressive behavior
  • AAS-induced decreases in brain serotonin and 5-HIAA - associated with aggression
  • Forebrain GABAergic mechanisms involved in AAS-induced aggression and anxiety
  • AAS exert reinforcing effects through GABA, opioid, and dopamine systems
• In human CSF studies, men treated with methyltestosterone showed significantly higher 5-HIAA levels vs. placebo, correlating with AAS-associated effects (increased energy, diminished sleep, sexual arousal)
• The hypothalamic-pituitary-testicular (HPT) axis is suppressed via feedback inhibition during exogenous AAS use, causing hypogonadism upon cessation

5. Psychiatric Disorders Associated with AAS Misuse

A. AAS Dependence

• Tolerance (progressively higher doses needed)
• Withdrawal symptoms on cessation
• Prolonged use and difficulty discontinuing (often fear of losing muscle mass)
• Spending large amounts of time in AAS-related activities (weightlifting, special diets, associating with other AAS users)
• Continued use despite adverse effects (gynecomastia, sexual dysfunction, cardiovascular toxicity)
• Craving and inability to cut down

• Some users experience euphoria, feelings of power, and aggressiveness with AAS use, which reinforces continued use
• The reinforcing effects operate via GABA, opioid, and dopamine systems - similar to classical drugs of abuse

B. AAS-Induced Mood Disorders

Dose-Response Relationship (critical to understand):

Hypomanic / Manic Episodes:

• 2-15% of AAS abusers experience hypomanic or manic episodes
• Features include: irritability, aggressiveness, euphoria, decreased need for sleep, racing thoughts, grandiosity, impulsive spending
• "Roid rage" - episodes of uncharacteristic violent behavior - is a recognized (though variable) phenomenon
• One study found 1.3% developed frank mania and 7.8% developed hypomania at ~500 mg/week doses

Depressive Syndromes:

• A brief, self-limited depression occurs upon AAS withdrawal, caused by suppression of the HPT axis
• This depression drives many users to resume AAS to alleviate the withdrawal state - a key maintaining factor of dependence
• Some develop major depression during withdrawal requiring antidepressant medication or even ECT
• Suicide is a recognized risk during AAS-induced depressive episodes

Symptom Summary Table (from Kaplan & Sadock's Synopsis):

C. AAS-Induced Psychotic Disorder

• Psychotic symptoms are rare but have been reported
• Primarily occur in those using > 1,000 mg testosterone equivalent/week
• Typically: grandiose or paranoid delusions, usually in the context of a manic episode; occasionally without frank mania
• In most reported cases, psychotic symptoms resolved promptly (within weeks) after stopping AAS
• Temporary antipsychotic treatment was sometimes required
• The mechanism is similar to the idiosyncratic psychotic reactions seen with corticosteroids (same chemical family)

D. AAS-Related Disorder NOS

• Panic disorder and social phobia symptoms can occur during AAS use or worsen during withdrawal
• Some individuals paradoxically report decreased anxiety during AAS use

• AAS use may serve as a gateway to opioid misuse - users begin using opioids (nalbuphine, oxycodone, heroin) to treat muscle aches from heavy training
• Concurrent alcohol, cocaine, and cannabis misuse is common in noncompetitive AAS users
• In one study of 223 men admitted to an addiction unit, 29 had past AAS use - but this was documented in physicians' notes in only 4 cases, illustrating the underdetection of AAS use in clinical settings

6. Withdrawal Syndrome

• Depression (most common - can be severe)
• Anxiety
• Fatigue
• Decreased libido and erectile dysfunction (due to HPT axis suppression causing hypogonadism)
• Craving and relapse pressure
• Body image distress - dissatisfaction with their physical state

7. Clinical Case Example (from Kaplan & Sadock)

Mr. A, a 26-year-old man, began lifting weights at age 17. At age 19, he started AAS cycles - first using methandienone 30 mg/day orally + testosterone cypionate 600 mg/week IM for 9 weeks, gaining 20 lb. Over 6 years, he completed 6 cycles. During his most ambitious cycle (testosterone cypionate 600 mg/wk + nandrolone decanoate 400 mg/wk + stanozolol + oxandrolone), he experienced euphoria, felt "invincible," had decreased need for sleep, racing thoughts, spent $2,700 impulsively, and became uncharacteristically irritable - ultimately punching through a car window during an argument. After the cycle ended, he became mildly depressed for 2 months. He also developed concurrent opioid misuse (nalbuphine IV) and classic features of muscle dysmorphia - checking his appearance compulsively, refusing to go to the beach despite having a 48-inch chest and 19-inch biceps.

8. Assessment Considerations

• Clinicians must actively ask about AAS use - in one study, 56% of AAS users had never disclosed use to any physician; 40% would trust a drug dealer's information over a physician's
• AAS use is frequently undetected on clinical assessment (documented in fewer than 14% of admitted patients with known AAS history in one study)
• Urine toxicology screens do not routinely test for AAS
• Always screen for concurrent substance use (opioids, alcohol, cocaine)
• Assess for muscle dysmorphia and body dysmorphic disorder
• Evaluate HPT axis function in those discontinuing

9. Treatment

Key Takeaways

1. AAS misuse is primarily driven by body image goals, not athletic performance
2. ~32.5% of AAS users develop formal dependence
3. Psychiatric effects are dose-dependent - risk rises sharply above 1,000 mg/week
4. Major risks: mania/"roid rage," depression/suicide on withdrawal, opioid gateway, psychosis at high doses
5. AAS use is severely underdetected in clinical settings - ask directly
6. Withdrawal hypogonadism drives relapse and requires active endocrine management