Day # 167: Marijuana & Other Cannabis Use Disorder
- Marcus Hunt
- 4 hours ago
- 6 min read
Today we will discuss cannabis use disorder (CUD). In this post, we’ll cover the history, neurobiology, epidemiology, clinical presentation, and evidence-based treatment strategies.
Today's Content Level: Intermediate to Advanced
History and Formulations
Cannabis has been used for thousands of years for medicine, textiles, and rituals.
Cannabis is the whole plant containing hundreds of compounds, including cannabinoids, which are the chemicals that act on the endocannabinoid system.
THC (Δ⁹-tetrahydrocannabinol) is the key psychoactive component and drives intoxication.
CBD (cannabidiol) is non-intoxicating and may have anxiolytic, anticonvulsant, and anti-inflammatory effects.
Cannabis goes by many names including weed, marijuana, pot, bud, ganja, hash, and THC.
Common formulations include smoked flower, vaped THC oils (“carts”), high-potency concentrates (wax, shatter, dabs), and edibles (gummies, brownies).
Cannabis remains illegal on a federal level (at this writing in 2025), although many states have legalized cannabis for recreational and medical use.
Modern cannabis is far more potent than in the past, with high-THC flower, concentrates, vapes, and edibles contributing to increased rates of cannabis use disorder. THC potency has risen dramatically over time. Cannabis flower in the 1960s–70s contained ~1–3% THC, by the 1990s it was 4–6%, and today many strains reach 15–25%, with concentrates up to 60–90%.
Synthetic cannabinoids (K2, Spice, Scooby Snacks, Black Mamba) are not natural cannabis and have far more dangerous, unpredictable effects.
Mechanism of Action
THC acts as a partial agonist at CB1 (central) and CB2 (peripheral) receptors within the endocannabinoid system → inhibits adenylate cyclase → ↓ cAMP → reduced neuronal excitability → alters neurotransmitter release → impacts reward pathways (notably dopamine).
Chronic use leads to downregulation and desensitization of CB1 receptors → tolerance and withdrawal. Receptor levels typically rebound toward baseline within 2–4 weeks of abstinence, though recovery may be slower in heavy daily users.
Medical uses
Medically, cannabis has shown some efficacy in treating chronic pain, chemotherapy-induced nausea, spasticity in multiple sclerosis, appetite stimulation in certain conditions, and decreased intraocular pressure in glaucoma.
Cannabis itself has no strong evidence-based role in treating primary psychiatric disorders and is more often linked to worsened depression, anxiety, PTSD symptoms, bipolar instability, and psychosis. However, individual cannabinoids have a few narrow, adjunctive uses: CBD (non-intoxicating) shows modest benefit for performance anxiety and may help with PTSD-related nightmares in some small studies, while nabilone, a synthetic cannabinoid, can reduce nightmares in select cases. These are not first-line treatments, and THC-containing products typically exacerbate psychiatric symptoms rather than improve them.
Diagnostic Criteria 4
Diagnostic criteria for all substance use disorders are the same, characterized by a ≥ 12-month period of problematic substance use that leads to impairment or distress and requires ≥2 additional criteria. See Day #160: Introduction to Substance Use Disorders for complete diagnostic criteria and severity specifiers.
Genetics, environmental influences, and mental health comorbidities contribute to vulnerability.
Prevalence: One of the most commonly used drugs worldwide. Millions meet criteria for CUD.
Age / Gender: Highest use in late teens to late 20s. Men > women in both use and CUD diagnoses.
Genetics/Biology: Variations in endocannabinoid signaling, dopamine pathways, and family history increase risk.
Certain genetic variants (polymorphisms), including variations in COMT (which influences dopamine regulation), AKT1 (involved in glucose metabolism), and CNR1 (cannabinoid receptor gene), can increase susceptibility to cannabis-related psychosis. Daily use in carriers may raise relative risk 2–10× above baseline, particularly in adolescents or with high-potency cannabis.
Other risk factors: Availability, social acceptance, early exposure, trauma, peer use, lower education, lower income, other SUD, comorbid psychiatric disorders, younger age at first use increases rate of progression to frequent use.
Psychiatric Comorbidity: Mood disorders, anxiety disorders, PTSD, psychotic disorders, personality disorders (e.g., borderline, antisocial).
Substance Comorbidity: Alcohol, nicotine, stimulants.
High-potency use (concentrates/dabs) and synthetic cannabinoids are associated with higher dependence risk and increased psychosis risk (& aggression, seizures) in vulnerable individuals.
History
General SUD: Obtain a detailed history (onset, frequency, quantity, last use, forms and routes), prior treatment attempts, periods of sobriety, withdrawal symptoms, impact on daily functioning, social history with triggers, legal obligations, and co-occurring psychiatric or medical conditions. Ask DSM-5 symptoms of SUD (loss of control, craving, risky use, tolerance, withdrawal, impairment). Ask about prescription misuse and illicit use. Ask about injection drug use, overdose history, co-use of other substances. Assess for other safety concerns related to use, including IV/IN use, sharing paraphernalia, needle licking, exchanging sex for drugs, body packing/stuffing, or impaired driving.
Cannabis specific
Route (smoked/vaped/edible) and potency (% THC).
Be aware that many “gas station” or “mushroom” gummies actually contain synthetic cannabinoids or potent THC analogs rather than psilocybin (despite “mushroom” branding), with highly unpredictable and unregulated potency.
Goals of use: Relaxation? Sleep? Anxiety? Recreation? Coping?
Chronic use may cause respiratory problems (e.g., asthma, chronic bronchitis), suppression of the immune system, *cancer, and possible effects on reproductive hormones.
*Heavy, long-term cannabis use has the most consistent association with testicular germ cell tumors, while links to other cancers remain unproven or inconsistent.
Pay special attention to:
Anxiety/panic
Perceptual disturbances
Paranoia or acute psychosis
Cyclic vomiting → Cannabinoid Hyperemesis Syndrome (CHS)
Labs / Diagnostics
Urine tox: Good for confirming recent(ish) use but does NOT indicate level of intoxication. THC metabolites can remain positive for days to weeks. UDS + for ~10 days after weekly use and up to ~3-4 weeks after daily use.
Standard drug screens do not detect synthetic cannabinoids, and although specialty send-out labs exist, they detect only a limited subset of older compounds. Many newer variants will still test negative.
Additional labs only if clinically indicated: electrolytes, glucose, CBC, CMP if severe intoxication, hyperemesis, or altered mental status.
Intoxication 9
Psychological Symptoms:
Euphoria
Relaxation
Time dilation (sensation of slowed time)
Heightened sensory perception (e.g., enhanced colors, sound appreciation, taste, smell).
Impaired short-term memory
Physical Symptoms
Tachycardia (generally mild)
Orthostatic hypotension
Ataxia & impaired coordination
Increased appetite
Dry mouth
Conjunctival injection (red eyes)
Severe presentations
Anxiety, panic attacks, paranoia
Delirium
Perceptual distortion/rare hallucinations
Acute psychosis in susceptible individuals
CHS (in chronic/high-potency users)
Treatment of Intoxication
Supportive care (most important): quiet room, reassurance, hydration
Benzodiazepines for severe anxiety/agitation.
Antipsychotics only if refractory psychosis is present (avoid overdiagnosing as intoxication often resolves with time).
Benzodiazepines are preferred for synthetic drug-induced psychosis or agitation due to less risk of medical complications (e.g., siezures, arrhythmia, hyperthermia).
Rule out metabolic, infectious, or toxic mimics in severe cases.
For CHS: hot showers (temporary relief) + cessation (only cure).
Withdrawal 10
Remember that withdrawal symptoms of a drug are usually opposite of its intoxication effects. For example, cannabis can cause relaxation and euphoria, but withdrawal can → post-intoxication anxiety or insomnia.
Symptoms:
Irritability
Anxiety & restlessness
Insomnia or vivid dreams
Depressed mood
Decreased appetite
Abdominal pain, nausea
Headaches, sweating, tremor
Starts around 24-48 hours after cessation, usually peaks within 2-6 days with mild/moderate use, lasts ~2-3 weeks with chronic/heavy use.
Treatment:
Supportive treatment: Hydration, provide reassurance (normalize symptoms and set expectations), sleep hygiene, exercise.
Symptomatic meds (none FDA-approved):
For severe withdrawal, can use dronabinol (synthetic Δ⁹-THC), gabapentin, and other symptomatic support.
Short-term trazodone or hydroxyzine for sleep/anxiety
NSAIDs for headaches
Antiemetics for nausea
•Effective treatment requires a combination of medical, psychological, and social interventions. A multi-disciplinary team—often including psychiatrists, primary care providers, therapists, social workers, and peer support specialists collaborates to address all aspects of the disorder.
Determine the Appropriate Treatment Setting: Choosing the right level of care depends on substance use severity, comorbid conditions, and prior treatment history. See Day 60: Intro to SUD for a description of each level of care.
Psychosocial Interventions:
Individual and/or group therapy should be part of every SUD treatment approach. See Day 60: Intro to SUD for a discussion of interventions that include behavioral therapies, peer support & 12-step programs, and family support resources.
Medications:
There is no approved medication for cannabis use disorder, but some evidence suggests benefit in specific situations.
Address psychiatric comorbidities, especially psychotic and mood disorders. Antidepressants treat comorbid depression/anxiety, but do not reduce cannabis use directly.
Gabapentin: may reduce withdrawal symptoms/craving in adults.
N-acetylcysteine (NAC): shows some promise, more/better data in adolescents.
Cannabinoid agonists (dronabinol, nabilone): can mitigate withdrawal and improve retention, but evidence for abstinence is mixed and clinical use is limited.
Conclusion
“Just weed” can cause dependence, withdrawal, and functional impairment.
Potency matters! Today’s cannabis has much higher THC levels.
Daily users often underestimate their withdrawal symptoms → relapse risk.
Cannabis can precipitate psychosis in vulnerable individuals; always screen for family history.
Don’t miss Cannabinoid Hyperemesis Syndrome.
Treatment is behavioral first; medications are adjunctive.
Always treat co-occurring disorders: improving anxiety, depression, or insomnia often reduces use.
Resources for today's post include:
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