Marijuana use disorder and psychosis often appear together in research articles and publications, but is there a difference between marijuana use disorder and psychosis? The relationship between cannabis use disorder and primary psychosis is complex, since the marijuana plant is composed of over 500 chemical substances, and only a small percentage of those chemicals have been studied, according to research published by the Alcohol and Drug Abuse Institute at the University of Washington. Cannabis use disorder has psychotomimetic effects, meaning that the effects mimic symptoms of psychosis. There is extensive evidence connecting marijuana intoxication to psychotomimetic effects such as paranoia, disorganized thinking, delusions, auditory and visual hallucinations, memory loss, and cognitive impairment.
Dr. Ruby S. Grewal and Dr. Tony George (2017) made a distinction between cannabis-induced psychosis (CIP) and primary psychosis. The eight distinguishing features of each are described as follows:
According to the 2017 National Survey on Drug Use and Health:
• Marijuana is the most widely used drug, followed by psychotherapeutic drugs (which include prescription opioids, sedatives, tranquilizers and stimulants), cocaine, hallucinogens, etc.
• Young adults (ages 18-25) reported the highest rate of marijuana use from 2015 to 2017
• Marijuana use among young women significantly increased from 2.8 million in 2015 to 3.3 million in 2017, compared to men (4.1 million in 2015 to 4.3 million in 2017)
• The rate of marijuana use disorder is highest among adults aged 18-25
• Marijuana use during pregnancy has been linked with fetal growth restriction, stillbirth, and premature birth, problems with neurological development leading to poor cognitive function and hyperactivity
• Among youth, marijuana use has resulted in poor academic performance, increased drop-out rates, and increased risks for psychotic disorders in adulthood
• For youth who are at risk for developing schizophrenia, marijuana use is linked with earlier onset
Primary psychosis: Marijuana’s main active ingredient, delta-9-tetrahydrocannabinol (THC), is sometimes present in the toxicology screening.
CIP: Positive drug test results indicate a clear timeline. The time of last drug use will indicate if psychotic symptoms are closely connected to cannabis intoxication or withdrawal effects. CIP symptoms include sudden onset of severe mood swings and paranoia as soon as 24 hours after use or within one week of use. A sudden increase in THC content usually precedes CIP.
Frequency of Use
Primary psychosis: If an individual has not consumed cannabis or experienced cannabis withdrawal symptoms for at least four weeks at the time of diagnosis but exhibits symptoms of psychosis, a diagnosis of primary psychosis is warranted. An individual may also display symptoms of psychosis prior to heavy cannabis use.
CIP: Heavy cannabis use within the past month precedes the onset of CIP.
Appearance of Symptoms
Primary psychosis: Symptoms appear prior to heavy substance use.
CIP: Symptoms appear only during heavy substance use or sudden increase in potency. Historically, CIP has been associated with fewer negative symptoms than schizophrenia; distinguishing between the two may be very difficult without a timeline of use, as both disorders share overlapping characteristics. Compared to primary psychosis, CIP has relatively more mood symptoms.
Duration of Symptoms
Primary psychosis: Symptoms persist even if the individual abstains from drug use.
CIP: Symptoms diminish or disappear after a period of abstinence from drug use. When assessing for CIP, it’s important to note the time of last drug use if psychotic symptoms resemble cannabis intoxication or cannabis withdrawal effects.
Primary psychosis: Antipsychotics improve symptoms.
CIP: Antipsychotics may or may not improve symptoms.
Primary psychosis: Individuals may experience delusions, hallucinations and cognitive impairment.
CIP: Acute cannabis intoxication is associated with a range of transient positive symptoms, mood symptoms and cognitive defects. Symptoms that persist beyond intoxication and withdrawal are categorized as CIP regardless of how cannabis is ingested (e.g., smoking, intravenous or oral).
Degree of Insight
Primary psychosis: The individual may lack awareness about symptoms of psychosis.
CIP: The individual may be aware of symptoms associated with cannabis use. Awareness of the clinical condition and the individual’s ability to identify symptoms as a manifestation of a disorder is one of the most distinguishing characteristics of CIP.
Primary psychosis: An individual with primary psychosis would present symptoms of disorganized thought and incoherent speech.
CIP: The individual’s thought process is more organized and sequential.
A number of psychosocial factors across multiple domains may put an individual at risk for cannabis use disorder, particularly personality traits, family, peer, work, neighborhood and habit of drug use (Brook, Lee, Finch, Koppel & Brook, 2011; Hayatbakhsh, Najman, Bor, O’Callaghan & Williams, 2009). Risk factors are described as follows:
• Personality traits: impulsivity and aggression, sensation-seeking, lack of planning, neuroticism
• Motivation: Desire to get high (anticipation of perceived positive effect of cannabis use)
• Gender: Male
• Family factor: Poor relationship with parents; poor marital relationships
• Peers: Friends and influential social circles
• Age: Underdeveloped brain is related to reduced ability to make decisions
• Drug habit/comorbidity: Current or prior tobacco and/or alcohol use
• Mental health: Clinical and subclinical symptoms of anxiety and depression
• Childhood sexual abuse
• Changes in mother’s marital status
• Maternal smoking
• Poor academic performance
An individual is diagnosed with cannabis use disorder (CUD) if he or she exhibits compulsive behaviors and persists in a pattern of repetitive use despite harmful consequences that severely impair one’s ability to function in school, at work or home. Symptoms may include physiological dependence on cannabis, such as tolerance or withdrawal symptoms, and recurrent use may result in health conditions and disabilities. The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V) lists 11 criteria for substance use disorders (SUD) which are used by practitioners to assess their patients’ use of cannabis within the past year. The criteria are as follows:
1. Use of cannabis was longer or more than intended
2. Multiple attempts to stop or reduce use have failed
3. Excessive time was spent on cannabis use or recovering from the effects of intoxication
4. Psychological preoccupation with cannabis use
5. Consumption or recovering from cannabis intoxication often interfered with responsibilities
6. Persistent use of cannabis despite interpersonal problems with loved ones
7. Social reclusion or reduced hobby activities due to cannabis use
8. Increased risky behaviors as a result of cannabis use (e.g., driving while intoxicated)
9. Continued and persistent use despite onset of anxiety, depression or other mental disorders
10. The need to use increasing amounts to get the same effect as initial use
11. Presence of withdrawal symptoms upon cessation of use
The number of criteria met by the individual would indicate the level of severity as noted below:
– Mild – two or three criteria
– Moderate – Four or five criteria
– Severe – Six or more
Symptoms of cannabis intoxication may include the following (Miller, Oberbarnschiedt & Gold, 2017):
– Euphoric high associated with inappropriate laughter
– Red eyes
– Chronic cough
– Cannabis odor on clothing
– Yellow fingers (from smoking joints)
– Increased appetite and craving for certain foods (e.g., “munchies”)
– Short-term memory loss
– Delusions of grandeur
– Inability to focus
Cannabis withdrawal symptoms start to appear within a week after heavy use:
– Hostile moods and behavior
– Anxiety and nervousness
– Sleep disturbance
– Loss in appetite or weight
– Depressive mood symptoms
– Abdominal pain
– Shaking, chills and headache
Although many people turn to marijuana to alleviate symptoms of anxiety and depression, long-term use of marijuana does the opposite: it worsens anxiety and other mood disorders over time, according to an article published in The New England Journal of Medicine. The article reviews 12 longitudinal studies of 11,959 patients diagnosed with post-traumatic stress disorder, panic disorder, bipolar disorder or major depression. The level of cannabis use ranged from one-time use to cannabis use disorder within six (6) months prior to the study. Findings suggest that higher rates of marijuana use are associated with anxiety and mood disorders.
Poor academic performance and quality of work can be attributed to apathy and lack of motivation associated with marijuana use. Amotivational syndrome, an effect of cannabis use, reduces self-efficacy by lowering one’s desire to take initiative and follow through to task completion. Compared to alcohol and tobacco, marijuana is the only substance associated with drastic changes in initiative and persistence, according to findings published in Prevention Science.
Physical effects of marijuana use depend on the method of use. Most people smoke marijuana using paper-wrapped joints, blunts, pipes and bongs, and it can be inhaled through vaping. Other marijuana products include brownies, baked goods, candy and other cannabis edibles. Smoking marijuana can damage the cell linings of the lungs, leading to respiratory problems, chronic bronchitis and chronic obstructive pulmonary disease (COPD). Regarding the causal effect between cannabis use and lung cancer, there is limited research and the results are mixed. Tobacco smoke is known to cause lung cancer, and marijuana smoke contains many of the same toxins as tobacco smoke, such as benzo(a)pyrene, phenols, nitrosamines, vinyl chlorides, reactive oxygen species, and benz(a)pyrene. Marijuana smokers tend to inhale more deeply than tobacco smokers, increasing lung exposure to toxins. Research literature on the cardiac effects of cannabis is limited, but current literature shows an association between cannabis use and ventricular tachycardia, a heart condition characterized by more than 100 heartbeats per minute.
In response to the rising rates of cannabis use and cannabis use disorder in the United States, clinical trials for the treatment of cannabis use disorder have increased, with an emphasis on psychotherapy treatments such as cognitive-behavioral therapy, motivational enhancement therapy and contingency management. A combination of these three modalities is recommended to produce the best treatment outcomes. As an adjunctive intervention to psychosocial treatment, pharmacotherapy has emerged and shown some promise, although the extent to which pharmacological interventions are effective is still unclear at this point (Sherman & McRae-Clark, 2016).
1 Brook, J. S., Lee, J. Y., Finch, S. J., Koppel, J., & Brook, D. W. (2011). Psychosocial factors related to cannabis use disorders. Substance abuse, 32(4), 242–251. doi:10.1080/08897077.2011.605696. Retrieved from https://www.ncbi.nlm.nih.gov/
2 Grewal, R. & George, T. (2017). 8 Distinguishing features of primary psychosis versus cannabis-induced psychosis. Psychiatric Times. Retrieved from https://www.psychiatrictimes.com/
3 Hayatbakhsh MR, Najman JM, Bor W, O’Callaghan MJ & Williams GM. (2009). Multiple risk factor model predicting cannabis use and use disorders: a longitudinal study. The American Journal of Drug and Alcohol Abuse, 35(6): 399-407. doi: 10.3109/00952990903353415.
4 Lee-Winn, A. E., Mendelson, T., & Johnson, R. M. (2018). Associations of personality traits with marijuana use in a nationally representative sample of adolescents in the United States. Addictive behaviors reports, 8, 51–55. doi:10.1016/j.abrep.2018.06.005
5 Miller NS, Oberbarnscheidt T, Gold MS. (2017). Marijuana Addictive Disorders: DSM-5 Substance-Related Disorders. Journal of Addiction Research and Therapy, doi:10.4172/2155-6105.1000S11-013
6 Sherman, B. J., & McRae-Clark, A. L. (2016). Treatment of Cannabis Use Disorder: Current Science and Future Outlook. Pharmacotherapy, 36(5), 511–535. doi:10.1002/phar.1747