top of page

Can Marijuana Cause Psychosis?


Several studies have linked marijuana use to increased risk for psychiatric disorders, including psychosis (schizophrenia), depression, anxiety, and substance use disorders, but whether and to what extent it actually causes these conditions is not always easy to determine.32 Recent research suggests that smoking high-potency marijuana every day could increase the chances of developing psychosis by nearly five times compared to people who have never used marijuana.113 The amount of drug used, the age at first use, and genetic vulnerability have all been shown to influence this relationship. The strongest evidence to date concerns links between marijuana use and psychiatric disorders in those with a preexisting genetic or other vulnerability.61


Research using longitudinal data from the National Epidemiological Survey on Alcohol and Related Conditions examined associations between marijuana use, mood and anxiety disorders, and substance use disorders. After adjusting for various confounding factors, no association between marijuana use and mood and anxiety disorders was found. The only significant associations were increased risk of alcohol use disorders, nicotine dependence, marijuana use disorder, and other drug use disorders.62

Recent research (see "AKT1 Gene Variations and Psychosis") has found that people who use marijuana and carry a specific variant of the AKT1 gene, which codes for an enzyme that affects dopamine signaling in the striatum, are at increased risk of developing psychosis. The striatum is an area of the brain that becomes activated and flooded with dopamine when certain stimuli are present. One study found that the risk of psychosis among those with this variant was seven times higher for those who used marijuana daily compared with those who used it infrequently or used none at all.63


Whether adolescent marijuana use can contribute to developing psychosis later in adulthood appears to depend on whether a person already has a genetically based vulnerability to the disorder. The AKT1 gene governs an enzyme that affects brain signaling involving the neurotransmitter dopamine. Altered dopamine signaling is known to be involved in schizophrenia. AKT1 can take one of three forms in a specific region of the gene implicated in susceptibility to schizophrenia: T/T, C/T, and C/C. Those who use marijuana daily (green bars) with the C/C variant have a seven times higher risk of developing psychosis than those who use it infrequently or use none at all. The risk for psychosis among those with the T/T variant was unaffected by whether they used marijuana.

Another study found an increased risk of psychosis among adults who had used marijuana in adolescence and also carried a specific variant of the gene for catechol-O-methyltransferase (COMT), an enzyme that degrades neurotransmitters such as dopamine and norepinephrine64 (see "Genetic Variations in COMT Influences the Harmful Effects of Abused Drugs"). Marijuana use has also been shown to worsen the course of illness in patients who already have schizophrenia. As mentioned previously, marijuana can produce an acute psychotic reaction in non-schizophrenic people who use marijuana, especially at high doses, although this fades as the drug wears off.

The influence of adolescent marijuana use on adult psychosis is affected by genetic variables. This figure shows that variations in a gene can affect the likelihood of developing psychosis in adulthood following exposure to cannabis in adolescence. The COMT gene governs an enzyme that breaks down dopamine, a brain chemical involved in schizophrenia. It comes in two forms: "Met" and "Val." Individuals with one or two copies of the Val variant have a higher risk of developing schizophrenic-type disorders if they used cannabis during adolescence (dark bars). Those with only the Met variant were unaffected by cannabis use.

Inconsistent and modest associations have been reported between marijuana use and suicidal thoughts and attempted suicide among teens.65,66 Marijuana has also been associated with an amotivational syndrome, defined as a diminished or absent drive to engage in typically rewarding activities. Because of the role of the endocannabinoid system in regulating mood and reward, it has been hypothesized that brain changes resulting from early use of marijuana may underlie these associations, but more research is needed to verify that such links exist and better understand them.


Adverse Consequences of Marijuana Use:


Acute (present during intoxication)

  • Impaired short-term memory

  • Impaired attention, judgment, and other cognitive functions

  • Impaired coordination and balance

  • Increased heart rate

  • Anxiety, paranoia

  • Psychosis (uncommon)

Persistent (lasting longer than intoxication, but may not be permanent)

  • Impaired learning and coordination

  • Sleep problems

Long-term (cumulative effects of repeated use)

  • Potential for marijuana addiction

  • Impairments in learning and memory with potential loss of IQ*

  • Increased risk of chronic cough, bronchitis

  • Increased risk of other drug and alcohol use disorders

  • Increased risk of schizophrenia in people with genetic vulnerability**

*Loss of IQ among individuals with persistent marijuana use disorder who began using heavily during adolescence

**These are often reported co-occurring symptoms/disorders with chronic marijuana use. However, research has not yet determined whether marijuana is causal or just associated with these mental problems.


Like tobacco smoke, marijuana smoke is an irritant to the throat and lungs and can cause a heavy cough during use. It also contains levels of volatile chemicals and tar that are similar to tobacco smoke, raising concerns about risk for cancer and lung disease.67

Marijuana smoking is associated with large airway inflammation, increased airway resistance, and lung hyperinflation, and those who smoke marijuana regularly report more symptoms of chronic bronchitis than those who do not smoke.67,68 One study found that people who frequently smoke marijuana had more outpatient medical visits for respiratory problems than those who do not smoke.69 Some case studies have suggested that, because of THC’s immune-suppressing effects, smoking marijuana might increase susceptibility to lung infections, such as pneumonia, in people with immune deficiencies; however, a large AIDS cohort study did not confirm such an association.67 Smoking marijuana may also reduce the respiratory system’s immune response, increasing the likelihood of the person acquiring respiratory infections, including pneumonia.68 Animal and human studies have not found that marijuana increases risk for emphysema.67

Reports of Deaths Related to Vaping Marijuana The Food and Drug Administration has alerted the public to hundreds of reports of serious lung illnesses associated with vaping, including several deaths. They are working with the Centers for Disease Control and Prevention (CDC) to investigate the cause of these illnesses. Many of the suspect products tested by the states or federal health officials have been identified as vaping products containing THC, the main psychotropic ingredient in marijuana. Some of the patients reported a mixture of THC and nicotine; and some reported vaping nicotine alone. No one substance has been identified in all of the samples tested, and it is unclear if the illnesses are related to one single compound. Until more details are known, FDA officials have warned people not to use any vaping products bought on the street, and they warn against modifying any products purchased in stores. They are also asking people and health professionals to report any adverse effects. The CDC has posted an information page for consumers.

Whether smoking marijuana causes lung cancer, as cigarette smoking does, remains an open question.67,70 Marijuana smoke contains carcinogenic combustion products, including about 50% more benzoprene and 75% more benzanthracene (and more phenols, vinyl chlorides, nitrosamines, reactive oxygen species) than cigarette smoke.67 Because of how it is typically smoked (deeper inhale, held for longer), marijuana smoking leads to four times the deposition of tar compared to cigarette smoking.71 However, while a few small, uncontrolled studies have suggested that heavy, regular marijuana smoking could increase risk for respiratory cancers, well-designed population studies have failed to find an increased risk of lung cancer associated with marijuana use.67

One complexity in comparing the lung-health risks of marijuana and tobacco concerns the very different ways the two substances are used. While people who smoke marijuana often inhale more deeply and hold the smoke in their lungs for a longer duration than is typical with cigarettes, marijuana’s effects last longer, so people who use marijuana may smoke less frequently than those who smoke cigarettes.

Additionally, the fact that many people use both marijuana and tobacco makes determining marijuana’s precise contribution to lung cancer risk, if any, difficult to establish. Cell culture and animal studies have also suggested THC and CBD may have antitumor effects, and this has been proposed as one reason why stronger expected associations are not seen between marijuana use and lung cancer, but more research is needed on this question.67

Within a few minutes after inhaling marijuana smoke, a person’s heart rate speeds up, the breathing passages relax and become enlarged, and blood vessels in the eyes expand, making the eyes look bloodshot. The heart rate—normally 70 to 80 beats per minute—may increase by 20 to 50 beats per minute or may even double in some cases. Taking other drugs with marijuana can amplify this effect.

Limited evidence suggests that a person’s risk of heart attack during the first hour after smoking marijuana is nearly five times his or her usual risk.72 This observation could be partly explained by marijuana raising blood pressure (in some cases) and heart rate and reducing the blood’s capacity to carry oxygen.73 Marijuana may also cause orthostatic hypotension (head rush or dizziness on standing up), possibly raising danger from fainting and falls. Tolerance to some cardiovascular effects often develops with repeated exposure.74 These health effects need to be examined more closely, particularly given the increasing use of "medical marijuana" by people with health issues and older adults who may have increased baseline vulnerability due to age-related cardiovascular risk factors (see "Is marijuana safe and effective as medicine?").

A few studies have shown a clear link between marijuana use in adolescence and increased risk for an aggressive form of testicular cancer (nonseminomatous testicular germ cell tumor) that predominantly strikes young adult males.75,76 The early onset of testicular cancers compared to lung and most other cancers indicates that, whatever the nature of marijuana’s contribution, it may accumulate over just a few years of use.

Studies have shown that in rare cases, chronic use of marijuana can lead to Cannabinoid Hyperemesis Syndrome—a condition marked by recurrent bouts of severe nausea, vomiting, and dehydration. This syndrome has been found to occur in persons under 50 years of age and with a long history of marijuana use. Cannabinoid Hyperemesis Syndrome can lead sufferers to make frequent trips to the emergency room, but may be resolved when a person stops using marijuana.77


The potential medicinal properties of marijuana and its components have been the subject of research and heated debate for decades. THC itself has proven medical benefits in particular formulations. The U.S. Food and Drug Administration (FDA) has approved THC-based medications, dronabinol (Marinol®) and nabilone (Cesamet®), prescribed in pill form for the treatment of nausea in patients undergoing cancer chemotherapy and to stimulate appetite in patients with wasting syndrome due to AIDS.

In addition, several other marijuana-based medications have been approved or are undergoing clinical trials. Nabiximols (Sativex®), a mouth spray that is currently available in the United Kingdom, Canada, and several European countries for treating the spasticity and neuropathic pain that may accompany multiple sclerosis, combines THC with another chemical found in marijuana called cannabidiol (CBD).

The FDA also approved a CBD-based liquid medication called Epidiolex® for the treatment of two forms of severe childhood epilepsy, Dravet syndrome and Lennox-Gastaut syndrome. It’s being delivered to patients in a reliable dosage form and through a reproducible route of delivery to ensure that patients derive the anticipated benefits. CBD does not have the rewarding properties of THC.

Researchers generally consider medications like these, which use purified chemicals derived from or based on those in the marijuana plant, to be more promising therapeutically than use of the whole marijuana plant or its crude extracts. Development of drugs from botanicals such as the marijuana plant poses numerous challenges. Botanicals may contain hundreds of unknown, active chemicals, and it can be difficult to develop a product with accurate and consistent doses of these chemicals. Use of marijuana as medicine also poses other problems such as the adverse health effects of smoking and THC-induced cognitive impairment. Nevertheless, a growing number of states have legalized dispensing of marijuana or its extracts to people with a range of medical conditions.

An additional concern with "medical marijuana" is that little is known about the long-term impact of its use by people with health- and/or age-related vulnerabilities—such as older adults or people with cancer, AIDS, cardiovascular disease, multiple sclerosis, or other neurodegenerative diseases. Further research will be needed to determine whether people whose health has been compromised by disease or its treatment (e.g., chemotherapy) are at greater risk for adverse health outcomes from marijuana use.


Medical Marijuana Laws and Prescription Opioid Use Outcomes

A new study underscores the need for additional research on the effect of medical marijuana laws on opioid overdose deaths and cautions against drawing a causal connection between the two. Early research suggested that there may be a relationship between the availability of medical marijuana and opioid analgesic overdose mortality. In particular, a NIDA-funded study published in 2014 found that from 1999 to 2010, states with medical cannabis laws experienced slower rates of increase in opioid analgesic overdose death rates compared to states without such laws.78 A 2019 analysis, also funded by NIDA, re-examined this relationship using data through 2017. Similar to the findings reported previously, this research team found that opioid overdose mortality rates between 1999-2010 in states allowing medical marijuana use were 21% lower than expected. When the analysis was extended through 2017, however, they found that the trend reversed, such that states with medical cannabis laws experienced an overdose death rate 22.7% higher than expected.79 The investigators uncovered no evidence that either broader cannabis laws (those allowing recreational use) or more restrictive laws (those only permitting the use of marijuana with low tetrahydrocannabinol concentrations) were asso