Let's be clear at the outset: Medical experts and scientists agree that we still don't have enough evidence that marijuana use can directly cause psychosis. Recent studies suggest a close relationship in people at risk, but more evidence is needed.
Thus, people with a family history of psychosis/schizophrenia or other vulnerability are advised to avoid marijuana. Strong-acting strains and smoking marijuana at a younger age are considered particularly risky. However, most studies have only dealt with associations, which means a causal relationship has not been established. For example, just because psychosis was associated with marijuana use does not mean that marijuana causes psychosis.
Also, even if research has shown that marijuana use contributes to psychosis, it is unlikely that this is the only cause. Complex disorders such as schizophrenia are always related to many possible factors, including genetics, brain chemistry, environment, and health conditions, which can vary from one person to another.
Common factors
Research shows that many factors can alter the relationship between marijuana and psychosis, including:
Thus, people with a family history of psychosis/schizophrenia or other vulnerability are advised to avoid marijuana. Strong-acting strains and smoking marijuana at a younger age are considered particularly risky. However, most studies have only dealt with associations, which means a causal relationship has not been established. For example, just because psychosis was associated with marijuana use does not mean that marijuana causes psychosis.
Also, even if research has shown that marijuana use contributes to psychosis, it is unlikely that this is the only cause. Complex disorders such as schizophrenia are always related to many possible factors, including genetics, brain chemistry, environment, and health conditions, which can vary from one person to another.
Common factors
Research shows that many factors can alter the relationship between marijuana and psychosis, including:
- Types of marijuana varieties and their effectiveness
- Patterns of use
- Age of use
- Genetics
- Childhood trauma
- Lifestyle
- Gender
- Race
- Social and cultural influences
- Other illnesses and/or addictions
Adverse effects of cannabis
The most common side effects caused by smoking cannabis or using a mouth spray containing cannabis extract are:
The most common side effects caused by smoking cannabis or using a mouth spray containing cannabis extract are:
- Headache
- Dizziness
- Drowsiness
- Fatigue
- Dry mouth
- Nausea
- Paranoid thinking and dissociation
A number of unconfirmed reports suggest that cannabis can cause a range of acute psychotic symptoms that include depersonalization, derealization, paranoia, anxiety, flight of ideas, disorganized thinking, delusions of persecution, grandiose delusions, auditory and visual hallucinations, attention disorders and memory.
Cannabis-induced psychosis
Small studies on healthy volunteers show that THC (from cannabis) can cause psychosis-like symptoms. However, some people seem to be more vulnerable to these negative effects than others. According to large recent studies in Europe and Brazil, daily smoking of potent marijuana was associated with an increased risk of developing psychosis almost five times that of people who had never used marijuana.
Another study involving 6,700 people concluded that people with marijuana-induced psychosis had a 47 percent chance of developing bipolar disorder or schizophrenia within three to five years. Substance-induced psychosis at a young age was associated with a higher risk of conversion to schizophrenia. Self-harm following substance-induced psychosis was associated with a higher risk of both schizophrenia and bipolar disorder.
On the other hand, no one knows for sure if cannabis causes schizophrenia (or bipolar disorder). Scientists say that people who are predisposed to schizophrenia may also be more likely to use cannabis. They are also more likely to smoke cigarettes.
However, another theory claims that some common factors may underlie both cannabis use and psychosis. Finally, a group of researchers believe that cannabis use in people with mental health problems is a way to «self-medicate» and alleviate the early symptoms of schizophrenia.
Effect of THC on neurotransmitters
Below are experimental and theoretical data related to the effects of THC on the neurotransmitter system.
Dopamine
Animal experiments show that THC increases dopamine in the striatum, which is thought to be a biological feature of schizophrenia and psychosis. Researchers believe that dopamine in the striatum can increase motivation. But if dopamine levels in the striatum are already high, cannabis can push it to its limit.
Activation of the CB1 receptor can also increase dopamine in the prefrontal cortex, which can lead to its nonspecific activation and disruption of normal signal processing, leading to poor cognitive integration of input. Scientists say that excessively high levels of dopamine may contribute to working memory deficits associated with cannabis exposure.
Structural and functional imaging studies show that chronic cannabis use causes the same negative changes in brain structure as in schizophrenia, such as decreased hippocampal and amygdala volume. According to one experimental hypothesis, this may be due to the neurotoxic effects of chronically elevated dopamine levels.
GABA
Activation of the CB1 receptor reduces the release of GABA in hippocampal neurons in animals. This is thought to disrupt the synchronization of neuronal activity, which interferes with memory consolidation and the brain's ability to make normal associations, ultimately leading to psychotic symptoms.
In other words, some scientists claim that GABA can stop «crazy» thoughts, but in some key places it is reduced when CB1 receptors are activated. Limited research suggests that people with schizophrenia may have lower levels of GABA in the brain, but more research is needed.
Glutamate
According to one theory, so-called cognitive gateway functions in the brain prevent illogical thoughts from entering the mind.
Animal studies show that cannabinoids reduce glutamate levels (and NMDA activation) in several brain regions involved in the regulation of gateway functions, such as the hippocampus, prefrontal cortex, adjoining nucleus and amygdala. Ketamine, an NMDA blocker, can also induce psychosis, highlighting the potential role of lower glutamate levels in certain areas and psychosis.
Genes and cannabis-induced psychosis
The following SNPs were found to be associated only with cannabis-induced psychosis. This does not mean that their presence increases the risk of cannabis-induced psychosis. More work is needed before the effect of cannabis use on psychosis in people with different genetic variations can be elucidated.
DRD2 (dopamine gene)
Limited experimental evidence suggests that dopamine D2 receptors and schizophrenia are closely related. There is an association between psychosis and relatively large numbers of D2 receptors in the striatum, a dopamine-rich region of the brain. In addition, DRD2 receptors are blocked by neuroleptics, which help control the symptoms of psychosis.
Scientists say that relatively excessive activation of dopamine D2 can lead to decreased «gateway» function. It is that people have reduced filtering of relevant information (reduced signal-to-noise ratio) as well as blocked distractions. These brain processes contribute to various higher-order cognitive functions and are actively involved in attention control.
Some studies show that patients with schizophrenia who perform attention tasks have less activity and lower levels of gray matter in the cingulate gyrus, an area of the brain that strongly influences attention processing and executive function. This area is influenced by D2 receptors.
SNP
The «A» allele of rs1076560 in the dopamine DRD2 gene was associated with cannabis-induced psychosis in one study. In another study, it was associated with a 10-fold increased risk of psychosis in daily cannabis users. This SNP has also been linked to behavior and brain activity during cognitive and emotional processing in healthy subjects and in patients with schizophrenia.
In healthy subjects, the interaction between the A DRD2 rs1076560 allele and the AKT1 rs1130233 allele was associated with decreased AKT1 protein levels and increased GSK-3β, as well as an altered cingulate response and impaired cognitive function during attention processing.
GSK3b is a protein that is thought to increase oxidative stress and inflammation in the brain. Certain factors may inhibit this. D2 stimulation by dopamine inhibits AKT1, which can increase GSK3b and has been associated with psychosis in limited studies. AKT1 levels in the prefrontal cortex in patients with schizophrenia have been reduced in some brain imaging studies. It has been suggested that antipsychotics help by increasing AKT1 and decreasing GSK-3β, but this has not been proven.
Cannabis-induced psychosis
Small studies on healthy volunteers show that THC (from cannabis) can cause psychosis-like symptoms. However, some people seem to be more vulnerable to these negative effects than others. According to large recent studies in Europe and Brazil, daily smoking of potent marijuana was associated with an increased risk of developing psychosis almost five times that of people who had never used marijuana.
Another study involving 6,700 people concluded that people with marijuana-induced psychosis had a 47 percent chance of developing bipolar disorder or schizophrenia within three to five years. Substance-induced psychosis at a young age was associated with a higher risk of conversion to schizophrenia. Self-harm following substance-induced psychosis was associated with a higher risk of both schizophrenia and bipolar disorder.
On the other hand, no one knows for sure if cannabis causes schizophrenia (or bipolar disorder). Scientists say that people who are predisposed to schizophrenia may also be more likely to use cannabis. They are also more likely to smoke cigarettes.
However, another theory claims that some common factors may underlie both cannabis use and psychosis. Finally, a group of researchers believe that cannabis use in people with mental health problems is a way to «self-medicate» and alleviate the early symptoms of schizophrenia.
Effect of THC on neurotransmitters
Below are experimental and theoretical data related to the effects of THC on the neurotransmitter system.
Dopamine
Animal experiments show that THC increases dopamine in the striatum, which is thought to be a biological feature of schizophrenia and psychosis. Researchers believe that dopamine in the striatum can increase motivation. But if dopamine levels in the striatum are already high, cannabis can push it to its limit.
Activation of the CB1 receptor can also increase dopamine in the prefrontal cortex, which can lead to its nonspecific activation and disruption of normal signal processing, leading to poor cognitive integration of input. Scientists say that excessively high levels of dopamine may contribute to working memory deficits associated with cannabis exposure.
Structural and functional imaging studies show that chronic cannabis use causes the same negative changes in brain structure as in schizophrenia, such as decreased hippocampal and amygdala volume. According to one experimental hypothesis, this may be due to the neurotoxic effects of chronically elevated dopamine levels.
GABA
Activation of the CB1 receptor reduces the release of GABA in hippocampal neurons in animals. This is thought to disrupt the synchronization of neuronal activity, which interferes with memory consolidation and the brain's ability to make normal associations, ultimately leading to psychotic symptoms.
In other words, some scientists claim that GABA can stop «crazy» thoughts, but in some key places it is reduced when CB1 receptors are activated. Limited research suggests that people with schizophrenia may have lower levels of GABA in the brain, but more research is needed.
Glutamate
According to one theory, so-called cognitive gateway functions in the brain prevent illogical thoughts from entering the mind.
Animal studies show that cannabinoids reduce glutamate levels (and NMDA activation) in several brain regions involved in the regulation of gateway functions, such as the hippocampus, prefrontal cortex, adjoining nucleus and amygdala. Ketamine, an NMDA blocker, can also induce psychosis, highlighting the potential role of lower glutamate levels in certain areas and psychosis.
Genes and cannabis-induced psychosis
The following SNPs were found to be associated only with cannabis-induced psychosis. This does not mean that their presence increases the risk of cannabis-induced psychosis. More work is needed before the effect of cannabis use on psychosis in people with different genetic variations can be elucidated.
DRD2 (dopamine gene)
Limited experimental evidence suggests that dopamine D2 receptors and schizophrenia are closely related. There is an association between psychosis and relatively large numbers of D2 receptors in the striatum, a dopamine-rich region of the brain. In addition, DRD2 receptors are blocked by neuroleptics, which help control the symptoms of psychosis.
Scientists say that relatively excessive activation of dopamine D2 can lead to decreased «gateway» function. It is that people have reduced filtering of relevant information (reduced signal-to-noise ratio) as well as blocked distractions. These brain processes contribute to various higher-order cognitive functions and are actively involved in attention control.
Some studies show that patients with schizophrenia who perform attention tasks have less activity and lower levels of gray matter in the cingulate gyrus, an area of the brain that strongly influences attention processing and executive function. This area is influenced by D2 receptors.
SNP
The «A» allele of rs1076560 in the dopamine DRD2 gene was associated with cannabis-induced psychosis in one study. In another study, it was associated with a 10-fold increased risk of psychosis in daily cannabis users. This SNP has also been linked to behavior and brain activity during cognitive and emotional processing in healthy subjects and in patients with schizophrenia.
In healthy subjects, the interaction between the A DRD2 rs1076560 allele and the AKT1 rs1130233 allele was associated with decreased AKT1 protein levels and increased GSK-3β, as well as an altered cingulate response and impaired cognitive function during attention processing.
GSK3b is a protein that is thought to increase oxidative stress and inflammation in the brain. Certain factors may inhibit this. D2 stimulation by dopamine inhibits AKT1, which can increase GSK3b and has been associated with psychosis in limited studies. AKT1 levels in the prefrontal cortex in patients with schizophrenia have been reduced in some brain imaging studies. It has been suggested that antipsychotics help by increasing AKT1 and decreasing GSK-3β, but this has not been proven.
Individual case
Teens have access to much more potent marijuana than their parents did at their age. Parents need to understand the risks, including psychosis
The father said that he and his wife had smoked quite a bit of cannabis themselves in college and tended to believe that «it was just pot». They persuaded their son to buy it from licensed stores rather than acquiring it «on the street».
In California, where I spoke with researchers and doctors studying the link between cannabis use and the development of psychosis, getting a medical marijuana card is easy — even for teenagers.
David started high school as a typically diligent student surrounded by a few friends. Gradually, he started using cannabis on a daily basis, first at parties with friends and then increasingly alone. His parents noticed his increasingly strange behavior: he blocked the camera on his laptop, taped the windows in his room with cardboard, stopped showering and refused to go to school.
Eventually, they decided to send him to a rehabilitation center for teenagers. There he abstained from using for three weeks, but his psychotic symptoms did not disappear, but even worsened. Simply stopping his use was not enough for recovery.
When the family contacted me, David had been exhibiting persistent delusions for over six months. He was convinced he was being watched by the government. While we can't say for sure if cannabis was the cause of his psychosis, it's surprising that the symptoms didn't go away after he stopped using. Perhaps marijuana altered the way his brain worked.
Today's cannabis is vastly different from what was used in the 1960s or 1980s, and even from 10 years ago. The new strains are very potent, making them more addictive and potentially dangerous. We are still learning exactly how this drug affects the developing teenage brain. As a scientist and parent, my advice is to avoid cannabis use until around age 25. While it is unrealistic to completely eliminate the risk, it is important to be aware of how much the composition of today's products has changed and the possible mental health effects they can have.
Today, not only are traditional joints and herbal cookies on the market, but also products with high THC content, such as vapes and edibles, are often very potent. In other words, what teens can buy today is much different than what their parents used.
More potent THC, marijuana use at a young age and frequent use increases the risk of developing psychosis. A Canadian study of more than 11,000 adolescents found that those who used cannabis had an 11 times higher risk of developing psychotic disorders compared to those who did not. There are many worrying aspects to such data, and some scientists are calling for more public awareness measures. However, it is still difficult to get the word out to parents, educators, and lawmakers. Although there is no complete consensus on a direct causal link between cannabis and psychosis, well-designed studies indicate that there is a link.
Another important question is why are adolescents so vulnerable to developing psychosis when using cannabis? It is thought to be due to the developmental patterns of their brains, which continue to remodel into their early thirties. The same molecules and receptors that THC (the endocannabinoid system) interacts with play a key role in shaping the brain. A growing body of evidence suggests that early exposure to cannabis can disrupt the development of neural connections and the brain's response to experience, further increasing the risk of mental disorders. Animal and human studies show that cannabis use at a young age can alter neuronal function and interfere with the formation of memories.
How do I talk to children about cannabis? When I work with adolescents at risk of psychosis, I ask them why they use cannabis and how they feel afterwards. I also find out if they can stop and are willing to stop if they need to. I suggest they try abstinence for a few days and see how their condition changes — it helps to know if they are addicted.
Some teens are confident they can quit at any time, others are not ready. For those, I advise avoiding high-THC products and favoring those with more CBD and less THC.
Regarding David's experience: he was recommended ongoing psychiatric treatment and family therapy because he suffered from a chronic psychotic disorder. If your child is experiencing distressing symptoms or unusual behavior — such as isolation, talking to imaginary companions, or hallucinations — it is important to seek professional help as soon as possible. A doctor or pediatrician will be able to make a referral to a specialist for diagnosis and treatment.
Overall, the changed landscape of available cannabis products and their widespread availability is an experiment that none of us consented to. The best we can do is to consciously prepare and inform our children to reduce risks and better understand what is happening.