Dr. Kiri Simms is an emergency psychiatrist in Victoria, British Columbia. Two years ago she saw her first patient with marijuana-induced psychosis. The person was very young and very disconnected from reality. “She was very, very ill.” Shatter, a butane hash oil product, was the only drug she used. In the past, most people did not become psychotic with marijuana use alone, Dr. Simms said. “That has changed with these butane hash oil products.”

Dr. Simms said she’s seeing an increased severity and intensity of symptoms with some people at her emergency department (ED). In the past year, she estimated she’s treated ten people who had used shatter and whose problems were severe enough to require a stay in psychiatric intensive care or on one of their inpatient wards. People are often surprised they experienced psychotic symptoms from using marijuana products, she said.

It used to be that people did not become psychotic from marijuana use alone. Infrequently, individuals with a family history of schizophrenia might have a psychotic experience after smoking marijuana, but not any more. It’s not like the old days, where symptoms would pass in a few hours or days. Now Dr. Simms said they are seeing people who sometimes take weeks and occasionally months for their psychotic symptoms to clear.

The above discussion was in an interview she did with Greg Craigie the host of the CBC radio program, On the Island. You can read excerpts or follow a link to hear the full interview here. Craigie followed the Simms interview with one he did with Rebecca Jessemen, the senior policy advisor for the Canadian Centre of Substance Abuse. She said they were really concerned with minimizing the risk of harm with youth, as marijuana legalization moves closer in Canada. “That includes key messages such as delaying initiation of use, reducing frequency of use, and reducing the quantity of use… Part of that is quantity in terms of concentration too.”

Not surprisingly, the interview and web story prompted several mostly negative Facebook comments rejecting a link between shatter and psychosis. Accusations were made of this being false news, that CBC was spreading anti-cannabis propaganda, etc. You can read an article about Craigie’s interview with Rebecca Jessemen here. But this is not fake news. There is a clear, known association of marijuana use and psychotic episodes. And with higher THC content in a marijuana product, the risk of a psychotic episode increases.

Do people react differently to the same dose of THC? Does cannabidiol (CBD) reduce the psychotic effects of THC? There was an experiment done at the Institute of Psychiatry at King’s College, London that looked at the relationship of the effects of the two main cannabinoids in cannabis, THC and CBD. You can watch a video of a reporter participating in the experiment here.

She was given pure THC and a mixture of THC and CBD. On the THC and CBD mixture, the reporter said she seemed flippant; on pure THC, she just didn’t care. The mixture of THC and CBD left her with the giggles: “No matter how hard I tried to take the experiment seriously, it all seems hilarious.”

With pure THC, she was suspicious, introverted; “weird.” Every question seemed to have a double meaning. She felt morbid. “It’s like a panic attack.” “It’s horrible. It’s like being at a funeral . . . Worse . . . It’s just so depressing. You want to top [kill] yourself.”

The researchers used the Positive and Negative Syndrome Scale (PNASS), a standard test to measure changes in psychotic symptoms. On the PNASS sub scale used, changes above four was clinically significant; changes that would be associated with schizophrenic psychosis. She scored fourteen. The effects on the reporter were temporary and would not be long lasting. But the video clearly shows how higher concentrations of THC can induce temporary psychotic symptoms in normal individuals.

In a NPR interview, Dr. Nora Volkow, the director of the National Institute for Drug Abuse (NIDA) said while no one would question that marijuana can trigger temporary symptoms of psychosis in some people, it is not clear whether cannabis alone can trigger schizophrenia. “You can have a psychotic episode from the use of marijuana without it turning into schizophrenia. . . . It’s very distressing, but you’ll get out of it.” While drugs like marijuana and methamphetamine can lead to experiencing symptoms like paranoia and disorganized thinking, that’s very different from schizophrenia.

Dr. Volkow suggested the studies show that people with schizophrenia tend to smoke pot. People with an emerging schizophrenic disorder maybe “trying to self-medicate because they just don’t feel right.” Volkow believes if someone has a vulnerability to schizophrenia smoking it could trigger a psychotic episode. Without the predisposition, “you can smoke all the marijuana you want and it will make no difference.” Volkow did acknowledge the dramatic increase in people showing up in the emergency department with a temporary psychotic episode could be related to “a much more potent marijuana.”

But not everyone has the same opinion; that there is a clear distinction between schizophrenia and marijuana-induced psychosis. Sir Robin Murray, a psychiatrist at King’s College in London said 20 years ago he would tell patients that cannabis was safe. “It’s only after you see all the patients that go psychotic that you realize—it’s not safe.”

Krista Lisdahl, a clinical neuropsychologist, said that if marijuana is causing schizophrenia, this happens during an individual’s early years of development. There hasn’t been an increase in the number of people with schizophrenia; the number still hovers around 1%. However, studies do show that the earlier someone starts using marijuana, the more likely they will develop a psychiatric disorder in general.

A report by DAWN (Drug Abuse Warning Network) found that ED visits due to marijuana increased by 52% between 2004 and 2011. This was lower than the increase in ED visits for anti-anxiety and insomnia medications (124%), narcotic pain relievers (153%), antipsychotics (71%), and stimulants like ADHD medications (292%).  Nevertheless, Sir Robin Murray said the data strengthens the case of an association between cannabis and the risk for schizophrenia. A study in The Lancet which he published suggested marijuana with around 15% THC could increase the risk of schizophrenia 5 times. “We think about 5 percent of people will go psychotic instead of 1 percent.”

Our findings show the importance of raising public awareness of the risk associated with use of high-potency cannabis, especially when such varieties of cannabis are becoming more available. The worldwide trend of liberalisation of the legal constraints on the use of cannabis further emphasises the urgent need to develop public education to inform young people about the risks of high-potency cannabis.

A 2014 article in Frontiers in Psychiatry, “Gone to Pot,” reviewed the emerging evidence of a connection between cannabis and psychosis/psychotic disorders, including schizophrenia. The review was comprehensive and suggested cannabis may be a component in the emergence of psychosis. But the precise nature of these associations remains unclear. However, the relationship has been evident since the mid 1800s. One of the earliest studies of marijuana and psychosis was done by the French psychiatrist Jacques-Joseph Moreau, and reported in his 1845 book, Hashish and Mental Illness. Moreau said hashish (cannabis resin) could precipitate:

 … acute psychotic reactions, generally lasting but a few hours, but occasionally as long as a week; the reaction seemed dose-related and its main features included paranoid ideation, illusions, hallucinations, delusions, depersonalization, confusion, restlessness, and excitement. There can be delirium, disorientation, and marked clouding of consciousness.

Consistent with the YouTube video of the King’s College experiment linked above, cannabis extract and THC alone have been shown to produce a range of transient symptoms similar to the positive symptoms of schizophrenia: “suspiciousness, paranoid and grandiose delusions, conceptual disorganization, fragmented thinking, and perceptual alterations. Additionally, cannabis and THC also result in depersonalization, derealization, alterations in sensory perception, and feelings of unreality.” A double-blind, randomized, placebo-controlled study by D’Souza et al. found that THC produced transient positive psychotic symptoms. A similar study replicated these findings in healthy individuals with a lower THC dose than D’Souza et al.

Several studies suggest a “window of opportunity” hypothesis, meaning there is a critical period during early adolescence “where the brain is particularly susceptible to the psychosis-inducing effects of cannabis.” The premise suggests cannabis may affect the brain during a critical period of development and maturation. Cannabis could disrupt one or more of these maturation processes.

By disrupting the endocannabinoid system and interfering with neurodevelopmental processes, exogenous [from outside of an organism] cannabinoids may provide a biologically plausible mechanism by which exposure to cannabinoids during adolescence may increase the risk for the development of schizophrenia.

While there has been a notable increase in the rates of cannabis use over the past four decades, there has not been an increase in the prevalence of schizophrenia. The authors admit these results are difficult to explain in the context of their review showing how “the relationship between cannabinoids and psychosis fulfills many but not all of the traditional criteria for causality.” One possible explanation is that schizophrenia rates are lagging behind increased rates of cannabis consumption. In other words, we need to look for a future increase of schizophrenia rates with a cannabis connection.

Given the evidence presented above, it is likely that cannabis is an important component cause in the development of psychotic disorders. This causal role is apparantly magnified when cannabis exposure occurs at an earlier age, in greater quantities, and over a longer time-course. Further, as was discussed in this review, specific populations (i.e., those with a genetic vulnerability or a history of childhood abuse) may be particularly susceptible to the causal effects of cannabis. In conclusion the authors said:

Acute exposure to both natural and synthetic cannabinoids can produce a full range of transient symptoms, cognitive deficits, and psychophysiological abnormalities that bear a striking resemblance to some of the features of schizophrenia. Also clear is that, in individuals with an established psychotic disorder, cannabinoids can exacerbate symptoms, trigger relapse, and have negative consequences on the course of the illness. Finally, exposure to cannabinoids in adolescence confers a higher risk for psychosis outcomes in later life and the risk is dose-related. However, it should be remembered that the majority of individuals who consume cannabis do not experience any kind of psychosis.

So the On the Island interview with Dr. Simms was not an example of fake news or anti-marijuana fear mongering. While the dangers of cannabis use don’t approach those portrayed in the classic cult film Reefer Madness, there is growing evidence of a risk of psychotic symptoms with higher levels of THC in marijuana products like shatter. And there is an increased risk of psychosis later in life for a subgroup of adolescents who use marijuana. The evidence is not conclusive at this time, but can we afford to just wait-and-see if wide spread recreational marijuana use conclusively causes the adverse effects discussed above before taking regulatory action?