For decades, the misunderstood relationship between cannabis and schizophrenia has sowed fear among regulators, healthcare providers, and law enforcement. Opposition to legalization has often come wrapped in alarm that rising cannabis consumption will trigger rising rates of psychosis and schizophrenia.
Yet, more than 80 years after the film “Reefer Madness” incited this panic about cannabis, we still know frustratingly little about whether the madness theory is true. In a confusing turn of events, newer research suggests that cannabinoid therapy may actually reduce the symptoms of psychosis and schizophrenia.
Although there has been substantial scientific attention given to this relationship over the last half-century, the current body of work faces issues related to the nature of epidemiological study and the inherent biases in cannabis research. By their very nature, population-wide studies simply cannot control for all the variables, which is especially true within the long-term studies needed to explore how cannabis relates to schizophrenia.
When it comes to cannabis, there is also the established inherent bias against the plant’s medicinal properties. As a recent analysis uncovered, research into the potential harms of cannabis received 20 times more funding over the last two decades than the plant’s therapeutic value. While new studies suggest cannabis and cannabinoids could help reduce the symptoms of schizophrenia, historic biases mean this is still an extremely challenging topic to fund and receive approval. Therefore, most research to date has focused on the negatives.
Thankfully, several publications and research centers have taken a more objective approach to this topic over the last few years. This new impartial assessment has not led to any breakthroughs—yet—but it has helped redefine and rebalance the current scientific landscape.
In 2019, Current Psychiatry Reports published “Cannabis and Psychosis: Are We any Closer to Understanding the Relationship?” by Ian Hamilton and Mark Monaghan. The authors succinctly summarize the three contemporary theories about the relationship between cannabis and schizophrenia.
Direct Relationship: Cannabis consumption can trigger psychosis and schizophrenia, even in people who would never have developed the mental health condition without cannabis use.
Reverse Causation: People with a predisposition to schizophrenia use cannabis to reduce symptoms, which in turn increases the risk of this condition developing.
Common Cause: Genetic predisposition, childhood trauma, and other factors increase the risk for both schizophrenia and cannabis use.
The direct relationship theory has “proved to be difficult to investigate with confidence,” as Hamilton and Monaghan detail. So far, it seems as if dose size and frequency may come into play, but the THC metabolite lingers in the human body much longer than the actual intoxication, which complicates the conclusions.
Depending on a variety of factors, patients may test positive for THC more than a month after consumption. It’s also challenging to study because dose size and frequency of use are generally self-reported by the patient, not clinically controlled. Whether or not a historical use of cannabis can be connected to a recent schizophrenia diagnosis remains suspect.
The second hypothesis, reverse causation, has gained more traction in recent years. Instead of cannabis directly triggering the onset of schizophrenia, the theory suggests it activates a predisposition toward the condition (genetic or environmental). Some literature suggests that cannabis appeals to schizophrenia patients for the purpose of reducing the early symptoms of the disease, although this remains unproven.
The final idea explores a shared genetic vulnerability, which would increase the likelihood of both cannabis use and schizophrenia. In a 2018 analysis published in Drug and Alcohol Dependence, researchers determined that “high schizophrenia vulnerability was associated with a stronger increase in cannabis use at age 16-20.” These findings support “a relation between genetic risk to schizophrenia and prospective cannabis use patterns during adolescence. In contrast, no relation between alcohol and smoking was established.”
Unfortunately, despite interesting research into these genetic connections, it is exponentially more challenging to assess any added environmental influences.
As Hamilton and Monaghan highlighted in their paper, “cannabidiols have been shown to provide therapeutic value in the treatment of schizophrenia with a relatively low risk of adverse effects.” Researchers now have a much better understanding of cannabis outside of the single intoxicating compound, tetrahydrocannabinol (Δ9-THC). Other compounds, like cannabidiol (CBD), are a novel target for research projects exploring potential new treatment options.
Cannabidiol is already an effective and proven antipsychotic when it comes to countering the psychoactive properties of THC. Now, this idea has expanded to explore CBD for the treatment of mental health disorders like schizophrenia. In one such study, researchers gave 88 patients with schizophrenia a dose of CBD or a placebo for six weeks. The CBD was over and above their regular antipsychotic prescriptions.
The results of this short study showed statistically significant reductions in what are called positive psychotic symptoms. It also demonstrated that CBD provided a greater improvement in cognitive performance. Better yet, rates of adverse effects were equal between the two groups.
This study strongly suggests that CBD could help treat schizophrenia and related disorders in a conjunctive role with traditional pharmaceuticals. It may also help explain why people with a predisposition to schizophrenia may already turn to cannabis to reduce systems. Since January 2018, more than 2,000 patients have reported using cannabis for schizophrenia within the RYAH Data ecosystem.
Despite more than 80 years of research, it is still incredibly challenging for patients and healthcare providers to navigate the relationship between cannabis consumption and schizophrenia. It is difficult to conclude whether cannabis helps, hinders, or directly triggers schizophrenic episodes, either in those with a predisposition or those without.
From Hamilton and Monaghan’s perspective on the direction of research: “As cannabis use and the development of psychosis are both influenced by social as well as biological factors, it is important that we keep pursuing a balanced blend of enquiry.”
From a patient perspective, caution is needed. Several factors, including genetic vulnerability, environmental factors, and cannabis potency, may increase the risk of consuming cannabis for some people. And while new research indicates cannabinoid therapy improves symptoms, this is a relatively new idea that requires much more research before it’s rolled out in practice.