From Hip to Harmful: the Ongoing Revision of the Cannabis-Schizophrenia Link

Much water has passed under the bridge since the idea of enhancing consciousness and creativity through the use of psychoactive substances was first introduced to a larger audience by musicians and artists in the 1960s. Smoking cannabis was hip and suited the innocent and curious atmosphere of that era. While cannabis products have gotten stronger and users younger since those days, researchers have also gradually started to recognize the potential of this drug to induce psychosis and possibly increase the risk for a chronic psychiatric illness.

Due to several large-scale epidemiologic studies, we now know that heavy cannabis use is associated with an increased likelihood of a psychotic disorder and with an earlier onset of its symptoms. However, debate continues about whether a causal link exists: Is cannabis an independent cause of a psychotic illness, or is their link better explained by common risk factors or reciprocal causality? Comments on the existing findings have gone somewhat beyond what has actually been shown, which suggests that cannabis has a specific potential to induce not only affective reactions but opinions, too.

In our register-based study, my colleagues and I were not seeking direct evidence for a causal link between cannabis and schizophrenia. Instead, we wanted to investigate a clinical population of patients that is well known in acute psychiatry: relatively young people with psychotic states seemingly induced by recent substance abuse. Using our comprehensive national hospital register, we were able to show that up to half of the patients being treated for a cannabis-induced psychosis for the first time will be given a diagnosis of schizophrenia within 5 years.

Among different psychosis-inducing substances, cannabis was the one most associated with subsequent conversion into a diagnosis of schizophrenia. The possible explanations for this are manifold. Our data do not allow us to speculate on the possible role of THC and the endocannabinoid system in regard to the cannabis–schizophrenia link. Instead, we now have to consider that, in the clinical world, we may be prone to either an initial misdiagnosis or difficulties in recognizing possible prodromal symptoms in the midst of problematic cannabis use. Regardless of the mechanism of the association, it should be noted that clinicians are now in fact being offered a very important target for early intervention in regard to such a high-risk population!

In the context of the complexity of the risk factors for schizophrenia, we know that cannabis is not a sufficient cause for schizophrenia. The risk is increased, however, in those who already have many other risk factors and who are vulnerable to both the chemical and psychosocial consequences of heavy cannabis use. From our study, the lesson to learn is to enhance our awareness in cases of substance-induced psychosis and provide better follow-up with proactive, integrated services. Cannabis use may still be hip for some people, but some will need protection from what it may bring with it.

Financial disclosure:Dr Pirkola had no relevant personal financial relationships to report.