Accumulating evidence suggests an association between cannabis use and psychosis. However, some concerns have been raised about the nature of this association, particularly whether it might be driven by other factors such as use of other substances. Another explanation would bring into play preexisting differences among cannabis users and nonusers in terms of psychosis-related symptomatology that would make cannabis users more prone to develop psychosis. Moreover, it has been argued that people with psychosis may use cannabis more in an attempt to self-medicate, thus implying that psychosis may itself predispose to cannabis use. Finally, evidence of a common genetic background predisposing to both psychosis and cannabis use would weaken the strength of any direct detrimental effect of cannabis use on later development of psychosis. The aim of this chapter is to bring together the available evidence specifically exploring the causality of the association between cannabis use and psychosis and to discuss it along with cause–effect criteria such as magnitude of the association, consistency of findings from other studies, specificity of the association, temporal sequence of association, biological gradient, coherence and experimental proof, and biological plausibility. Collectively, there is robust evidence for an association between cannabis use and psychosis. Convergent evidence from prospective and experimental studies points in the direction of a causal relationship. Although the size of the effect appears modest, the psychosis-inducing effects of cannabis may be particularly high among frequent users, users of potent forms of cannabis, and in the context of specific genetic or neurobiological vulnerability.

Is there sufficient evidence that cannabis use is a risk factor for psychosis?

Colizzi, Marco;
2020-01-01

Abstract

Accumulating evidence suggests an association between cannabis use and psychosis. However, some concerns have been raised about the nature of this association, particularly whether it might be driven by other factors such as use of other substances. Another explanation would bring into play preexisting differences among cannabis users and nonusers in terms of psychosis-related symptomatology that would make cannabis users more prone to develop psychosis. Moreover, it has been argued that people with psychosis may use cannabis more in an attempt to self-medicate, thus implying that psychosis may itself predispose to cannabis use. Finally, evidence of a common genetic background predisposing to both psychosis and cannabis use would weaken the strength of any direct detrimental effect of cannabis use on later development of psychosis. The aim of this chapter is to bring together the available evidence specifically exploring the causality of the association between cannabis use and psychosis and to discuss it along with cause–effect criteria such as magnitude of the association, consistency of findings from other studies, specificity of the association, temporal sequence of association, biological gradient, coherence and experimental proof, and biological plausibility. Collectively, there is robust evidence for an association between cannabis use and psychosis. Convergent evidence from prospective and experimental studies points in the direction of a causal relationship. Although the size of the effect appears modest, the psychosis-inducing effects of cannabis may be particularly high among frequent users, users of potent forms of cannabis, and in the context of specific genetic or neurobiological vulnerability.
2020
9780128132029
Cannabidiol, Cannabis, Delta-9-tetrahydrocannabinol, Psychosis, Schizophrenia
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11562/1014617
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