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Relationship between cannabis use and schizophrenia

INTRODUCTION: Numerous studies have shown evidence that cannabis use increases the appearance of psychotic symptoms and disorders, and worsens the course of the disease in those with schizophrenia. However, a causal relationship between cannabis and schizophrenia has not been well established yet. O...

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Detalles Bibliográficos
Autores principales: Vazquez Vazquez, J.J., Gutiérrez Rodríguez, M.M., Corral Y Alonso, M.D.L.A., Moreno Menguiano, C., Garcia Sánchez, F.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cambridge University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9568200/
http://dx.doi.org/10.1192/j.eurpsy.2022.1191
Descripción
Sumario:INTRODUCTION: Numerous studies have shown evidence that cannabis use increases the appearance of psychotic symptoms and disorders, and worsens the course of the disease in those with schizophrenia. However, a causal relationship between cannabis and schizophrenia has not been well established yet. OBJECTIVES: In this presentation we try to review the relationship between cannabis use and prevalence of schizophrenia. METHODS: We performed a search of Medline looking for systematic reviews and methodologically robust studies in the field published in English in the last 5 years. RESULTS: A number of studies, both cross-sectional and prospective, find a prevalence of schizophrenia several times higher among cannabis users than in non-users. This association becomes stronger the lower the age of cannabis use onset, the higher the amount consumed and the higher the THC concentration are. Half of the patients with a cannabis-induced psychotic disorder turn into a diagnosis of schizophrenia within a few years. So far, it has not been possible to demonstrate a global increased prevalence of schizophrenia in relation to the increase of cannabis use in the population in recent decades. CONCLUSIONS: Cannabis and schizophrenia have a complex relationship model; we still cannot clearly establish whether it is causal or the first works as a trigger for pathology in vulnerable subjects. DISCLOSURE: No significant relationships.