Javier Vázquez-Bourgon1, Víctor Ortiz-García de la Foz2, Irene Suarez-Pereira3, Paula Iruzubieta4, María Teresa Arias-Loste5, Esther Setién-Suero6, Rosa Ayesa-Arriola7, Marcos Gómez-Revuelta6, Javier Crespo8, Benedicto Crespo Facorro9. 1. Department of Psychiatry, University Hospital Marqués de Valdecilla, Instituto de Investigación Sanitaria Valdecilla, Santander, Spain; Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Instituto de Salud Carlos III, Spain; Department of Medicine and Psychiatry, School of Medicine, University of Cantabria, Santander, Spain. Electronic address: javier.vazquez@scsalud.es. 2. Department of Psychiatry, University Hospital Marqués de Valdecilla, Instituto de Investigación Sanitaria Valdecilla, Santander, Spain; Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Instituto de Salud Carlos III, Spain. Electronic address: newvtro@gmail.com. 3. Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Instituto de Salud Carlos III, Spain; Neuropsychopharmacology & Psychobiology Research Group, University of Cádiz, Spain; Instituto de Investigación e Innovación en Ciencias Biomédicas de Cádiz, INiBICA, Edificio "Andrés Segovia", Cádiz, Spain. Electronic address: irene.suarez@uca.es. 4. Gastroenterology and Hepatology Unit, University Hospital de Valdecilla, Instituto de Investigación Sanitaria Valdecilla, Santander, Spain. Electronic address: paula.iruzubieta@scsalud.es. 5. Gastroenterology and Hepatology Unit, University Hospital de Valdecilla, Instituto de Investigación Sanitaria Valdecilla, Santander, Spain. Electronic address: mteresa.arias@scsalud.es. 6. Department of Psychiatry, University Hospital Marqués de Valdecilla, Instituto de Investigación Sanitaria Valdecilla, Santander, Spain; Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Instituto de Salud Carlos III, Spain; Department of Medicine and Psychiatry, School of Medicine, University of Cantabria, Santander, Spain. 7. Department of Psychiatry, University Hospital Marqués de Valdecilla, Instituto de Investigación Sanitaria Valdecilla, Santander, Spain; Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Instituto de Salud Carlos III, Spain; Department of Medicine and Psychiatry, School of Medicine, University of Cantabria, Santander, Spain. Electronic address: rayesa@idival.org. 8. Department of Medicine and Psychiatry, School of Medicine, University of Cantabria, Santander, Spain; Gastroenterology and Hepatology Unit, University Hospital de Valdecilla, Instituto de Investigación Sanitaria Valdecilla, Santander, Spain. Electronic address: digcgj@humv.es. 9. Department of Psychiatry, University Hospital Marqués de Valdecilla, Instituto de Investigación Sanitaria Valdecilla, Santander, Spain; Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Instituto de Salud Carlos III, Spain; Department of Medicine and Psychiatry, School of Medicine, University of Cantabria, Santander, Spain. Electronic address: benedicto.crespo@unican.es.
Abstract
INTRODUCTION: Increased incidence of obesity and excess weight lead to an increased incidence of non-alcoholic fatty liver disease (NAFLD). Recent evidence indicates a protective effect of cannabis consumption on weight gain and related metabolic alterations in psychosis patients. Overall, patients are at greater risk of presenting fatty diseases, such as NAFLD, partly due to lipid and glycemic metabolic disturbances. However, there are no previous studies on the likely effect of cannabis on liver steatosis. We aimed to explore if cannabis consumption had an effect on hepatic steatosis, in a sample of first-episode (FEP) non-affective psychosis. MATERIAL AND METHODS: A total of 390 patients were evaluated at baseline and after 3 years of initiating the antipsychotic treatment. Anthropometric measurements and liver, lipid, and glycemic parameters were obtained at both time points. All but 6.7% of patients were drug-naïve at entry, and they self-reported their cannabis use at both time points. Liver steatosis and fibrosis were evaluated through validated clinical scores (Fatty Liver Index [FLI], Fibrosis-4 [FIB-4], and NAFLD). RESULTS: At 3-year follow-up, cannabis users presented significantly lower FLI scores than non-users (F = 13.874; p < .001). Moreover, cannabis users less frequently met the criteria for liver steatosis than non-users (X2 = 7.97, p = .019). Longitudinally, patients maintaining cannabis consumption after 3 years presented the smallest increment in FLI over time, which was significantly smaller than the increment in FLI presented by discontinuers (p = .022) and never-users (p = .016). No differences were seen in fibrosis scores associated with cannabis. CONCLUSIONS: Cannabis consumption may produce a protective effect against liver steatosis in psychosis, probably through the modulation of antipsychotic-induced weight gain.
INTRODUCTION: Increased incidence of obesity and excess weight lead to an increased incidence of non-alcoholic fatty liver disease (NAFLD). Recent evidence indicates a protective effect of cannabis consumption on weight gain and related metabolic alterations in psychosispatients. Overall, patients are at greater risk of presenting fatty diseases, such as NAFLD, partly due to lipid and glycemic metabolic disturbances. However, there are no previous studies on the likely effect of cannabis on liver steatosis. We aimed to explore if cannabis consumption had an effect on hepatic steatosis, in a sample of first-episode (FEP) non-affective psychosis. MATERIAL AND METHODS: A total of 390 patients were evaluated at baseline and after 3 years of initiating the antipsychotic treatment. Anthropometric measurements and liver, lipid, and glycemic parameters were obtained at both time points. All but 6.7% of patients were drug-naïve at entry, and they self-reported their cannabis use at both time points. Liver steatosis and fibrosis were evaluated through validated clinical scores (Fatty Liver Index [FLI], Fibrosis-4 [FIB-4], and NAFLD). RESULTS: At 3-year follow-up, cannabis users presented significantly lower FLI scores than non-users (F = 13.874; p < .001). Moreover, cannabis users less frequently met the criteria for liver steatosis than non-users (X2 = 7.97, p = .019). Longitudinally, patients maintaining cannabis consumption after 3 years presented the smallest increment in FLI over time, which was significantly smaller than the increment in FLI presented by discontinuers (p = .022) and never-users (p = .016). No differences were seen in fibrosis scores associated with cannabis. CONCLUSIONS: Cannabis consumption may produce a protective effect against liver steatosis in psychosis, probably through the modulation of antipsychotic-induced weight gain.
Authors: Patricia Rivera; Antonio Vargas; Antoni Pastor; Anna Boronat; Antonio Jesús López-Gambero; Laura Sánchez-Marín; Dina Medina-Vera; Antonia Serrano; Francisco Javier Pavón; Rafael de la Torre; Ekaitz Agirregoitia; María Isabel Lucena; Fernando Rodríguez de Fonseca; Juan Decara; Juan Suárez Journal: Br J Pharmacol Date: 2020-04-15 Impact factor: 8.739
Authors: Giulia Cisbani; Alex Koppel; Adam H Metherel; Mackenzie E Smith; Kankana N Aji; Ana C Andreazza; Romina Mizrahi; Richard P Bazinet Journal: Lipids Date: 2022-01-24 Impact factor: 1.880
Authors: Jonathan Gorelick; Tal Assa-Glazer; Gil Zandani; Anna Altberg; Noa Sela; Abraham Nyska; Zecharia Madar Journal: J Cannabis Res Date: 2022-05-30