title: Cannabinoids influence lipid-arachidonic acid pathways in schizophrenia.
abstract: Increasing evidence suggests modulating effects of cannabinoids on time of onset, severity, and outcome of schizophrenia. Efforts to discover the underlying pathomechanism have led to the assumption of gene x environment interactions, including premorbid genetical vulnerability and worsening effects of continuing cannabis use. The objective of this cross-sectional study is to investigate the relationship between delta-9-tetrahydrocannabinol intake and niacin sensitivity in schizophrenia patients and healthy controls. Intensity of niacin skin flushing, indicating disturbed prostaglandin-mediated processes, was used as peripheral marker of lipid-arachidonic acid pathways and investigated in cannabis-consuming and nonconsuming schizophrenia patients and in healthy controls. Methylnicotinate was applied in three concentrations onto the forearm skin. Flush response was assessed in 3-min intervals over 15 min using optical reflection spectroscopy. In controls, skin flushing was significantly decreased in cannabis-consuming as compared to nonconsuming individuals. When comparing the nonconsuming subgroups, patients showed significantly decreased flush response. The populations as a whole (patients and controls) showed an inverse association between skin flushing and sum scores of Symptom Check List 90-R. Results demonstrate an impact of long-term cannabis use on lipid-arachidonic acid pathways. Considering pre-existing vulnerability of lipid metabolism in schizophrenia, observed effects of cannabis use support the notion of a gene x environment interaction.
authors.affiliation: Department of Psychiatry, Friedrich-Schiller-University Jena, Philosophenweg 3, D-07743 Jena, Germany. stefan.smesny@med.uni-jena.de
authors.forename: Stefan
authors.initials: S
authors.lastname: Smesny
authors.forename: Timm
authors.initials: T
authors.lastname: Rosburg
authors.forename: Kati
authors.initials: K
authors.lastname: Baur
authors.forename: Nicole
authors.initials: N
authors.lastname: Rudolph
authors.forename: Heinrich
authors.initials: H
authors.lastname: Sauer
mesh_terms: D000328:Adult; D001095:Arachidonic Acids / Q000378:metabolism*; D015415:Biomarkers; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D002186:Cannabinoids / Q000494:pharmacology*; D003430:Cross-Sectional Studies; D013759:Dronabinol / Q000494:pharmacology; D004347:Drug Interactions; D005260:Female; D006801:Humans; D050356:Lipid Metabolism / Q000187:drug effects* / Q000502:physiology; D008297:Male; D009525:Niacin / Q000494:pharmacology*; D009539:Nicotinic Acids; D011453:Prostaglandins / Q000378:metabolism; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012559:Schizophrenia / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D012867:Skin / Q000098:blood supply / Q000187:drug effects / Q000503:physiopathology; D012882:Skin Tests; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D001095:Arachidonic Acids; D015415:Biomarkers; D002186:Cannabinoids; D009539:Nicotinic Acids; D011453:Prostaglandins; D009525:Niacin; C008473:methyl nicotinate; D013759:Dronabinol