Abstract
Schizophrenia is a complex psychiatric disorder strongly associated with substance use disorders. Theoretically, schizophrenia and SUD may share endocannabinoid alterations in the brain reward system. The main endocannabinoids, anandamide, and 2-arachidonoylglycerol, are lipids which bind cannabinoid receptors. Oleoylethanolamide (OEA), a fatty-acid ethanolamide, binds peroxisome proliferator-activated receptors. The endocannabinoid system has been shown to be impaired in schizophrenia, and recently, our group has shown that schizophrenia patients with SUD have elevated peripheral levels of anandamide and OEA that do not normalize after 3-month treatment with quetiapine. Objective For comparative purposes, we aimed to measure endocannabinoids in non-psychosis substance abusers and non-abusing schizophrenia patients. Methods Using liquid chromatography and mass spectrometry, we measured plasma levels of anandamide and OEA in non-psychosis SUD patients, non-abusing schizophrenia patients, and healthy controls. In an open-label manner, all patients received 12-week treatment with quetiapine. Results Anandamide and OEA were reduced in substance abusers without schizophrenia, relative to healthy controls (p < 0.05). Both endocannabinoids were unchanged in non-abusing schizophrenia patients. After quetiapine, anandamide, and OEA levels remained significantly reduced the SUD group (p < 0.05). Discussion Taken together with results of our previous study performed in dual-diagnosis patients, our results suggest that peripheral anandamide and OEA levels are impaired in patients with SUD in opposite ways according to the presence or absence of schizophrenia. Endocannabinoid alterations did not change with treatment, suggesting that they are trait markers. Further studies are necessary to understand the role of endocannabinoids in substance abusers with and without schizophrenia and to examine therapeutic implications.
Highlights
Schizophrenia is a complex disease encompassing 0.87% of the general population (Perala et al, 2007)
We report plasma anandamide and OEA concentrations in substance abusers without schizophrenia and in non-abusing schizophrenia patients assessed in the same clinical conditions and included following the same criteria as the patients with dual-diagnosis
Plasma anandamide levels were reduced in substance use disorder (SUD) patients, but normal in non-abusing schizophrenia patients, and both anandamide and OEA levels remained reduced in the SUD group after quetiapine treatment
Summary
Schizophrenia is a complex disease encompassing 0.87% of the general population (Perala et al, 2007). Psychiatric symptoms and comorbidities such as substance use disorder (SUD) contribute to the associated disability. The lifetime prevalence of SUD is approximately 40% in schizophrenia (Regier et al, 1990). It has a negative impact on drug compliance, psychotic relapses, and on prognosis. Patients with schizophrenia are more prone to substance abuse than the general population and 25% have a lifetime prevalence of cannabis abuse/dependence, the most widely used illicit psychoactive substance worldwide (Jablensky, 2000). Cannabinoid intoxication can provoke cognitive deficits and psychiatric symptoms akin to the cognitive and positive symptoms of schizophrenia (D’Souza et al, 2004). Cannabinoid intoxication has become a valid psychosis model, because its effects are representative of the full spectrum of schizophrenia symptoms. The endogenous cannabinoid (ECB) system may help to understand the link between schizophrenia and substance abuse
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