Abstract
Cannabis use in adolescence has been linked with increased risk of developing depression in adulthood and chronic cannabis use has a blunting effect on the endocannabinoid signalling. We investigated the role of cannabis use in the mechanisms underlying depression development and the impact of cannabis use on the endocannabinoid signalling in 74 patients receiving interferon-alpha treatment for hepatitis-C-viral. We measured serum endocannabinoids, anandamide (AEA) and 2-arachidonoylglycerol (2-AG) at baseline and treatment week 4 (TW4), using High Performance Liquid Chromatography with Tandem Mass Spectrometry. We used M.I.N.I. International Neuropsychiatric Interview to assess depression development and Cannabis Experience Questionnaire to determine cannabis use during lifetime. Our results show that the proportion of patients who smoke cannabis at baseline is 3.73 greater amongst those who develop depression during treatment compared to those who do not develop depression. When we looked at the effect of interferon-alpha on endocannabinoid levels, we found a significant increase in 2-AG levels, from baseline to TW4, only in patients who never used cannabis and those who used cannabis in the past. Levels of AEA were significantly increased from baseline to TW4 only in patients who never used cannabis. Our findings suggest that current cannabis use may increased the likelihood of developing depression during interferon-alpha treatment in hepatitis-C-viral patients. Cannabis use may have a blunting effect on eCB signaling in response to interferon-alpha treatment.
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