Marc D Ferger, Christine Sigrist, Susanne Brodesser, Michael Kaess, Julian Koenig
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引用次数: 0
Abstract
Non-suicidal self-injury (NSSI) is a highly prevalent phenomenon in adolescence, often associated with prior traumatic experiences. The development and maintenance of NSSI is associated with dysregulation of the stress response, and evidence suggests that the hypothalamic-pituitary-adrenal (HPA) axis plays an important role. The endocannabinoid system is a neuromodulatory system in close functional interaction with the HPA axis. Several studies have reported alterations of the endocannabinoid system in adult patients with post-traumatic stress disorder. However, the role of the endocannabinoid system in children and adolescents with NSSI is less clear, and previously no study examined endocannabinoids in youth with experiences of maltreatment. N-arachidonyl ethanolamide (AEA) and 2-arachidonyl glycerol (2-AG) were quantified alongside sociodemographic and clinical characteristics in n = 148 adolescents (12-17 years of age). Analyses addressed group differences comparing healthy controls (HC, n = 38), patients with NSSI without (NSSI - CMT, n = 42) and with a history of childhood maltreatment (NSSI + CMT, n = 68). We show that AEA is reduced in adolescents with NSSI independent of childhood maltreatment. Further, we present first evidence for a negative association between AEA and NSSI frequency as well as AEA and the severity of childhood maltreatment. This is the first study providing evidence for alterations in the endocannabinoid system in children and adolescents engaging in repetitive NSSI. Findings from the study support current endocannabinoid-hypotheses on the neurobiology of trauma and adversity, extending existing findings of altered endocannabinoid signaling following exposure to traumatic events to a well-powered sample of children and adolescents.
期刊介绍:
Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.