Harm Avoidance And Childhood Adversities In Patients With Obsessive-Compulsive Disorder And Unaffected First-Degree Relatives: Evidence For A Diathesis-Stress Model

Background Obsessive-compulsive disorder (OCD) is a severe psychiatric disorder, which aggregates in families. Its etiology is assumed to involve interactions between genetically determined vulnerability factors and critical environmental influences. In the present study, we aim to investigate how the personality trait harm avoidanceand the experience of different childhood adversities contribute to the development of OCD. Methods One hundred and sixty-nine patients with OCD, 157 healthy comparison subjects and 57 unaffected first-degree relativesof OCD patients were examined by trained clinical psychologists using the Structured Clinical Interviewfor DSM-IV(SKID). Harm avoidancewas assessed using the Temperamentand Character Inventory(TCI) and the severity of childhood adversities was measured with the Childhood Adversity Questionnaire (CTQ). Associations with depressive and obsessive-compulsive symptoms were investigated using the Beck Depression Inventory-II (BDI-II) and the Obsessive-Compulsive Inventory-Revised (OCI-R). Results Both OCD patients and unaffected relatives showed elevated levels of harm avoidancecompared to healthy volunteers. Furthermore, patients exhibited significantly higher scores than relatives. This linear pattern was observed throughout all subscales of harm avoidance, and remained stable after controlling for the severity of depressive and obsessive-compulsive symptoms. With regards to childhood adversities, OCD patients reported higher levels than unaffected relatives and healthy volunteers, specifically on the subscales emotional abuse, emotional neglect, and experience of inconsistencies. Discussion The present findings support the role of harm avoidanceas a potential endophenotypeof OCD, and provide further evidence for a diathesis-stress model. While patients with OCD and unaffected first-degree relativesshare elevated levels of harm avoidance, a heightened severity of childhood adversity was only observed in patients. A predisposition to exaggerated anxiety responses may thus take different trajectories depending on adverse environmental influences during childhood. In future research, we aim to investigate the genetic and epigenetic mechanisms underlying these findings.