Dissociative disorders are a common and frequently undiagnosed group of psychiatric disorders, characterized by disruptions in the normal integration of awareness, personality, emotion and behavior. The available evidence suggests that these disorders arise from an interaction between genetic vulnerability and stress, particularly traumatic stress, but the attention paid to the underlying genetic diatheses has been sparse. In this paper, the existing literature on the molecular genetics of dissociative disorders, as well as of clinically significant dissociative symptoms not reaching the threshold of a disorder, is reviewed comprehensively across clinical and non-clinical samples. Association studies suggest a link between dissociative symptoms and genes related to serotonergic, dopaminergic and peptidergic transmission, neural plasticity and cortisol receptor sensitivity, particularly following exposure to childhood trauma. Genome-wide association studies have identified loci of interest related to second messenger signaling and synaptic integration. Though these findings are inconsistent, they suggest biologically plausible mechanisms through which traumatic stress can lead to pathological dissociation. However, methodological concerns related to phenotype definition, study power, and correction for the confounding factors limit the value of these findings, and they require replication and extension in studies with better design.
Keywords: depersonalization; derealization; dissociative amnesia; dissociative disorder; dissociative fugue; dissociative identity disorder; dissociative symptoms; genetics; genome-wide association study.