DNA methylation differences with respect to early life adversity and social anxiety disorder

 

Introduction Social anxiety disorder (SAD) is a severe mental disorder characterized by an excessive fear of negative evaluation, being the focus of attention and embarrassing oneself. The etiology of anxiety is influenced by genetic as well as environmental factors, most importantly stressful life events. The contribution of early life adversities (ELA) to pathophysiological processes which lead to an increased risk for SAD later in life, has been consistently described. The underlying biological mechanisms are still poorly understood, but evidence is emerging that epigenetic regulation of gene expression like DNA methylation is involved in mediating this effect.

Methods For the present study, we investigated genome-wide whole blood DNA methylation of 143 participants of Caucasian descent. SAD status was determined by a Structured Clinical Interview for DSM-IV (SCID) and ELA was assessed using the Childhood Trauma Questionnaire (CTQ). Thus, four groups emerged: healthy controls with low (n = 47) and high (n = 30) levels of ELA and patients suffering SAD with low (n = 35) and high levels of ELA (n = 31).

Results Several differentially methylated regions (DMRs) were identified with respect to SAD and ELA as well as their interaction. Amongst others, these DMRs are associated with genes of the solute carrier (SLC) family.

Conclusion Our results support the idea that epigenetic mechanisms are involved in pathophysiological processes underlying psychiatric disorders but further studies are needed to increase power and to investigate the underlying pathways.