Reduced discrimination between signals of danger and safety but not overgeneralization is linked to exposure to childhood adversity in healthy adults

Abstract

AbstractExposure to adverse childhood experiences (ACEs) is a strong predictor for developing behavioral, somatic and psychopathological conditions. Exposure to threat-related early adversity has been suggested to be specifically linked to altered emotional learning as well as changes in neural circuits involved in emotional responding and fear. Learning mechanisms are particularly interesting as they are central mechanisms through which environmental inputs shape emotional and cognitive processes and ultimately behavior. Multiple theories on the mechanisms underlying this association have been suggested which, however, differ in the operationalization of ACEs. 1,402 physically and mentally healthy participants underwent a fear conditioning paradigm including a fear acquisition and generalization phase while skin conductance responses (SCRs) and different subjective ratings were acquired. ACEs were retrospectively assessed through the childhood trauma questionnaire and participants were assigned to individuals exposed or unexposed to at least moderate adverse childhood experiences according to established cut-off criteria. In addition, we provide exploratory analyses aiming to shed light on different theoretical accounts on how ACE’s impact individual risk profiles (i.e., cumulative risk account, specificity model, dimensional model). During fear acquisition training and generalization, we observed reduced discrimination in SCRs between the CS+ and the CS-, primarily due to reduced CS+ responding in exposed individuals. During fear generalization, no differences in generalization gradients were observed between exposed and unexposed individuals but generally blunted physiological responses in exposed individuals. No differences between the groups were observed in ratings in any of the experimental phases. The lower CS discrimination in SCRs in exposed individuals was evident across operationalizations according to the cumulative risk account, specificity as well as dimensional model. However, none of these theories showed clear explanatory superiority. Our results stand in stark contrast to typical patterns observed in patients suffering from anxiety and stress-related disorders (i.e., reduced CS discrimination due to increased responses to safety signals). Thus, reduced CS+ responding in individuals exposed to ACEs, yet not showing signs of psychopathology, may represent a specific characteristic of this resilient subgroup that warrants further investigation with respect to its relation to risk and resilience. In addition, we conclude that theories linking ACEs to psychopathology need refinement.