Adverse childhood experiences and internalizing symptoms: the moderating role of neural responses to threat

Abstract

Adverse childhood experiences (ACEs) increase vulnerability to internalizing symptoms, namely symptoms characterized primarily by processes within the self, such as anxiety and depression, but the underlying processes are still unclear. One possible mechanism is that ACEs alter the neural correlates responsible for the preferential processing unpleasant stimuli, a key feature of anxiety. Another mechanism could be a stress-induced disruption in the processing of pleasant stimuli, which is mostly linked with depressive symptoms. In this study, we examined how ACEs and neural correlates of different emotional processing stages (affective engagement, anticipation, elaboration) interact in the association with internalizing symptoms in a sample of university students (n = 46, 28 females). Participants completed the Adverse Childhood Experiences Questionnaire (ACE-Q), and the anxiety and depression subscale of the Brief Symptoms Inventory Checklist to assess depression and anxiety. An S1-S2 paradigm, a task in which a cue (S1) anticipates the valence of a succeeding emotional image (S2), was used during an electroencephalographic (EEG) recording. Three event-related potentials (ERPs) reflecting different stages of emotional processing were assessed: the Cue-P300 (reflecting cue-evaluation and affective engagement), the Stimulus Preceding Negativity (SPN; reflecting outcome anticipation), and the P300/late positive potential (LPP) complex (reflecting affective processing). ACEs were linked to greater P300/LPP for unpleasant stimuli, suggesting that childhood adversities may be related to increased elaboration of threatening information. Moreover, ACEs were associated with dampened engagement (Cue-P300) and processing (P300/LPP) of pleasant content. Interestingly, the interaction between the P300/LPP to unpleasant stimuli and ACEs was significantly associated with greater symptoms of anxiety, whereas there was no effect in the link with depression. Specifically, individuals exposed to ACEs only reported heightened anxiety symptoms when their P300/LPP complex to unpleasant stimuli was larger. No significant effect emerged for the other ERPs components. Taken together, these findings suggest that an increased sensitivity to unpleasant content in adulthood might moderate the association between ACEs and anxiety symptoms.