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•We tested a SEM model with BIS/BAS predicting psychopathology, and anger rumination as mediator•BIS predicted higher anxiety and depression, and BAS predicted higher aggression scores•BIS×BAS interaction only predicted anxiety symptoms•Angry memories and thoughts of revenge mediated the link between BIS and psychopathology•Implications for importance of cultivating forgiveness in individuals with high BIS sensitivity

This study investigated the longitudinal effects of the Behavioral Inhibition System (BIS) and the Behavioral Activation System (BAS) on anxiety symptomatology and tested the indirect effect of cognitive emotion regulation as a possible mechanism underlying this link. In this study, 274 individuals were assessed two times (T1 and T2), at a 5-year interval. We found an excellent fit for the hypothesized model, with BIS (T1) predicting both maladaptive cognitive emotion regulation (mCER) and T2-anxiety even after controlling for T1-anxiety. Further, mCER significantly mediated the relationship between BIS and T2-anxiety, and between T1-anxiety and T2-anxiety. However, an alternative model, supposing that BIS and T1-anxiety indirectly affect mCER through T2-anxiety, showed a similar fit. While BAS predicted higher levels of adaptive cognitive emotion regulation (aCER), it was unrelated to mCER and showed a small positive association with anxiety only at higher levels of BIS. These findings provide longitudinal support for BIS as a risk for anxiety symptoms and support the importance of targeting mCER in the prevention and treatment of anxiety, especially among individuals with BIS sensitivity. Finally, the results suggest a possible overlap between anxiety and mCER that requires further longitudinal research to clarify the direction of their relationship.

Childhood abuse and neglect (CAN) is considered as a risk factor for substance use disorder (SUD). Based on the drinking to cope model, this study investigated the association of two trauma-relevant emotions (shame and sadness) and substance use. Using ecological momentary assessment we compared real-time emotion regulation in situations with high and low intensity of shame and sadness in currently abstinent patients with CAN and lifetime SUD (traumaSUD group), healthy controls with CAN (traumaHC group), and without CAN (nontraumaHC group). Multilevel analysis showed a positive linear relationship between high intensity of both emotions and substance use for all groups. The traumaSUD group showed heightened substance use in low, as well as in high, intensity of shame and sadness. In addition, we found an interaction between type of emotion, intensity, and group: the traumaHC group exhibited a fourfold increased risk for substance use in high intense shame situations relative to the traumaSUD group. Our findings provide evidence for the drinking to cope model. The traumaSUD group showed a reduced distress tolerance for variable intensity of negative emotions. The differential effect of intense shame for the traumaHC group emphazises its potential role in the development of SUD following CAN. In addition, shame can be considered a relevant focus for therapeutic preinterventions and interventions for SUD after CAN.

The current study investigates the effect of adolescent harm avoidance (HA) on maladaptive cognitive emotion regulation strategies (mCER) in early adulthood. The mediating role of inhibitory control and the moderating effect of gender on this link were also examined. Longitudinal data from 261 adolescents (147 female) were collected in three phases (T0, T1 and T2) over approximately 10 years. Results revealed that, after controlling for HA in adulthood (T2), female adolescents' HA (T0) significantly predicted mCER strategies after 10 years (T2), whereas male adolescents' HA only predicted catastrophizing. In addition, attentional impulsivity (T1) significantly mediated the relation between HA and mCER, though only among women. There was no significant indirect effect for emotional interference and stop-signal reaction time. Results revealed gender and measure specific associations between HA and inhibitory control and suggest that HA could induce inhibitory deficits leading to mCER.