There is an extensive literature on the negativity bias, including its conceptualization, measurement, temporal stability (individual differences), and neural and genetic associations. Hibbing et al. posit that the difference across individuals in the negativity bias is a key factor in determining political predisposition. The measures and paradigms developed in this literature provide a means of testing this hypothesis.

Patient characteristics may partly explain individual differences in long-term maintenance of treatment gains in response to cognitive and behavioral therapies (CBT). This study evaluated the relative contribution of negative cognitive style, behavioral activation, and personality patterns, measured at the end of treatment among treatment responders, towards the risk of relapse of major depressive disorder over a 2-year prospective follow-up. The sample included depressed adults who were randomized and received an adequate dose of one of three forms of CBT, who then fully responded and completed a 2-year prospective follow-up (N = 93) (Jacobson et al., 1996; Gortner, Gollan, Dobson and Jacobson, 1998). Cox regression analyses revealed that for treatment responders, self-devaluative depressogenic cognitive style did not predict relapse during the 2-year follow-up. Separate cox regression analyses indicated that without considering the contribution of personality patterns, it was important to distinguish the level of behavioral activation (e.g. frequency of pleasant events) from its associated pleasure in predicting relapse. With the introduction of personality patterns; however, an integrated model revealed that only dependent personality pattern was associated with hazard of relapse during the 2-year prospective follow-up. Dependent personality pattern may increase relapse through behavioral passivity.

The aim of this paper is to clarify how neural mechanisms at the molecular level, specifically the serotonergic (5-HT) system and the hypothalamic–pituitary–adrenal axis system (HPA) in conjunction with early life stress may contribute to the emergence of aggression, self-directed and otherwise, in borderline personality disorder (BPD). Chronic dysregulation of these biological systems, which function to regulate stress and emotion, may potentiate the development of impulsive aggression in borderline personality conditions. Our central premise in this paper is that brain development, stress regulation, and early pathonomic experience are interactive and cumulative in their mutual influence on the development of impulsive aggression in BPD. We review the parameters of impulsive aggression in BPD, followed by a discussion of the neurobiological and neuroendocrine correlates of impulsive aggression with and without BPD. We then focus on the developmental continuities in BPD with attention to brain maturation of 5-HT and HPA axis function during the life span and the influence of early adverse experiences on these systems. Finally, we comment on the data of the relative stability of aggression in BPD, adolescence as a developmental stage of potential vulnerability, and the course of aggressive behavior during the life span.The authors thank Caroline Cozza, Michael McCloskey, and Kurt Knoblett for their comments during the preparation of this manuscript. This research was supported by research funding from the American Foundation of Suicide Prevention (J.K.G.), Grant MH066888-01 (R.L.), and the Borderline Personality Disorder Research Foundation (E.F.C.).