Developmental models of borderline personality disorder (BPD) emphasize the effects of youths’ biological vulnerabilities and their experiences of parental responses to emotion, as well as the interaction between these two elements. The current study evaluated the independent and interactive effects of two indices of autonomic nervous system response and parental responses to youth negative emotions on severity and exacerbation of youths’ BPD features during the transition to adolescence. The sample consisted of 162 psychiatric youth (10–14 years; 47.2% female) and their parents. At baseline, youth and their parents completed a lab-based conflict discussion during which parasympathetic and sympathetic nervous system response were measured and indices of sympathetic-parasympathetic balance and coactivation/coinhibition were calculated. Youth also reported on supportive and non-supportive parental responses. At baseline and after 9 months, youth self-reported on their BPD features. Results demonstrated that shifting toward sympathetic dominance independently predicted exacerbation of BPD across 9 months. Additionally, fewer experiences of supportive parental responses and more non-supportive parental responses were associated with greater severity of BPD features in youth. This study highlights the role of autonomic response to parent-child conflict as well as the significance of parental responses to youth emotion for the development of BPD during this developmental window.

While the Research Domain Criteria (RDoC) acknowledges that environmental and developmental influences represent important elements of the RDoC framework, there is little specificity regarding how and when to systematically examine the impact of these dimensions on domains of function. The primary aims of this paper are to demonstrate the ways in which the RDoC can be expanded to include an explicit emphasis on (a) assessing within-individual change in developmental processes over time and (b) evaluating the extent to which selective and measurable environmental influences drive meaningful change during key developmental periods. We provide data from an ongoing randomized control trial as a proof of concept to highlight how repeated assessments within an experimental intervention design affords the unique opportunity to test the impact of environmental influences on within-individual change. Using preliminary data from 77 mother–child dyads repeatedly assessed across 12 months during the sensitive preschool period, we demonstrate the impact of change in maternal emotion regulation (ER) on within-individual growth in child ER and link that growth to fewer teacher-reported externalizing problems. In line with this Special Issue, findings are discussed within the context of expanding and clarifying the existing RDoC framework to explicitly incorporate environmental and developmental dimensions.

Early threat exposure is a transdiagnostic risk factor for psychopathology, and evidence suggests that genetic variation in the oxytocin receptor (OXTR) moderates this association. However, it is unclear if this gene-by-environment (G×E) interaction is tied to unique risk for disorder-specific outcomes or instead increases shared risk for general psychopathology. Moreover, little is known about how this G×E interaction increases risk. The current study utilized a prospective, longitudinal sample of females (n = 2,020) to examine: (a) whether the interaction between early threat exposure and OXTR variation (rs53576, rs2254298) confers risk for disorder-specific outcomes (depression, anxiety, borderline and antisocial personality disorders) and/or general psychopathology in early adulthood; and (b) whether social–emotional deficits (emotion dysregulation, callousness, attachment quality) during adolescence constitute mediating mechanisms. Consistent with hypotheses, the interactive effects of early threat exposure and OXTR variation (rs53576) predicted general psychopathology, with threat-exposed women carrying at least one copy of the rs53576 A-allele at greatest risk. This interaction was mediated via emotional dysregulation in adolescence, with threat-exposed A-allele carriers demonstrating greater emotion dysregulation, and greater emotion dysregulation predicting general psychopathology in early adulthood. Findings suggest that this G×E places women at risk for a broad range of psychopathology via effects on emotion dysregulation.

Research consistently demonstrates that common polymorphic variation in monoamine oxidase A (MAOA) moderates the influence of childhood maltreatment on later antisocial behavior, with growing evidence that the “risk” allele (high vs. low activity) differs for females. However, little is known about how this Gene × Environment interaction functions to increase risk, or if this risk pathway is specific to antisocial behavior. Using a prospectively assessed, longitudinal sample of females (n = 2,004), we examined whether changes in emotional reactivity (ER) during adolescence mediated associations between this Gene × Environment and antisocial personality disorder in early adulthood. In addition, we assessed whether this putative risk pathway also conferred risk for borderline personality disorder, a related disorder characterized by high ER. While direct associations between early maltreatment and later personality pathology did not vary by genotype, there was a significant difference in the indirect path via ER during adolescence. Consistent with hypotheses, females with high-activity MAOA genotype who experienced early maltreatment had greater increases in ER during adolescence, and higher levels of ER predicted both antisocial personality disorder and borderline personality disorder symptom severity. Taken together, findings suggest that the interaction between MAOA and early maltreatment places women at risk for a broader range of personality pathology via effects on ER.