Considerable attention has been directed towards studying co-occurring psychopathology through the lens of a general factor (p-factor). However, the developmental trajectory and stability of the p-factor have yet to be fully understood. The present study examined the explanatory power of dynamic mutualism theory – an alternative framework that suggests the p-factor is a product of lower-level symptom interactions that strengthen throughout development. Data were drawn from a population-based sample of girls (N = 2450) who reported on the severity of internalizing and externalizing problems each year from age 14 to age 21. Predictions of dynamic mutualism were tested using three distinct complementary statistical approaches including: longitudinal bifactor models, random-intercept cross-lagged panel models (RI-CLPMs), and network models. Across methods, study results document preliminary support for mutualistic processes in the development of co-occurring psychopathology (that is captured in p). Findings emphasize the importance of exploring alternative frameworks and methods for better understanding the p-factor and its development.

Childhood maltreatment (CM) is a known risk factor for adolescent pregnancy. Sleep disturbances and psychological distress, both common negative sequelae of CM, often co-occur during pregnancy, although directionality remains unclear. Furthermore, little is known about how CM affects sleep–distress associations during pregnancy. In pregnant adolescents, we examined: (a) whether there are significant predictive associations from CM to sleep quality and distress and (b) bidirectional influences of distress and sleep quality. Healthy pregnant adolescents (n = 204) were recruited before or during the 2nd trimester. CM was assessed at enrollment; sleep quality and distress were assessed in the 2nd and 3rd trimesters. Hypotheses were tested using path analysis. Findings revealed that CM was associated with worse 2nd trimester sleep quality and distress (β = .19, p < .05 for sleep; β = .30, p < .001 for distress). Higher levels of 2nd trimester distress were associated with lower 3rd trimester sleep quality (β = .19, p < .05). Findings provide novel information about (a) associations from CM to prenatal mood and sleep in pregnant adolescents, and (b) sleep–distress directionality over the course of pregnancy. These results have implications for better understanding the ways in which CM potentially exerts influences later in life, and for targeting interventions to address physical and mental health during pregnancy.

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.

Emotional distress during pregnancy is likely influenced by both maternal history of adversity and concurrent prenatal stressors, but prospective longitudinal studies are lacking. Guided by a life span model of pregnancy health and stress sensitization theories, this study investigated the influence of intimate partner violence (IPV) during pregnancy on the association between childhood adversity and prenatal emotional distress. Participants included an urban, community-based sample of 200 pregnant women (aged 18–24) assessed annually from ages 8 to 17 for a range of adversity domains, including traumatic violence, harsh parenting, caregiver loss, and compromised parenting. Models tested both linear and nonlinear effects of adversity as well as their interactions with IPV on prenatal anxiety and depression symptoms, controlling for potential confounds such as poverty and childhood anxiety and depression. Results showed that the associations between childhood adversity and pregnancy emotional distress were moderated by prenatal IPV, supporting a life span conceptualization of pregnancy health. Patterns of interactions were nonlinear, consistent with theories conceptualizing stress sensitization through an “adaptive calibration” lens. Furthermore, results diverged based on adversity subdomain and type of prenatal IPV (physical vs. emotional abuse). Findings are discussed in the context of existing stress sensitization theories and highlight important avenues for future research and practice.

Childhood exposure to stress can induce prolonged negative effects on health, which in turn confer risks for the next generation, but greater specificity is needed to inform intervention. A first step is to measure individual differences in emotional reactivity to stress early in life in ways that can account for heterogeneity in child exposure. The present study tested the hypothesis that mothers’ childhood exposure to stress would be differentially associated with patterns of positive and negative emotional reactivity in their offspring, suggesting transmission of stress response across generations. Participants were 268 young mothers (age 14–23 years) followed longitudinally since childhood, and their infants aged 3–9 months. Latent class analysis of infant emotions expressed before and during the still-face paradigm yielded five subgroups that varied in valence, intensity, and reactivity. After accounting for sociodemographic factors, infant temperament, and postpartum depression, multinomial regression models showed that, relative to an emotionally regulated still-face response, infants showing low negative reactivity were more likely to have mothers exposed to childhood emotional abuse, and infants showing high and increasing negative reactivity were more likely to have mothers exposed to childhood emotional neglect. Mechanisms by which early maternal stress exposure influences emotional reactivity in offspring are discussed.

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.

Negative emotionality is a distinguishing feature of borderline personality disorder (BPD). However, this person-level characteristic has not been examined as a marker of vulnerability in the development of this disorder. The current study utilized a multimethod approach to examine the interplay between negative emotional reactivity and cumulative exposure to family adversity on the development of BPD symptoms across 3 years (ages 16–18) in a diverse, at-risk sample of adolescent girls (N = 113). A latent variable of negative emotional reactivity was created from multiple assessments at age 16: self-report, emotion ratings to stressors from ecological assessments across 1 week, and observer-rated negative affectivity during a mother–daughter conflict discussion task. Exposure to family adversity was measured cumulatively between ages 5 and 16 from annual assessments of family poverty, single parent household, and difficult life circumstances. The results from latent growth curve models demonstrated a significant interaction between negative emotional reactivity and family adversity, such that exposure to adversity strengthened the association between negative emotional reactivity and BPD symptoms. In addition, family adversity predicted increasing BPD symptoms during late adolescence. These findings highlight negative emotional reactivity as a marker of vulnerability that ultimately increases risk for the development of BPD symptoms.

Nonsuicidal self-injury (NSSI) is a common behavior among females that has been shown to confer risk for continued self-injury and suicidal attempts. NSSI can be viewed conceptually as behavior that is pathognomonic with aggression and/or depression. Empirical research on concurrent correlates supports this concept: numerous and diverse factors are shown to be significantly associated with self-harm, including depression, emotion dysregulation, impulsivity, and aggression and other conduct problems, as well as environmental stressors such as bullying, harsh parenting, and negative life events. In the present study, we test hypotheses regarding developmental precursors (measured from ages 8 to 12 years) to NSSI in young adolescent girls (ages 13–14 years), specifically whether aggression, depression, and environmental stressors distinguish girls with and without self-harm, and whether there is evidence for multiple developmental pathways to NSSI. Data were derived from the longitudinal Pittsburgh Girls Study. In this community sample of girls, the prevalence of NSSI at ages 13 or 14 years of age was 6.0%. Initial levels in dimensions measured within the depression, aggression, and environmental stressor domains accounted for variance in NSSI in early adolescence. Changes over time in relational aggression and assertiveness were also significantly associated with risk for NSSI. To a large extent, adolescent NSSI was predicted by psychological deficits and stress exposure that began early in childhood. Risk indices were calculated using the 85th or 15th percentile. Close to 80% of girls who engaged in NSSI during adolescence were identified by at least one risk domain in childhood. A sizable proportion of adolescent girls who later engaged in NSSI had childhood risk scores in all three domains; the remaining girls with adolescent NSSI were relatively evenly distributed across the other risk domain profiles. The observation that multiple pathways to NSSI exist suggests that deficits underlying the behavior may vary and require different modes of prevention.

Theories of borderline personality disorder (BPD) postulate that high-risk transactions between caregiver and child are important for the development and maintenance of the disorder. Little empirical evidence exists regarding the reciprocal effects of parenting on the development of BPD symptoms in adolescence. The impact of child and caregiver characteristics on this reciprocal relationship is also unknown. Thus, the current study examines bidirectional effects of parenting, specifically harsh punishment practices and caregiver low warmth, and BPD symptoms in girls aged 14–17 years based on annual, longitudinal data from the Pittsburgh Girls Study (N = 2,451) in the context of child and caregiver characteristics. We examined these associations through the use of autoregressive latent trajectory models to differentiate time-specific variations in BPD symptoms and parenting from the stable processes that steadily influence repeated measures within an individual. The developmental trajectories of BPD symptoms and parenting were moderately associated, suggesting a reciprocal relationship. There was some support for time-specific elevations in BPD symptoms predicting subsequent increases in harsh punishment and caregiver low warmth. There was little support for increases in harsh punishment and caregiver low warmth predicting subsequent elevations in BPD symptoms. Child impulsivity and negative affectivity, and caregiver psychopathology were related to parenting trajectories, while only child characteristics predicted BPD trajectories. The results highlight the stability of the reciprocal associations between parenting and BPD trajectories in adolescent girls and add to our understanding of the longitudinal course of BPD in youth.