Adverse childhood experiences (ACEs) have an impact on women's adaptation to parenthood, but mechanisms are poorly understood. Autonomic nervous system reactivity was tested as a potential mediating mechanism in a sample of 193 at-risk primiparous women. ACEs were measured retrospectively during pregnancy. A baby cry-response task was administered during pregnancy while indicators of sympathetic reactivity (pre-ejection period; PEP) and parasympathetic reactivity (respiratory sinus arrhythmia; RSA) were recorded. Parenting self-efficacy, anxiety, and depressive symptoms were measured during pregnancy and 1 year after giving birth. Harsh discipline was measured 2 years after giving birth. Structural equation modeling was employed to test whether baseline PEP and RSA and reactivity mediated links between ACEs and postnatal outcomes, adjusted for prenatal variables. High ACEs predicted less RSA reactivity (p = .02), which subsequently predicted increases in depressive symptoms (p = .03). The indirect effect was not significant (p = .06). There was no indirect link between high ACEs and harsh parenting through PEP nor RSA (n = 98). The parasympathetic nervous system may be involved in negative affective responses in the transition to parenthood among women exposed to childhood trauma.

Understanding factors increasing susceptibility to social contexts and predicting psychopathology can help identify targets for prevention. Persistently high externalizing behavior in adolescence is predictive of psychopathology in adulthood. Parental monitoring predicts low externalizing behavior, yet youth likely vary in the degree to which they are affected by parents. Genetic variants of GABA receptor subunit alpha-2 (GABRA2) may increase susceptibility to parental monitoring, thus impacting externalizing trajectories. We had several objectives: (a) to determine whether GABRA2 (rs279827, rs279826, rs279858) moderates the relationship between a component of parental monitoring, parental knowledge, and externalizing trajectories; (b) to test the form of this interaction to assess whether GABRA2 variants reflect risk (diathesis–stress) or susceptibility (differential susceptibility) factors; and (c) to clarify GABRA2 associations on the development of problem behavior. This prospective study (N = 504) identified three externalizing trajectory classes (i.e., low, decreasing, and high) across adolescence. A GABRA2 × Parental Monitoring effect on class membership was observed, such that A-carriers were largely unaffected by parental monitoring, whereas class membership for those with the GG genotype was affected by parental monitoring. Findings support differential susceptibility in GABRA2.

Accumulating behavioral and genetic research suggests that most forms of psychopathology share common genetic and neural vulnerabilities and are manifestations of a relatively few core underlying processes. These findings support the view that comorbidity mostly arises, not from true co-occurrence of distinct disorders, but from the behavioral expression of shared vulnerability processes across the life span. The purpose of this review is to examine the role of the prefrontal cortex (PFC) in the shared vulnerability mechanisms underlying the clinical phenomena of comorbidity from a transdiagnostic and ontogenic perspective. In adopting this perspective, we suggest complex transactions between neurobiologically rooted vulnerabilities inherent in PFC circuitry and environmental factors (e.g., parenting, peers, stress, and substance use) across development converge on three key PFC-mediated processes: executive functioning, emotion regulation, and reward processing. We propose that individual differences and impairments in these PFC-mediated functions provide intermediate mechanisms for transdiagnostic symptoms and underlie behavioral tendencies that evoke and interact with environmental risk factors to further potentiate vulnerability.

Maltreatment adversely impacts the development of children across a host of domains. One way in which maltreatment may exert its deleterious effects is by becoming embedded in the activity of neurophysiological systems that regulate metabolic function. This paper reviews the literature regarding the association between childhood maltreatment and the activity of three systems: the parasympathetic nervous system, the sympathetic nervous system, and the hypothalamic–pituitary–adrenal axis. A particular emphasis is placed on the extent to which the literature supports a common account of activity across these systems under conditions of homeostasis and stress. The paper concludes with an outline of directions for future research and the implications of the literature for policy and practice.

Two studies examined the nature and processes underlying the joint role of interparental aggression and maternal antisocial personality as predictors of children's disruptive behavior problems. Participants for both studies included a high-risk sample of 201 mothers and their 2-year-old children in a longitudinal, multimethod design. Addressing the form of the interplay between interparental aggression and maternal antisocial personality as risk factors for concurrent and prospective levels of child disruptive problems, the Study 1 findings indicated that maternal antisocial personality was a predictor of the initial levels of preschooler's disruptive problems independent of the effects of interparental violence, comorbid forms of maternal psychopathology, and socioeconomic factors. In attesting to the salience of interparental aggression in the lives of young children, latent difference score analyses further revealed that interparental aggression mediated the link between maternal antisocial personality and subsequent changes in child disruptive problems over a 1-year period. To identify the family mechanisms that account for the two forms of intergenerational transmission of disruptive problems identified in Study 1, Study 2 explored the role of children's difficult temperament, emotional reactivity to interparental conflict, adrenocortical reactivity in a challenging parent–child task, and experiences with maternal parenting as mediating processes. Analyses identified child emotional reactivity to conflict and maternal unresponsiveness as mediators in pathways between interparental aggression and preschooler's disruptive problems. The findings further supported the role of blunted adrenocortical reactivity as an allostatic mediator of the associations between parental unresponsiveness and child disruptive problems.

The influence of five monoamine candidate genes on depressive symptom trajectories in adolescence and young adulthood were examined in the Add Health genetic sample. Results indicated that, for all respondents, carriers of the dopamine receptor D4 5-repeat allele were characterized by distinct depressive symptom trajectories across adolescence and early adulthood. Similarly, for males, individuals with the monoamine oxidase A 3.5-repeat allele exhibited unique depressive symptom trajectories. Specifically, the trajectories of those with the dopamine receptor D4 5-repeat allele were characterized by rising levels in the transition to adulthood, while their peers were experiencing a normative drop in depressive symptom frequency. Conversely, males with the monoamine oxidase A 3.5-repeat allele were shown to experience increased distress in late adolescence. An empirical method for examining a wide array of allelic combinations was employed, and false discovery rate methods were used to control the risk of false positives due to multiple testing. Special attention was given to thoroughly interrogate the robustness of the putative genetic effects. These results demonstrate the value of combining dynamic developmental perspectives with statistical genetic methods to optimize the search for genetic influences on psychopathology across the life course.

Nicki Crick initiated a generative line of theory and research aimed at exploring the implications of exposure to overt and relational aggression for youth development. The present study aimed to continue and expand this research by examining whether early (second grade) and increasing (second–sixth grade) levels of victimization during elementary school contributed to youths’ tendencies to move against, away from, or toward the world of peers following the transition to middle school. Youth (M age in second grade = 7.96 years, SD = 0.35; 338 girls, 298 boys) reported on their exposure to victimization and their social goals (performance-approach, performance-avoidance, or mastery). Teachers reported on youths’ exposure to victimization and their engagement in antisocial, socially helpless, and prosocial behavior. Latent growth curve analyses revealed that early and increasing levels of both overt and relational victimization uniquely contributed to multifinality in adverse developmental outcomes, predicting all three social orientations (high conflictual engagement, high disengagement, and low positive engagement). The pattern of effects was robust across sex and after adjusting for youths’ early social motivation. These findings confirm that both forms of victimization leave an enduring legacy on youths’ social health in adolescence. Given that profiles of moving against and away from the world can contribute to subsequent psychopathology, understanding and preventing this legacy is pivotal for developing effective intervention programs aimed at minimizing the effects of peer adversity.

The field of developmental psychopathology has seen growth in research focusing on interdisciplinarity and normative developmental processes, including context-linked coping and adaptations. However, there continues to be an uncomfortable and unarticulated perspective to view others as having culture and “the self” as representing the standard. A call for explicit cultural considerations in research is needed to augment the impact of these new and other significant conceptual contributions noted. Sociopolitical influences on social contexts relevant to the different trajectories associated with youths' opportunities and challenges are presented. We focus on macrolevel factors that frame contexts in which individual development occurs. A federal and educational policy is used to illustrate how unexamined cultural traditions and patterns embedded in research and policy impact development. These examples provide insight in presenting issues of vulnerability, particularly for youth, and afford opportunities to present advances and challenges paralleled in the developmental psychopathology field.

Poor self-regulation has been implicated as a significant risk factor for the development of multiple forms of psychopathology. This research examined the proposition that self-regulation deficits differentially predict aggressive behavior and depressive symptoms, depending on children's social approach versus avoidance motivation. A prospective, multiple-informant approach was used to test this hypothesis in 419 children (M age = 8.92, SD = 0.36). Parents rated children's inhibitory control. Children completed measures of social approach–avoidance motivation and depressive symptoms. Teachers rated children's aggressive behavior. As anticipated, poor inhibitory control predicted aggressive behavior in boys with high but not low approach motivation and low but not high avoidance motivation, whereas poor inhibitory control predicted depressive symptoms in girls with high but not low avoidance motivation. This research supports several complementary theoretical models of psychopathology and provides insight into the differential contributions of poor self-regulation to maladaptive developmental outcomes. The findings suggest the need for targeted intervention programs that consider heterogeneity among children with self-regulatory deficits.

The present paper focuses on the trait domain of conscientiousness, its development, and its relation to psychopathology. The definition of conscientiousness and its interface with specific forms of psychopathology, such as externalizing psychopathology, are discussed first. Then an overview of the known developmental changes in conscientiousness across the life course is provided, as well as the potential shared developmental etiology of conscientiousness and externalizing psychopathology. Given the lack of data, testing etiological factors that may contribute to the development of both conscientiousness and externalizing disorders, we report on three studies examining the childhood experiences associated with both conscientiousness and externalizing behaviors. Last, future directions are discussed.

Despite the substantial heritability of nearly all psychological traits, it has been difficult to identify specific genetic variants that account for more than a tiny percentage of genetic variance in phenotypes. Common explanations for this “missing heritability” include massive polygenicity, rare variants, epigenetics, epistasis, and gene–environment interactions. Gene–trait (G × T) interaction is another concept useful for understanding the lack of obvious genetic main effects. Both genes and environments are distal contributors to human behavior, but the brain is the proximal driver of behavior. The effect of any single genetic variant is dependent on the configuration of the brain in which it is expressed. One method to begin studying how single genes interact with variations in the rest of the brain is to investigate G × T interactions. A psychological trait reflects a characteristic pattern of psychological function (and, therefore, of brain function), which has its origin in the cumulative effects of both the genome and the environment. A trait therefore describes variation in the broad organismic context in which any single gene operates. We describe the nature and significance of G × T interactions for understanding psychopathology and normal trait variation, which are illustrated with empirical examples.

Researchers have long been interested in whether particular temperamental traits in childhood connote risk for depressive disorders. For example, children characterized as having high negative emotionality (NE; sadness, fear, anger) and low positive emotionality (PE; anhedonia, listlessness, and lack of enthusiasm) are hypothesized to be at risk for depression. Few studies, however, have examined whether (and how) these two temperamental dimensions interact to confer risk. In a sample of 329 preschoolers, the present study addressed this question by examining the relation between PE and NE and asymmetry in resting EEG activity in frontal and posterior regions, which are putative biomarkers for depression. Using a laboratory battery to define temperament, we found an interaction of PE and NE on posterior asymmetry. Specifically, when PE was high, NE was associated with greater relative right activity. When PE was low, NE was not related to posterior asymmetry. These results were driven by differences in EEG activity in right posterior regions, an area associated with emotional processing and arousal, and were specific to girls. We found no relation between temperament and frontal asymmetry. These findings suggest that, at least for girls, PE and NE may have an interactive effect on risk for depression.

Despite extensive theoretical and empirical advances in the last two decades, little attention has been paid to the development of statistical techniques suited for the analysis of data gathered in studies of developmental psychopathology. As in most other studies of developmental processes, research in this area often involves complex constructs, such as intelligence and antisocial behavior, measured indirectly using multiple observed indicators. Relations between pairs of such constructs are sometimes reported in terms of latent variables (LVs): linear combinations of the indicators of each construct. We introduce the assumptions and procedures associated with one method for exploring these relations: partial least squares (PLS) analysis, which maximizes covariances between predictor and outcome LVs; its coefficients are correlations between observed variables and LVs, and its LVs are sums of observable variables weighted by these correlations. In the least squares logic of PLS, familiar notions about simple regressions and principal component analyses may be reinterpreted as rules for including or excluding particular blocks in a model and for “splitting” blocks into multiple dimensions. Guidelines for conducting PLS analyses and interpreting their results are provided using data from the Goteborg Daycare Study and the Seattle Longitudinal Prospective Study on Alcohol and Pregnancy. The major advantages of PLS analysis are that it (1) concisely summarizes the intercorrelations among a large number of variables regardless of sample size, (2) yields coefficients that are readily interpretable, and (3) provides straightforward decision rules about modeling. The advantages make PLS a highly desirable technique for use in longitudinal research on developmental psychopathology. The primer is written primarily for the nonstatistician, although formal mathematical details are provided in Appendix 1.

Exposure to childhood adversity is a critical risk factor for the development of psychopathology. A growing field of research examines how exposure to childhood adversity is translated into biological risk for psychopathology through alterations in immune system functioning, most notably heightened levels of inflammation biomarkers. Though our knowledge about how childhood adversity can instantiate biological risk for psychopathology is growing, there remain many challenges and gaps in the field to understand how inflammation from childhood adversity contributes to psychopathology. This paper reviews research on the inflammatory outcomes arising from childhood adversity and presents four major challenges that future research must address: (a) the measurement of childhood adversity, (b) the measurement of inflammation, (c) the identification of mediators between childhood adversity and inflammation, and (d) the identification of moderators of inflammatory outcomes following childhood adversity. We discuss synergies and inconsistencies in the literature to summarize the current understanding of the association between childhood adversity, a proinflammatory phenotype, and the biological risk for psychopathology. We discuss the clinical implications of the inflammatory links between childhood adversity and psychopathology, including possibilities for intervention. Finally, this review conclude by delineates future directions for research, including issues of how best to detect, prevent, and understand these “hidden wounds” of childhood adversity.

An important function of the brain is to scan incoming sensory information for the presence of relevant signals and act on this information. For humans, the most salient signals are often social in nature, such as the identity and the emotional expression of the faces we encounter in our everyday lives. It can be argued that our survival as a species depends in large measure on these skills.

Family Minds is a brief group psychoeducational parenting intervention designed to increase the reflective functioning (RF) and mentalization skills of foster parents. RF is important for foster parents who have to build relationships with children whose adverse experiences increase their risk for psychosocial challenges. A randomized controlled trial (RCT) for Family Minds was conducted in Texas with 89 foster parents. The main aims of this study were to examine whether the intervention could significantly increase the RF/mentalization skills of the foster parents and decrease their parenting stress. After 6 weeks, compared with the control group, intervention foster parents improved their RF via a lowering of pre-mentalizing and also significantly decreased parenting stress related to parent–child dysfunctional interactions. Other measures of RF and parenting stress showed no significant differences between groups. Foster child behavior was not significantly different between groups, although data at 6 months showed a possible lowering of internalizing symptoms for children of intervention parents. This RCT provides some encouraging evidence that Family Minds may increase RF in foster parents, improve parental sensitivity and their ability to emotionally regulate, decrease parenting stress related to challenging interactions with their foster children, and possibly decrease children's internalizing behavior.

The interplay of parenting and environmental sensitivity on children’s behavioral adjustment during, and immediately after, the COVID-19 lockdown restrictions was investigated in two longitudinal studies involving Italian preschoolers (Study 1, N = 72; 43% girls, Myears = 3.82(1.38)) and primary school children (Study 2, N = 94; 55% girls, Myears = 9.08(0.56)). Data were collected before and during the first-wave lockdown (Studies 1 and 2) and one month later (Study 1). Parental stress and parent–child closeness were measured. Markers of environmental sensitivity in children were temperamental fearfulness and Sensory Processing Sensitivity. Results showed little change in externalizing and internalizing behaviors over time, but differences emerged when considering parenting and children’s environmental sensitivity. In preschoolers, greater parenting stress was related to a stronger increase in internalizing and externalizing behaviors, with children high in fearful temperament showing a more marked decrease in externalizing behaviors when parenting stress was low. In school-aged children, parent–child closeness emerged as a protective factor for internalizing and externalizing behaviors during COVID-19, with children high in Sensory Processing Sensitivity showing a marked decrease in internalizing behaviors when closeness was high. Implications for developmental theory and practice in times of pandemic are discussed.

In this paper I review evidence and viewpoints on developmental plasticity in the cerebral cortex. Although there is some degree of plasticity in the cortex during early postnatal life in the human infant, this plasticity is constrained by various factors. Three working hypotheses about postnatal cortical specialization of function are advanced, and some specific predictions about the limits and extent of plasticity are assessed through both empirical evidence from infants and simulations on simple cortical network models.

This article considers the implications of theory and research in developmental psychopathology for existing and emerging social policy concerning treatment of child and adolescent psychopathology. Based on the concept that all psychopathology is a process, four core principles of a developmental psychopathology perspective are discussed. In turn, each is applied to an evaluation of policy issues with implications for intervention, including mental health parity, treatment guidelines, mental health reimbursement, and level of intervention. It is concluded that social policy on treatment must be based on an empirically supported theory of developmental psychopathology and on evidence-based interventions that link treatments to pathogenic processes.