Dysregulation in children's physiological stress systems is a key process linking early adversity to poor health and psychopathology. Thus, interventions that improve children's stress physiology may help prevent deleterious health outcomes. Reminiscing and Emotion Training (RET) is a brief relational intervention designed to improve maternal caregiving support by enhancing maltreating mothers’ capacity to reminisce with their young children. This study evaluated associations between maltreatment, intimate partner violence, and the RET intervention with changes in children's diurnal cortisol regulation across the 1 year following the intervention, and the extent to which improvements in maternal elaborative reminiscing differed between intervention groups and mediated change in children's physiological functioning. Participants were 237 children (aged 36 to 86 months) and their mothers. Results indicated that the RET intervention was associated with significant positive change in elaborative reminiscing, which was sustained over time. Mothers’ elaboration immediately after the intervention served as a mediator of RET's effects on improvements in children's diurnal cortisol regulation (steeper diurnal slopes) from baseline to 1 year following intervention. This suggests RET is effective in facilitating physiological regulation among maltreated children.

Discrimination has been associated with adverse mental health outcomes, though it is unclear how early in life this association becomes apparent. Implicit emotion regulation, developing during childhood, is a foundational skill tied to a range of outcomes. Implicit emotion regulation has yet to be tested as an associated process for mental illness symptoms that can often emerge during this sensitive developmental period. Youth aged 9–11 were recruited for the Adolescent Brain Cognitive Development (ABCD) study. Associations between psychotic-like experiences, depressive symptoms, and total discrimination (due to race, ethnicity, nationality, weight, or sexual minority status) were tested, as well as associations with implicit emotion regulation measures (emotional updating working memory and inhibitory control). Analyses examined whether associations with symptoms were mediated by implicit emotion regulation. Discrimination related to decreased implicit emotion regulation performance, and increased endorsement of depressive symptoms and psychotic-like experiences. Emotional updating working memory performance partially mediated the association between discrimination and psychotic-like experiences, while emotional inhibitory control did not. Discrimination and implicit emotion regulation could serve as putative transdiagnostic markers of vulnerability. Results support the utility of using multiple units of analysis to improve understanding of complex emerging neurocognitive functions and developmentally sensitive periods.

The United States is entering a pivotal period in history, led by extraordinary shifts in the demographic makeup of children who are in need of medical, educational, and developmental services. For the first time in this country's history, the majority of children are being born to non-white populations. Simultaneously, racism (personal, institutional, and systemic) is now being recognized as a powerful social determinant of children's mental and physical health by the time they enter kindergarten. It is crucial to evaluate how early childhood development (ECD) settings are prepared to authentically engage racially diverse children. In this paper, we critically analyze the narratives of the architect of Head Start, Dr. Edward Zigler, and investigate his evolving contributions to early childhood programming. We propose that Zigler's conceptualization of culture and its impact on children's development, although advanced for his time, had historical limitations that have perpetuated the personal, institutional, and systemic racism that children of color experience in early childhood settings. This paper concludes with suggestions to include topics covering implicit bias, white privilege, and the impact of slavery, colonization, and oppression as core principles in professional training. Only then will we be able to eliminate racism across early childhood settings in the United States.

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.

The way that people internalize adverse experiences plays an important role in the development of psychopathology. The Pathogenic Belief Scale (PBS) is intended to operationalize a transtheoretical understanding of repetitive patterns of emotion-laden beliefs that develop in childhood and continue to influence people's current experience. Using a cross-sectional survey design, we recruited a large heterogeneous sample of 246 clinic outpatients and 732 adults in the community. Besides the PBS, measures of adverse parenting experiences and common psychopathology were administered. An exploratory factor analysis of the total sample of 978 participants was conducted followed by a convergent validity analysis for the 246 clinic outpatients. The three-factor solution included “cannot rely on others,” “undeserving,” and “interpersonal guilt,” and it showed good psychometric properties, including convergent validity with the measures of adverse parenting experiences and psychopathology. The 34-item PBS offers a promising self-report measure that could help delineate and understand the pathogenic beliefs that heterogeneous samples of patients may hold. Pathogenic beliefs may be relevant to the psychotherapy process, regardless of model or theoretical context.

Aggression coincides with emotional underarousal in childhood, but we still lack an understanding of how underarousal contributes to aggression. With an ethnically diverse sample of 8-year-olds (N = 150), we tested whether physiological underarousal and lower fear recognition were indirectly associated with heightened aggression through dampened guilt feelings. Caregivers rated children's aggressive behavior. We assessed children's skin conductance (SC) and respiratory sinus arrhythmia (RSA) while they imagined transgressing norms and measured their fear recognition with a facial morph task. Children reported guilt or lack thereof after hypothetically transgressing. The interaction of decreasing SC and increasing RSA (i.e., physiological underarousal) and poor fear recognition were indirectly associated with higher aggression through their associations with lower guilt. Emotional underarousal may contribute to aggression by disrupting the normative development of guilt. We discuss strategies to improve social-emotional acuity and reduce aggression in children with blunted physiological arousal and fear recognition.

Over 50% of adoptions are transracial, involving primarily White parents and children of color from different ethnic or racial backgrounds. Transracial adoptive (TRA) parents are tasked with providing ethnic–racial socialization processes (ERS) to support TRA adoptees’ ethnic–racial identity development and prepare them to cope with ethnic–racial discrimination. However, unlike nonadoptive families of color, TRA parents lack shared cultural history with adoptees and have limited experience navigating racial discrimination. Knowledge of ERS among TRA families has centered on unidirectional processes between parenting constructs, ERS processes, and children's functioning. However, ERS processes in this population have complexities and nuances that warrant more sensitive and robust conceptualization. This paper proposes a process-oriented dynamic ecological model of the system of ERS, situating transacting processes in and across multiple family levels (parent, adoptee, family) and incorporating developmental and contextual considerations. With its framing of the complexities in ERS among TRA families, the model offers three contributions: a conceptual organization of parenting constructs related to ERS, a more robust understanding of ERS processes that inform how parents provide ERS, and framing of transacting processes within and between parenting constructs, ERS processes, and children's functioning. Implications for research, policy, and practice are discussed.

Chronic health conditions are hypothesized to disrupt the typical trajectory of child and adolescent development, and subsequently lead to increased levels of mental illness. However, due to methodological limitations in existing studies, this theory remains to be fully substantiated by empirical research. This study aimed to more thoroughly test hypotheses in the field. This study used data from the Avon Longitudinal Study of Parents and Children to examine the co-occurrence of mental illness among children with chronic illness in late childhood into early adolescence and explore mediating factors in these outcomes. Children with chronic health problems presented with a disproportionate rate of psychiatric illness at 10 years, and these chronic health problems continued to be associated with poor mental health outcomes at 13 years and 15 years. These outcomes were mediated by high levels of peer victimization and health-related school absenteeism. This study suggests that chronic illness may impact on functioning and social development in early adolescence, and consequently lead to increased rates of mental illness. Examining rates of school absenteeism and peer victimization may be key to identifying children at risk over time.

Childhood adversity appears to sensitize youth to stress, increasing depression risk following stressful life events occurring throughout the lifespan. Some evidence suggests hypothalamic–pituitary–adrenal (HPA) axis-related and serotonergic genetic variation moderates this effect, in a “gene-by-environment-by-environment” interaction (G × E × E). However, prior research has tested single genetic variants, limiting power. The current study uses a multilocus genetic profile score (MGPS) approach to capture polygenic risk relevant to HPA axis and serotonergic functioning. Adolescents (N = 241, Mage = 15.90) completed contextual-threat-based interviews assessing childhood adversity and acute life events, and diagnostic interviews assessing depression. Established MGPSs indexed genetic variation linked to HPA axis (10 single nucleotide polymorphisms [SNPs]) and serotonergic (five SNPs) functioning. Results showed significant MGPS × Childhood Adversity × Recent Life Stress interactions predicting depression for both HPA axis and serotonergic MGPSs, with both risk scores predicting stronger Childhood Adversity × Recent Stress interactions. Serotonergic genetic risk specifically predicted sensitization to major interpersonal stressors. The serotonergic MGPS G × E × E was re-tested in an independent replication sample of early adolescent girls, with comparable results. Findings support the notion that genetic variation linked to these two neurobiological symptoms alters stress sensitization, and that gene-by-environment (G × E) interactions may be qualified by environmental exposures occurring at different points in development.

The relationships infants and young children have with their caregivers are fundamental to their survival and well-being. Theorists and researchers across disciplines have attempted to describe and assess the variation in these relationships, leading to a general acceptance that caregiving is critical to understanding child functioning, including developmental psychopathology. At the same time, we lack consensus on how to assess these fundamental relationships. In the present paper, we first review research documenting the importance of the caregiver–child relationship in understanding environmental risk for psychopathology. Second, we propose that the National Institute of Mental Health's Research Domain Criteria (RDoC) initiative provides a useful framework for extending the study of children's risk for psychopathology by assessing their caregivers’ social processes. Third, we describe the units of analysis for caregiver social processes, documenting how the specific subconstructs in the domain of social processes are relevant to the goal of enhancing knowledge of developmental psychopathology. Lastly, we highlight how past research can inform new directions in the study of caregiving and the parent–child relationship through this innovative extension of the RDoC initiative.

Maternal stress during pregnancy can cause alterations to the fetal hypothalamus–pituitary–adrenal (HPA) axis, a phenomenon known as fetal programming that may have lasting effects on offspring outcomes, including depression. Evidence suggests that these effects may vary with respect to the offspring's genetic risk. Nonetheless, few studies have examined these effects into adulthood, when risk for depression onset is highest. The present study builds upon the extant literature by examining the interaction of maternal prenatal perceived stress (MPPS) and offspring HPA-axis polygenic risk to predict offspring depression in early adulthood. A total of 381 mother–child dyads participated in a prospective, longitudinal study that spanned from pregnancy until offspring were 20 years of age. Polygenic risk was defined by a multilocus genetic profile score (MGPS) that reflected the additive risk of three HPA-axis candidate genes. The results indicated that the interaction of MPPS and HPA-axis MGPS confers risk for offspring depression at age 20, in line with the differential susceptibility model. This interaction may be specific to prenatal stress, as maternal stress during early childhood did not interact with genetic risk to predict depression. These findings provide the first evidence that genetic variants that are associated with the HPA axis may act in a polygenic, additive fashion to moderate the association between fetal programming and adult depression.

Maternal depression is associated with instability within the family environment and increases in offspring substance use across adolescence. Rates of delay discounting, or the tendency to select smaller rewards that are immediately available relative to larger, but delayed rewards, are also associated with steeper increases in substance use among youth. Moreover, recent research suggests that early unstable environments may reinforce youths’ propensity towards opportunistic decision making and delay discounting specifically. The current prospective, longitudinal study examined links between maternal depressive symptoms, adolescent delay discounting, and subsequent substance use. Participants included 247 adolescents and their mothers who were assessed annually over a 6-year period (from ages 13 to 19 years). Results supported a small but significant mediation effect. Specifically, maternal depressive symptoms predicted increases in adolescent delay discounting, which, in turn, predicted steeper increases in adolescent substance use over time. Thus, youth decision making may represent a mechanism linking maternal depression and adolescent risk behaviors. Findings indicate the potential for interventions targeting parental psychopathology to prevent subsequent adolescent substance use.

The National Institute of Mental Health's Research Domain Criteria (RDoC) framework has prompted a paradigm shift from categorical psychiatric disorders to considering multiple levels of vulnerability for probabilistic risk of disorder. However, the lack of neurodevelopmentally based tools for clinical decision making has limited the real-world impact of the RDoC. Integration with developmental psychopathology principles and statistical methods actualize the clinical implementation of RDoC to inform neurodevelopmental risk. In this conceptual paper, we introduce the probabilistic mental health risk calculator as an innovation for such translation and lay out a research agenda for generating an RDoC- and developmentally informed paradigm that could be applied to predict a range of developmental psychopathologies from early childhood to young adulthood. We discuss methods that weigh the incremental utility for prediction based on intensity and burden of assessment, the addition of developmental change patterns, considerations for assessing outcomes, and integrative data approaches. Throughout, we illustrate the risk calculator approach with different neurodevelopmental pathways and phenotypes. Finally, we discuss real-world implementation of these methods for improving early identification and prevention of developmental psychopathology. We propose that mental health risk calculators can build a needed bridge between the RDoC multiple units of analysis and developmental science.

This paper critically reviews the opportunities and challenges in designing and conducting actionable research on the learning and development of children in conflict- and crisis-affected countries. We approached our review through two perspectives championed by Edward Zigler: (a) child development and social policy and (b) developmental psychopathology in context. The aim of the work was to answer the following questions: What works to enhance children's learning and development in such contexts? By what mechanisms? For whom? Under what conditions? How do experiences and conditions of crisis affect the basic processes of children's typical development? The review is based on a research–practice partnership started in the Democratic Republic of the Congo in 2010 and expanded to research in Niger and Lebanon in 2016. The focus of the research is on the impact of Healing Classrooms (a set of classroom practices) and Healing Classrooms Plus (an additional set of targeted social and emotional learning activities), developed by the International Rescue Committee, on children's academic outcomes and social and emotional learning. We sought to extract lessons from this decade of research for building a global developmental science for action. Special attention is paid to the importance of research–practice partnerships, conceptual frameworks, measurement and methodology. We conclude by highlighting several essential features of a global developmental science for action.

There is mounting evidence to implicate the intrauterine environment as the initial pathogenic stage for neuropsychiatric disease. Recent developments in magnetic resonance imaging technology are making a multimodal analysis of the fetal central nervous system a reality, allowing analysis of structural and functional parameters. Exposures to a range of pertinent risk factors whether preconception or in utero can now be indexed using imaging techniques within the fetus’ physiological environment. This approach may determine the first “hit” required for diseases that do not become clinically manifest until adulthood, and which only have subtle clinical markers during childhood and adolescence. A robust characterization of a “multi-hit” hypothesis may necessitate a longitudinal birth cohort; within this investigative paradigm, the full range of genetic and environmental risk factors can be assessed for their impact on the early developing brain. This will lay the foundation for the identification of novel biomarkers and the ability to devise methods for early risk stratification and disease prevention. However, these early markers must be followed over time: first, to account for neural plasticity, and second, to assess the effects of postnatal exposures that continue to drive the individual toward disease. We explore these issues using the schizophrenia spectrum disorders as an illustrative paradigm. However, given the potential richness of fetal magnetic resonance imaging, and the likely overlap of biomarkers, these concepts may extend to a range of neuropsychiatric conditions.

We investigate how early exposure to parental externalizing behaviors (EB) may contribute to development of alcohol use disorders (AUD) in young adulthood, testing a developmental cascade model focused on competencies in three domains (academic, conduct, and work) in adolescence and emerging adulthood, and examining whether high parental education can buffer negative effects of parental EB and other early risk factors. We use data from 451,054 Swedish-born men included in the national conscript register. Structural equation models showed parental EB was associated with academic and behavioral problems during adolescence, as well as with lower resilience, more criminal behavior, and reduced social integration during emerging adulthood. These pathways led to elevated rates of AUD in emerging and young adulthood. Multiple groups analysis showed most of the indirect pathways from parental EB to AUD were present but buffered by higher parental education, suggesting early life experiences and competencies matter more for young men from lower socioeconomic status (SES) families than from higher SES families. Developmental competencies in school, conduct, and work are important precursors to the development of AUD by young adulthood that are predicted by parental EB. Occupational success may be an overlooked source of resilience for young men from low-SES families.

Based on attachment theory and a social-cognitive model of posttraumatic stress disorder (PTSD), this study examined the roles of parent–child communication, perceived parental depression, and intrusive rumination in the association between insecure attachment to parents and PTSD among adolescents following the Jiuzhaigou earthquake. In this study, 620 adolescents were recruited to complete self-report questionnaires. The results showed that the direct association between anxious attachment and PTSD was significant, but that between avoidant attachment and PTSD was non-significant. In addition, both anxious and avoidant attachment had indirect associations with PTSD via the mediating effects of parent–child communication openness and problems, perceived parental depression, and intrusive rumination. However, the specific paths between anxious and avoidant attachment and PTSD were different. The findings indicated that insecure attachment among adolescents following the earthquake was predictive for their PTSD, and the mechanisms underlying the association between anxious attachment and PTSD and the association between avoidant attachment and PTSD were distinct. To alleviate PTSD, more attention should be paid to improving the quality of parent–child communication for adolescents with avoidant attachment to parents, and to reducing negative cognition in adolescents with anxious attachment.

Informed by the National Institute of Mental Health's Research Domain Criteria (RDoC) and developmental psychopathology frameworks, the current study used cortisol area under the curve with respect to ground (AUCg) as an index of differential sensitivity to context, which was expected to predispose young children with elevated vulnerability to adverse caregiving experiences and adaptive sensitivity to intervention effects. Particularly, the study aimed to determine whether improving caregivers’ responsive parenting through the Filming Interactions to Nurture Development (FIND) intervention would buffer children's biologically embedded vulnerability to caregivers’ depressive symptoms. Data were derived from a randomized controlled trial using pretest–posttest design with low-income families of children aged 4 to 36 months (N = 91). Young children's differential sensitivity was measured using cortisol AUCg during a structured stress paradigm. As hypothesized, children whose cortisol AUCg indicated greater sensitivity to social context exhibited more internalizing and externalizing behaviors in relation to caregivers’ elevated depressive symptoms. Critically, the intervention program was effective in attenuating psychopathology symptoms among the more biologically sensitive children. As proven by rigorous statistical tests, the findings of this study partially supported the differential susceptibility hypotheses, indicating both greater vulnerability to adverse conditions and responsiveness to intervention among children with high levels of cortisol AUCg.

Parents’ comparisons of siblings have been understudied among sibling research, especially in Chinese societies where the government recently relaxed its one-child policy. This study, using a two-wave longitudinal design, explored how parents’ comparisons of siblings were associated with adolescents’ internalizing and externalizing problems. Study participants were 260 Chinese adolescents who had siblings and completed questionnaires that assessed their internalizing and externalizing problems, as well as their perceptions of parents’ critical comparisons of siblings. Cross-lagged modeling analysis showed that parents’ comparisons of siblings predicted more internalizing and externalizing problems in adolescents 6 months later. Moreover, adolescents’ externalizing problems but not internalizing problems predicted more parents’ comparisons of siblings over time. These findings underscore the importance of reciprocal relations between parents’ comparisons of siblings and adolescents’ externalizing problems and the implication of cultural context in understanding associations between parental practices and adolescents’ adjustment.

I present a theory of adaptive intelligence and discuss why I believe adaptive intelligence, rather than general intelligence, is the kind of intelligence upon which we should focus in today's world. Adaptive intelligence is the ability to adapt to, shape, and select real-world environments in ways that result in positive outcomes not only for oneself, but also for others and the world. Edward Zigler was among the first to recognize the importance of levels of adaptation to intellectual deficiency, arguing from early on that intellectual challenges needed to be recognized not just in terms of IQ but also in terms of adaptive functioning. Adaptive intelligence is compared to and contrasted with general intelligence, which is usually defined as the first factor in a factor analysis of psychometric tests. I first introduce the main issues in the article. Then I discuss how one even would decide what intelligence is. Next I discuss broader theories of intelligence and especially the theory of adaptive intelligence. Then I talk about the perishability of theories of intelligence and other things—to what extent are they set up so that people are willing and able to move beyond them? Finally, I discuss how individual outcomes do not necessarily predict collective outcomes.