Improved characterization of quantitative traits and dimensionally distributed complex behaviors during toddlerhood may improve early identification of autism spectrum disorder and related neurodevelopmental disorders. Parents of 205 community-ascertained toddlers (age: mean = 20.2, SD = 2.6 months) completed the Repetitive Behavior Scales for Early Childhood (RBS-EC) and the Video-Referenced Rating of Reciprocal Social Behavior (vrRSB), with longitudinal follow-up of behavioral assessments and/or another round of parent-report questionnaires. Criterion validity was examined both concurrently and longitudinally using the Infant Toddler Social Emotional Assessment (ITSEA) as a criterion anchor. Reciprocal social behavior as measured by the vrRSB was significantly associated with social competence as measured by the ITSEA, longitudinally and concurrently. Reciprocal social behavior was not associated with the externalizing subscale on the ITSEA, providing evidence of discriminant validity. Higher-order repetitive behaviors (restricted interests; rituals and routines) as measured by RBS-EC subscales were associated with the dysregulation and internalizing subscales of the ITSEA, longitudinally and concurrently. All RBS-EC subscales (excepting repetitive motor) were associated concurrently and longitudinally with the dysregulation subscale of the ITSEA. We report evidence of criterion-oriented and discriminant validity for the constructs/domains captured by the RBS-EC and vrRSB. These instruments may be particularly useful in characterizing dimensional variability across the typical-to-atypical continuum.

Childhood adversity is common and associated with elevated risk for transdiagnostic psychopathology. Reward processing has been implicated in the link between adversity and psychopathology, but whether it serves as a mediator or moderator is unclear. This study examined whether alterations in behavioral and neural reward processing function as a mechanism or moderator of psychopathology outcomes following adversity experiences, including threat (i.e., trauma) and deprivation. A longitudinal community sample of 10–15-year-old youths was assessed across two waves (Wave 1: n = 228; Wave 2: n = 206). Wave 1 assessed adverse experiences, psychopathology symptoms, reward processing on a monetary incentive delay task, and resting-state fMRI. At Wave 2, psychopathology symptoms were reassessed. Greater threat experiences were associated with blunted behavioral reward sensitivity, which, in turn, predicted increases in depression symptoms over time and mediated the prospective association between threat and depression symptoms. In contrast, reward sensitivity moderated the association between deprivation experiences and prospective externalizing symptoms such that the positive association of deprivation with increasing externalizing symptoms was absent for children with high levels of reward sensitivity.

Building on research on cumulative risk and psychopathology, this study examines how cumulative risk exposure is associated with altered diurnal cortisol rhythms in an ethnically diverse, low-income sample of youth. In addition, consistent with a diathesis-stress perspective, this study explores whether the effect of environmental risk is moderated by allelic variation in the serotonin transporter linked polymorphic region (5-HTTLPR) gene. Results show that youth with greater cumulative risk exposure had flatter diurnal cortisol slopes, regardless of 5-HTTLPR genotype. However, the association of cumulative risk with average cortisol output (area under the curve [AUC]) was moderated by the 5-HTTLPR genotype. Among youth homozygous for the long allele, greater cumulative risk exposure was associated with lower cortisol AUC, driven by significant reductions in cortisol levels at waking. In contrast, there was a trend-level association between greater cumulative risk and higher cortisol AUC among youth carrying the short allele, driven by a trend-level increase in bedtime cortisol levels. Findings are discussed with regard to the relevance of dysregulated diurnal cortisol rhythms for the development of psychopathology and the implications of genetically mediated differences in psychophysiological adaptations to stress.

There is increasing evidence that resilience in youth may have a neurobiological basis. However, the existing literature lacks a consistent way of operationalizing resilience, often relying on arbitrary judgments or narrow definitions (e.g., not developing PTSD) to classify individuals as resilient. Therefore, this study used data-driven, continuous resilience scores based on adversity and psychopathology to investigate associations between resilience and brain structure in youth. Structural MRI data from 298 youth aged 9–18 years (Mage = 13.51; 51% female) who participated in the European multisite FemNAT-CD study were preprocessed using SPM12 and analyzed using voxel-based morphometry. Resilience scores were derived by regressing data on adversity exposure against current/lifetime psychopathology and quantifying each individual’s distance from the regression line. General linear models tested for associations between resilience and gray matter volume (GMV) and examined whether associations between resilience and GMV differed by sex. Resilience was positively correlated with GMV in the right inferior frontal and medial frontal gyri. Sex-by-resilience interactions were observed in the middle temporal and middle frontal gyri. These findings demonstrate that resilience in youth is associated with volume in brain regions implicated in executive functioning, emotion regulation, and attention. Our results also provide evidence for sex differences in the neurobiology of resilience.

High levels of early emotionality (of either negative or positive valence) are hypothesized to be important precursors to early psychopathology, with attention-deficit/hyperactivity disorder (ADHD) a prime early target. The positive and negative affect domains are prime examples of Research Domain Criteria (RDoC) concepts that may enrich a multilevel mechanistic map of psychopathology risk. Utilizing both variable-centered and person-centered approaches, the current study examined whether levels and trajectories of infant negative and positive emotionality, considered either in isolation or together, predicted children's ADHD symptoms at 4 to 8 years of age. In variable-centered analyses, higher levels of infant negative affect (at as early as 3 months of age) were associated with childhood ADHD symptoms. Findings for positive affect failed to reach statistical threshold. Results from person-centered trajectory analyses suggest that additional information is gained by simultaneously considering the trajectories of positive and negative emotionality. Specifically, only when exhibiting moderate, stable or low levels of positive affect did negative affect and its trajectory relate to child ADHD symptoms. These findings add to a growing literature that suggests that infant negative emotionality is a promising early life marker of future ADHD risk and suggest secondarily that moderation by positive affectivity warrants more consideration.

In the past decades, there has been an overemphasis of a descriptive/behavioral approach to study conduct disorder. In an equifinal perspective, we aimed to examine the developmental multitrajectory groups of psychological features (irritability, interpersonal callousness, hyperactivity/impulsivity, and depressive–anxiety symptoms) and their associations with conduct problems. In a population-based cohort (n = 1,309 participants followed from 5 months to 17 years old), latent-class growth analysis was performed for each psychological feature to identify a two-trajectory model (from ages 6 to 12 years). Based on parameter estimates of the two-trajectory models for each of the four psychological features, a parallel process growth mixture model identified eight significant developmental patterns that were subsequently compared with typically developing children. Furthermore, we observed that while interpersonal callousness conferred an increased risk for childhood and adolescence conduct problems, its co-occurrence with hyperactivity/impulsivity, irritability, and/or depressive–anxiety symptoms heightened the general risk, but also predicted distinct subtypes of conduct problems (i.e., aggressive and rule-breaking behaviors). Thus, by studying complex developmental combinations of psychological features, we observed qualitatively distinct pathways towards conduct problems. A multitrajectory framework of psychological features should be considered as a significant step towards unveiling the multiple etiological pathways leading to conduct disorder and its substantial clinical heterogeneity.

Parental depression has significant implications for family functioning, yet much of the literature does not consider family-level dynamics in investigating individual, parenting and child outcomes. In the current study we apply a new index of couple-level support, partner reflective functioning (RF), or the romantic partner’s ability to consider how the partner’s mental states can guide behavior, to study familial resiliency in the face of prenatal parental depression among first-time parents. We investigate how partner RF buffers the association between prenatal parental depression and outcomes of postnatal parental depression, parenting style, and child effortful control. Maternal and paternal depression were measured in 91 primiparous couples during the sixth month of pregnancy and parental depression, partner RF, parental RF at 6 months postnatally. Outcomes of parental depression, permissive parenting, and children’s effortful control were assessed 24 months postnatally. Results indicate that average and high levels of paternal partner (not parental) RF attenuate risk for maternal postnatal depression, maternal permissive parenting, and deficits in child effortful control. Implications are discussed from a family systems approach.

Children differ in their response to environmental exposures, with some being more sensitive to contextual factors than others. According to theory, such variability is the result of individual differences in neurobiological sensitivity to environmental features, with some individuals generally more affected by both negative and/or positive experiences. In this exploratory study we tested whether left and right amygdala and hippocampus volumes (corrected for total brain size) account for individual differences in response to environmental influences in a sample of 62 boys. Cumulative general environmental quality, ranging from low to high, was measured across the first 9 years and child behavior was reported by teachers when boys were 12–13 years old. According to analyses, only the left amygdala volume – not any of the other brain volumes – emerged as an important brain region for sensitivity to positive environmental aspects. Boys with a larger left amygdala benefited significantly more from higher environmental quality than boys with a smaller left amygdala whilst not being more vulnerable to lower quality. Besides providing preliminary evidence for differences in environmental sensitivity due to brain structure, the results also point to the left amygdala as having a specific role regarding the response to environmental influences.

Some children are more affected by specific family environments than others, as a function of differences in their genetic make-up. However, longitudinal studies of genetic moderation of parenting effects during early childhood have not been conducted. We examined developmental profiles of child behavior problems between 18 months and age 8 in a longitudinal parent–offspring sample of 361 adopted children. In toddlerhood (18 months), observed structured parenting indexed parental guidance in service of task goals. Biological parent psychopathology served as an index of genetic influences on children’s behavior problems. Four profiles of child behavior problems were identified: low stable (11%), average stable (50%), higher stable (29%), and high increasing (11%). A multinominal logistic regression analysis indicated a genetically moderated effect of structured parenting, such that for children whose biological mother had higher psychopathology, the odds of the child being in the low stable group increased as structured parenting increased. Conversely, for children whose biological mother had lower psychopathology, the odds of being in the low stable group was reduced when structured parenting increased. Results suggest that increasing structured parenting is an effective strategy for children at higher genetic risk for psychopathology, but may be detrimental for those at lower genetic risk.

Relational victimization typically emerges first during the elementary school period, and has been associated with increased levels of internalizing symptoms in children. Individual differences in autonomic nervous system functioning have been suggested as a potential factor linking social stressors and internalizing symptoms. The aim of this study was therefore to examine whether heart rate and heart rate variability mediated the association between relational victimization and internalizing symptoms in 373 mainstream elementary school children. Children were assessed in 2015 (T0; Grades 3–5, M age = 9.78 years, 51% boys) and reassessed in 2016 (T1). Heart rate and heart rate variability were assessed during a regular school day at T1. A multi-informant (teacher and peer report) cross-time measure of relational victimization, and a multi-informant (self- and teacher report) measure of internalizing problems at T1 was used. Results showed that heart rate variability, but not heart rate, mediated the association between relational victimization and internalizing symptoms. This study provides tentative support that in children from a general population sample, a psychobiological factor may mediate the association of relational victimization with internalizing symptoms.

Recent research suggests that psychosocial resources and life stressors are mediating pathways explaining socioeconomic variation in young adults' health risks. However, less research has examined both these pathways simultaneously and their genetic moderation. A nationally representative sample of 11,030 respondents with prospective data collected over 13 years from the National Study of Adolescent to Adult Health was examined. First, the association between early cumulative socioeconomic adversity and young adults' (ages 25–34) cardiometabolic disease risk, as measured by 10 biomarkers, through psychosocial resources (educational attainment) and life stressors (accelerated transition to adulthood) was examined. Second, moderation of these pathways by the serotonin transporter linked polymorphic region gene (5-HTTLPR) was examined. There was evidence for the association between early socioeconomic adversity and young adults' cardiometabolic disease risk directly and indirectly through educational attainment and accelerated transitions. These direct and mediating pathways were amplified by the 5-HTTLPR polymorphism. These findings elucidate how early adversity can have an enduring influence on young adults' cardiometabolic disease risk directly and indirectly through psychosocial resources and life stressors and their genetic moderation. This information suggests that effective intervention and prevention programs should focus on early adversity, youth educational attainment, and their transition to young adulthood.

To understand the complex relationships between autism spectrum disorder (ASD) and other frequently comorbid conditions, a growing number of studies have investigated the emergence of ASD during infancy. This research has suggested that symptoms of ASD and highly related comorbid conditions emerge from complex interactions between neurodevelopmental vulnerabilities and early environments, indicating that developing treatments to prevent ASD is highly challenging. However, it also suggests that attenuating the negative effects of ASD on future development once identified is possible. The present paper builds on this by conceptualizing developmental delays in nonsocial skills as the potential product of altered caregiver–infant interactions following the emergence of ASD during infancy. And, following emerging findings from caregiver–infant dyadic head-mounted eye-tracking (D-ET) research, it also suggests that a multiple pathway model of joint attention can provide mechanistic insights into how ASD alters the ability of caregiver and infant to create a context for infant learning. The potential for this view to inform early intervention is further discussed and illustrated through D-ET data collected prior to and following a brief, parent-mediated intervention for infant ASD. While promising, further research informing how a multiple pathway model of joint attention can inform ASD early intervention is needed.

Early adversity is a major risk factor for the emergence of psychopathology across development. Identifying mechanisms that support resilience, or favorable mental health outcomes despite exposure to adversity, is critical for informing clinical intervention and guiding policy to promote youth mental health. Here we propose that caregivers play a central role in fostering resilience among children exposed to adversity via caregiving influences on children’s corticolimbic circuitry and emotional functioning. We first delineate the numerous ways that caregivers support youth emotional learning and regulation and describe how early attachment lays the foundation for optimal caregiver support of youth emotional functioning in a developmental stage-specific manner. Second, we outline neural mechanisms by which caregivers foster resilience—namely, by modulating offspring corticolimbic circuitry to support emotion regulation and buffer stress reactivity. Next, we highlight the importance of developmental timing and sensitive periods in understanding caregiving-related mechanisms of resilience. Finally, we discuss clinical implications of this line of research and how findings can be translated to guide policy that promotes the well-being of youth and families.

According to differential susceptibility theory (DST), some children may be more sensitive to both positive and negative features of the environment. However, research has generated a list of widely disparate temperamental traits that may reflect differential susceptibility to the environment. In addition, findings have implicated these temperament × environment interactions in predicting a wide variety of child outcomes. This study uses a novel evolutionary model of temperament to examine whether differential susceptibility operates in a domain-general or domain-specific manner. Using a racially and socioeconomically diverse sample of 243 preschoolers and their parents (56% female; 48% African American), we examined the interactions between maternal and paternal parenting quality and two evolutionary informed temperament profiles (i.e., Hawks and Doves) in predicting changes in teacher-reported conduct problems and depressive symptoms from preschool to first grade. Results suggest that differential susceptibility operates in a domain-specific fashion. Specifically, the “Hawk” temperament was differentially susceptible to maternal parenting in predicting externalizing problems. In contrast, the “Dove” temperament was susceptible to both paternal and maternal parenting quality in predicting changes in depressive symptoms. Findings provide support for an integrative framework that synthesizes DST with an evolutionary, function-based approach to temperament.

There has been growing evidence that autistic traits are more represented in children with attention-deficit hyperactivity disorder (ADHD). The purpose of this study was to investigate autistic traits associated with responding joint attention (RJA) abilities and face scanning patterns using eye-tracking in children with ADHD, and to compare with typically developing peers (TDs). All child participants viewed a series of videos related to male and female children under congruent and incongruent conditions during eye-tracking evaluation. The object and face regions of the models within the videos were determined as areas of interest (AOIs). Children with ADHD had significantly elevated ratings of autistic traits than TDs. Time course analysis of the proportion of fixations (PoF) on object region determined that children with ADHD tended to show more interest in the objects and had higher PoF on face interest area, including eyes and mouth compared to TD children in the videos when the male/female model shifts his/her gaze to the corner. Higher SRS scores were associated with higher PoF on the Face AOI in both groups. Given these findings, social skill interventions directly targeting the core deficits of RJA and problems in facial scanning appears to be beneficial in children with ADHD.

This study examined the intergenerational transmission of parental invalidation and whether parental difficulties in emotion regulation mediated the association between past experiences of invalidation and current invalidating parenting practices. We also aimed to investigate whether gender might influence the transmission of parental invalidation. We recruited a community sample of 293 dual-parent families (adolescent and their parents) based in Singapore. Parents and adolescents each completed measures of childhood invalidation, whereas parents additionally reported on their difficulties in emotion regulation. Results based on path analyses demonstrated that past parental invalidation experienced by fathers positively predicted current perceived invalidation by their children. The association between mothers’ childhood invalidation and current invalidating practices was fully mediated by mothers’ difficulties with emotion regulation. Further analyses revealed that parents’ current invalidating behaviors were not predicted by their past experiences of paternal or maternal invalidation. These findings point to the importance of considering the family invalidating environment as a whole when examining the influence of past experienced parental invalidation on emotion regulation and invalidating behaviors of second-generation parents. Our study provides empirical support for the intergenerational transmission of parental invalidation and highlights the need to address childhood experiences of parental invalidation in parenting programs.

Difficulty recognizing negative emotions is linked to aggression in children. However, it remains unclear how certain types of emotion recognition (insensitivities vs. biases) are associated with functions of aggression and whether these relations change across childhood. We addressed these gaps in two diverse community samples (study 1: aged 4 and 8; N = 300; study 2: aged 5 to 13, N = 374). Across studies, children performed a behavioral task to assess emotion recognition (sad, fear, angry, and happy facial expressions) while caregivers reported children’s overt proactive and reactive aggression. Difficulty recognizing fear (especially in early childhood) and sadness was associated with greater proactive aggression. Insensitivity to anger – perceiving angry faces as showing no emotion – was associated with increased proactive aggression, especially in middle-to-late childhood. Additionally, greater happiness bias – mistaking negative emotions as being happy – was consistently related to higher reactive aggression only in early childhood. Together, difficulty recognizing negative emotions was related to proactive aggression, however, the strength of these relations varied based on the type of emotion and developmental period assessed. Alternately, difficulty determining emotion valence was related to reactive aggression in early childhood. These findings demonstrate that distinct forms of emotion recognition are important for understanding functions of aggression across development.

We present a theory of atypical development based on a developmental theory of the typical mind integrating developmental, cognitive, and psychometric theory and research. The paper comprises three parts. First, it outlines the theory of typical development. The theory postulates central cognitive mechanisms, such as relational integration, executive and inferential processes, and domain-specific processes underlying different environmental relations, such as visuospatial or quantitative relations. Cognitive development advances in cycles satisfying developmental priorities in mastering these systems, such as executive control from 2–6 years, inferential control from 7–11 years, and truth control from 12–18 years. Second, we discuss atypical development, showing how each neurodevelopmental disorder emerges from deficiencies in one or more of the processes comprising the architecture of the mind. Deficiencies in relational integration mechanisms, together with deficiencies in social understanding, yield autism spectrum disorder. Deficiencies in executive processes yield attention-deficit and hyperactivity disorder. Deficiencies in symbolic representation yield specialized learning difficulties, such as dyslexia and dyscalculia. Finally, we discuss clinical and educational implications, suggesting the importance of early diagnosis of malfunctioning in each of these dimensions and specific programs for their remediation.

Maternal substance use has often been associated with insecure and disorganized child attachment. We evaluated this association with a meta-analysis of young children and, further, systematically reviewed mediating and moderating factors between maternal substance use and child attachment. We performed a systematic database search of quantitative English language studies on child attachment that included substance-using mothers and their children below 6 years of age. Eleven studies (N = 1,841) met the inclusion criteria and were included in the meta-analysis of attachment security and seven (N = 1,589) studies were included in the meta-analysis of attachment disorganization. We found that maternal substance use was negatively associated with secure attachment in children, but the effect size was small (r = −.10). The association with disorganized attachment was not significant (r = .15). Related to moderating and mediating factors (k = 6), we found evidence on the role of teratogenic and sociological factors on child attachment. Most importantly, the impact of cumulative risks was vital. However, literature was scarce, and studies varied in risk of bias, leaving many unanswered questions on other potential factors underlying the development of attachment in these high-risk children. We discuss the results considering clinical implications and future directions.

This study aimed to articulate the roles of social support and coping strategies in the relation between childhood maltreatment (CM) and subsequent major depressive disorder (MDD) with a comprehensive exploration of potential factors in a longitudinal community-based cohort. Parallel and serial mediation analyses were applied to estimate the direct effect (DE) (from CM to MDD) and indirect effects (from CM to MDD through social support and coping strategies, simultaneously and sequentially). Sociodemographic characteristics and genetic predispositions of MDD were considered in the modeling process. A total of 902 participants were included in the analyses. CM was significantly associated with MDD (DE coefficient (β) = 0.015, 95% confidence interval (CI) = 0.002∼0.028). This relation was partially mediated by social support (indirect β = 0.004, 95% CI = 0.0001∼0.008) and negative coping (indirect β = 0.013, 95% CI = 0.008∼0.020), respectively. Social support, positive coping, and negative coping also influenced each other and collectively mediated the association between CM and MDD. This study provides robust evidence that although CM has a detrimental effect on later-on MDD, social support and coping strategies could be viable solutions to minimize the risk of MDD. Intervention and prevention programs should primarily focus on weakening negative coping strategies, then strengthening social support and positive coping strategies.