Adverse effects of early exposure to parental mood disturbance on child adjustment have been documented for both mothers and fathers, but are rarely examined in tandem. Other under-researched questions include effects of changes over time in parental well-being, similarities and contrasts between effects of parental mood disturbance on children's internalizing versus externalizing problems, and potential mediating effects of couple relationship quality. The current study involved 438 couples who reported symptoms of depression and anxiety at each of four time points (i.e., last trimester of pregnancy and 4, 14, and 24 months postbirth). Mothers and fathers also rated their couple relationship quality and their child's socioemotional adjustment at 14 months, as well as internalizing and externalizing problems at 24 months. Latent growth models indicated direct effects of (a) maternal prenatal well-being on externalizing problems at 24 months, and (b) paternal prenatal well-being on socioemotional problems at 14 months. Internalizing symptoms at 24 months showed only indirect associations with parental well-being, with couple relationship quality playing a mediating role. Our findings highlight the importance of prenatal exposure to parental mood disturbance and demonstrate that, even in a low-risk sample, poor couple relationship quality explains the intergenerational stability of internalizing problems.

Children who spend their early lives in institutions experience profound psychosocial deprivation that is associated with altered stress response system development. Here, we used data from a longitudinal randomized controlled trial of foster care for institutionally reared children to examine whether caregiving quality and stressful life events (SLEs) in early adolescence (age 12) influence patterns of hypothalamic–pituitary–adrenal (HPA) axis and sympathetic nervous system (SNS) reactivity. Controlling for the effect of institutional care, higher caregiving quality at age 12 was associated with heightened cortisol and SNS reactivity. However, moderation analysis revealed that the latter effect was only observed among never-institutionalized children, whereas ever-institutionalized children demonstrated a persistently blunted SNS response regardless of recent caregiving quality. Among institutionally reared children, SLEs interacted with prior random assignment to foster care, such that those placed in foster care early in development had a SNS response that approximated never-institutionalized children when SLEs at age 12 were low. In contrast, SNS reactivity was persistently blunted among those with prolonged deprivation, regardless of recent SLEs. Early-life deprivation is associated with persistent blunting of stress response systems, but normalization may be achievable if SLEs are limited following placement into enriched family-based care.

Harsh and restrictive parenting are well-established contributors to the development of oppositional defiant disorder (ODD) among children. However, few studies have explored whether interpersonal relationships that develop outside the family environment attenuate the risk for ODD that is associated with harsh parenting. The current study tested multireporter measures of teacher–child closeness and peer acceptance as moderators of the association between harsh parenting and children's ODD as children's social worlds widen during the kindergarten year (N = 338 children, 48% girls, M age = 5.32 years). Harsh parenting interacted with peer nominations of peer acceptance and children's report of teacher–child closeness to predict children's ODD symptoms in the spring, adjusting for fall symptoms. Children exposed to harsh parenting exhibited greater symptom increases when they were less liked/accepted playmates and in the context of lower teacher–child closeness. However, harsh parenting was not associated with symptom change among children with higher levels of peer-nominated acceptance and those who reported closer relationships with teachers. There were no significant interactions using teacher's report of peer acceptance or teacher's report of teacher–child closeness. Findings highlight positive peer and teacher relationships as promising targets of intervention among children exposed to harsh parenting and support the importance of assessing multiple perspectives of children's social functioning.

Additive and bidirectional effects of executive control and hypothalamic–pituitary–adrenal (HPA) axis regulation on children's adjustment were examined, along with the effects of low income and cumulative risk on executive control and the HPA axis. The study utilized longitudinal data from a community sample of preschool age children (N = 306, 36–39 months at Time 1) whose families were recruited to overrepresent low-income contexts. We tested the effects of low income and cumulative risk on levels and growth of executive control and HPA axis regulation (diurnal cortisol level), the bidirectional effects of executive control and the HPA axis on each other, and their additive effects on children's adjustment problems, social competence and academic readiness. Low income predicted lower Time 4 executive control, and cumulative risk predicted lower Time 4 diurnal cortisol level. There was little evidence of bidirectional effects of executive control and diurnal cortisol. However, both executive control and diurnal cortisol predicted Time 4 adjustment, suggesting additive effects. There were indirect effects of income on all three adjustment outcomes through executive control, and of cumulative risk on adjustment problems and social competence through diurnal cortisol. The results provide evidence that executive control and diurnal cortisol additively predict children's adjustment and partially account for the effects of income and cumulative risk on adjustment.

Prospective longitudinal studies of idiopathic autism spectrum disorder (ASD) have provided insights into early symptoms and predictors of ASD during infancy, well before ASD can be diagnosed at age 2–3 years. However, research on the emergence of ASD in disorders with a known genetic etiology, contextualized in a developmental framework, is currently lacking. Using a biobehavioral multimethod approach, we (a) determined the rate of ASD in N = 51 preschoolers with fragile X syndrome (FXS) using a clinical best estimate (CBE) procedure with differential diagnoses of comorbid psychiatric disorders and (b) investigated trajectories of ASD symptoms and physiological arousal across infancy as predictors of ASD in preschoolers with FXS. ASD was not diagnosed if intellectual ability or psychiatric disorders better accounted for the symptoms. Our results determined that 60.7% of preschoolers with FXS met the Diagnostic and Statistical Manual of Mental Disorders (fifth edition) (DSM-5) criteria for ASD using the CBE procedure. In addition, 92% of these preschoolers presented with developmental delay and 45.4% also met criteria for psychiatric disorders, either anxiety, ADHD, or both. ASD diagnoses in preschoolers with FXS were predicted by elevated scores on traditional ASD screeners in addition to elevated autonomic arousal and avoidant eye contact from infancy.

The confluence model theorizes that dynamic transactions between peer rejection and deviant peer clustering amplify antisocial behavior (AB) within the school context during adolescence. Little is known about the links between peer rejection and AB as embedded in changing networks. Using longitudinal social network analysis, we investigated the interplay between rejection, deviant peer clustering, and AB in an ethnically diverse sample of students attending public middle schools (N = 997; 52.7% boys). Adolescents completed peer nomination reports of rejection and antisocial behavior in Grades 6–8. Results revealed that rejection status was associated with friendship selection, and adolescents became rejected if they were friends with others who were rejected. Youth befriended others with similar levels of AB. Significant patterns of peer influence were documented for AB and rejection. As hypothesized, rejected youth with low AB were more likely to affiliate with others with high AB instead of similarly low AB. In contrast, nonrejected youth preferred to befriend others with similarly high or low AB. Results support an updated confluence model of a joint interplay between rejection and AB as ecological conditions that lead to self-organization into deviant clusters in which peer contagion on problem behaviors operates.

The majority of children living in foster care in the United States have a history of maltreatment and/or disrupted caregiving. Maltreatment in early childhood adversely affects development at many levels, including neurobiology and behavior. One neurobiological measure associated with maltreatment is alpha electroencephalogram (EEG) asymmetry. Prior research has found greater right frontal asymmetry among children with a history of maltreatment. However, little research has been extended developmentally downward to examine alpha asymmetry and its behavioral correlates among toddlers in foster care; this was the purpose of the present study. Differences in EEG asymmetry were examined between a sample of foster toddlers (mean age = 3.21 years, n = 38) and a community comparison, low-income sample without a history of foster care (mean age = 3.04 years, n = 16). The toddlers in the foster care group exhibited greater right alpha asymmetry, primarily driven by differences in parietal asymmetry. Neither frontal nor parietal asymmetry were clearly related to internalizing or externalizing behaviors, measured concurrently or at previous time points. These findings reveal differences in alpha EEG asymmetry among toddlers in foster care, and highlight the need to better understand associations between neurobiological and behavioral functioning following early adversity.

Child maltreatment is a robust risk factor for suicidal ideation and behaviors during adolescence. Elevations in internalizing and externalizing symptomology have been identified as two distinct developmental pathways linking child maltreatment and adolescent risk for suicide. However, recent research suggests that the co-occurrence of internalizing and externalizing symptomology may form a distinct etiological pathway for adolescent risk behaviors. Using the Longitudinal Studies on Child Abuse and Neglect (LONGSCAN) sample (N = 1,314), the present study employed a person-centered approach to identify patterns of concurrent change in internalizing and externalizing psychopathology over five time points from early childhood to adolescence in relation to previous experiences of child maltreatment and subsequent suicidal ideation and behaviors. Results indicated four distinct bivariate externalizing and internalizing growth trajectories. Group membership in a heightened comorbid internalizing and externalizing symptom trajectory mediated the association between childhood abuse and adolescent suicidal ideation and suicidal behaviors. These findings suggest that the concurrent development of externalizing and internalizing symptoms in childhood and adolescence may constitute a unique developmental trajectory that confers risk for suicide-related outcomes.

Autism spectrum disorder (ASD) is a common neurodevelopmental disorder characterized by deficits in social communication and presence of restricted, repetitive behaviors, and interests. However, individuals with ASD vary significantly in their challenges and abilities in these and other developmental domains. Gene discovery in ASD has accelerated in the past decade, and genetic subtyping has yielded preliminary evidence of utility in parsing phenotypic heterogeneity through genomic subtypes. Recent advances in transcriptomics have provided additional dimensions with which to refine genetic subtyping efforts. In the current study, we investigate phenotypic differences among transcriptional subtypes defined by neurobiological spatiotemporal co-expression patterns. Of the four transcriptional subtypes examined, participants with mutations to genes typically expressed highly in all brain regions prenatally, and those with differential postnatal cerebellar expression relative to other brain regions, showed lower cognitive and adaptive skills, higher severity of social communication deficits, and later acquisition of speech and motor milestones, compared to those with mutations to genes highly expressed during the postnatal period across brain regions. These findings suggest higher-order characterization of genetic subtypes based on neurobiological expression patterns may be a promising approach to parsing phenotypic heterogeneity among those with ASD and related neurodevelopmental disorders.

Effective social functioning requires a broad range of social communication skills that are impaired in psychosis populations. However, little is known about early childhood (4- to 5-year period) social communication during the premorbid (pre-illness) stage of psychosis. The present study utilized retrospective parent reports to examine total early childhood social communication deficits, as well as deficits in two distinct domains, reciprocal social interaction (social smiling/eye gaze) and communication (social chat/gesture), in youth at clinical high-risk (CHR) for psychosis (ages 13–21; 37.2% female). Furthermore, associations between early childhood social communication and CHR youth's current functioning (social, academic/work), symptoms (positive/negative), and risk for conversion to psychosis were examined. Compared to healthy controls, CHR individuals had greater deficits in total and communication-specific early childhood social communication. Early childhood total, communication, and reciprocal social interaction deficits were associated with worse current functioning and greater current negative symptom severity (amotivation/anhedonia) in CHR youth. Early childhood total and reciprocal social interaction deficits were also associated with increased risk for conversion. These findings inform the field's understanding of the etiology and pathophysiology of psychosis by extending the current developmental literature on premorbid deficits in psychosis populations to specific domains of social behavior in a critical developmental period.

Children who have difficulty using reparative behaviors following transgressions display a wide range of poorer social and emotional outcomes. Despite the importance of reparative skills, no study has charted the developmental trajectory of these behaviors or pinpointed predictors of poorer reparative abilities. To address these gaps in the literature, this study applied growth mixture modeling to parent reports of children's reparative behaviors (N = 230) in a 9-year longitudinal data set spanning from preschool to early adolescence. Three distinct trajectories of reparative behaviors were found: a low-stable, moderate-stable, and high-stable latent class. Poorer emotion understanding, social withdrawal, social rejection, and maladaptive guilt in the preschool period predicted membership in a low-stable reparative trajectory. Externalizing diagnoses, particularly conduct disorder and oppositional defiant disorder, also predicted membership in a low-stable reparative trajectory. Preschool-onset depression predicted membership in a low-stable reparative trajectory through high levels of maladaptive guilt. The findings from this study suggest that socioemotional deficits in the preschool period set children on longstanding trajectories of impaired reparative responding. Thus, emotion understanding, social functioning, maladaptive guilt, and early psychiatric symptoms should be targeted in early preventive interventions.

Maternal thyroid dysfunction during pregnancy may contribute to offspring neurobehavioral disorders. In this paper, we investigate the relationship between maternal thyroid function during pregnancy and offspring depression and anxiety. Data were taken from the Avon Longitudinal Study of Parents and Children. A total of 2,920 mother-child pairs were included. Thyroid-stimulating hormone levels, free thyroxine (FT4), and thyroid peroxidase antibodies were assessed during the first trimester of pregnancy because maternal supply is the only source of thyroid hormone for the fetus during the first 12 weeks of gestation. Child symptoms of depression and anxiety were assessed using the Development and Well-Being Assessment at ages 7.5 and 15 years. The odds of presenting with depression and anxiety were estimated using the generalized estimating equation. The level of FT4 during the first trimester of pregnancy was associated with child depression combined at ages 7.5 and 15 (odds ratio = 1.21, 95% confidence interval [1.00, 1.14]. An increase of 1 standard deviation of FT4 during pregnancy increased the odds of child depression by 28% after adjustment made for potential confounders. No association was found among maternal levels of thyroid-stimulating hormone, FT4, and thyroid peroxidase antibodies and childhood anxiety. In conclusion, increased levels of FT4 during the first trimester of pregnancy appear be linked to greater risk of offspring depression.

Extensive research has established a positive association between caregiver-child behavioral synchrony and child developmental functioning. Burgeoning research examining physiological synchrony has yet to elucidate its impact for children’s developing self-regulation. The objectives of this systematic review were to: 1) determine whether there is evidence that caregiver-child physiological synchrony promotes positive child development, 2) examine developmental differences in physiological synchrony and its correlates, and 3) explore whether context, risk, and/or stress influence patterns of synchrony. Sixty-nine studies met the following criteria on PubMed and PsycINFO: 1) peer-reviewed empirical articles in English that 2) examine autonomic, hypothalamic-pituitary-adrenocortical, and/or central nervous system activity 3) for caregivers and children 4) in response to a task and 5) directly examine the association between caregiver and child physiology. Findings varied based on developmental period and current behavioral context. Functional differences may exist across physiological systems and contexts. Synchrony may have different developmental consequences for dyads with and without certain risk factors. Few studies examine physiological synchrony across multiple systems or contexts, nor do they measure child characteristics associated with synchrony. Statistical and methodological challenges impede interpretation. Findings generally support the idea that physiological synchrony may support children’s developing self-regulation. Longitudinal research is needed to examine child developmental outcomes over time.

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.

Individual differences in social-emotional functioning emerge early and have long-term implications for developmental adaptation and competency. Research is needed that specifies multiple early risk factors and outcomes simultaneously to demonstrate specificity. Using multigroup longitudinal path analysis in a sample of typically developing children (N = 541), we examined child temperament dimensions (surgency, negative affectivity, and regulation/effortful control) and maternal anxiety in infancy and age 2 as predictors of child externalizing, internalizing, dysregulation, and competence behaviors at age 3. Four primary patterns emerged. First, there was stability in temperament dimensions and maternal anxiety from infancy to age 3. Second, negative affectivity was implicated in internalizing problems and surgency in externalizing problems. Third, effortful control at age 2 was a potent mediator of maternal anxiety in infancy on age 3 outcomes. Fourth, there was suggestive evidence for transactional effects between maternal anxiety and child effortful control. Most pathways operated similarly for boys and girls, with some differences, particularly for surgency. These findings expand our understanding of the roles of specific temperamental domains and postnatal maternal anxiety in a range of social-emotional outcomes in the preschool period, and have implications for efforts to enhance the development of young children's social-emotional functioning and reduce risk for later psychopathology.

Experiencing poverty increases vulnerability for dysregulated hypothalamic–pituitary–adrenal (HPA) axis functioning and compromises long-term health. Positive parenting buffers children from HPA axis reactivity, yet this has primarily been documented among families not experiencing poverty. We tested the theorized power of positive parenting in 124 parent–child dyads recruited from Early Head Start (Mage = 25.21 months) by examining child cortisol trajectories using five samples collected across a standardized stress paradigm. Piecewise latent growth models revealed that positive parenting buffered children's stress responses when controlling for time of day, last stress task completed, and demographics. Positive parenting also interacted with income such that positive parenting was especially protective for cortisol reactivity in families experiencing greater poverty. Findings suggest that positive parenting behaviors are important for protecting children in families experiencing low income from heightened or prolonged physiologic stress reactivity to an acute stressor.

Cognitive ability, externalizing symptoms, and internalizing symptoms are correlated in children. However, it is not known why they combine in the general child population over time. To address this, we used data on 17,318 children participating in the UK Millennium Cohort Study and followed-up five times between ages 3 and 14 years. We fitted three parallel-process latent growth curve models to identify the parallel unfolding of children's trajectories of internalizing symptoms, externalizing symptoms, and cognitive ability across this period. We also examined the effects of time-invariant (ethnicity, birth weight, maternal education and age at birth, and breastfeeding status) and time-varying covariates (maternal psychological distress and socioeconomic disadvantage) on the growth parameters of the trajectories. The results showed that the intercepts of the trajectories of cognitive ability and, particularly, externalizing symptoms were inversely correlated. Their linear slopes were also inversely correlated, suggesting parallel development. Internalizing symptoms were correlated positively with externalizing symptoms and inversely (and more modestly) with cognitive ability at baseline, but the slope of internalizing symptoms correlated (positively) only with the slope of externalizing symptoms. The covariates predicted 9% to 41% of the variance in the intercepts and slopes of all domains, suggesting they are important common risk factors. Overall, it appears that externalizing symptoms develop in parallel with both cognitive ability and internalizing symptoms from early childhood through to middle adolescence. Children on an increasing trajectory of externalizing symptoms are likely both increasing in internalizing symptoms and decreasing in cognitive skills as well, and are thus an important group to target for intervention.

Being born small for gestational age (SGA) is considered a developmental vulnerability. Alternatively, SGA may be viewed as a marker for individual susceptibility to environmental experiences. The aim was to test if individuals born SGA are more susceptible to both negative and positive environmental experiences assessed by sensitive parenting in childhood compared with those born appropriate for gestational age (AGA). The target outcome was wealth in young adulthood. A total of 438 participants (SGA, n = 109; AGA, n = 329) were studied as part of the prospective Bavarian Longitudinal Study of neonatal at-risk children. Maternal sensitivity was observed during a standardized mother-child interaction task, and IQ was assessed with the Kaufman Assessment Battery for Children at age 6 years. At age 26, participants’ wealth was assessed with a comprehensive composite score. Individuals born SGA were found to be more susceptible to the effects of sensitive parenting after controlling for gestational age and IQ at age 6 years. When maternal sensitivity was lower than average, SGA adults did worse than AGA adults, but when exposed to above-average maternal sensitivity in childhood, they obtained significantly higher wealth than their AGA peers by 26 years of age.

Depression is associated with a multiplicity of adverse outcomes in adolescence, including peer victimization and low self-esteem. Depressive symptoms, peer victimization, and self-esteem are linked in cross-sectional studies, but no longitudinal study has been conducted assessing their developmental pathways in one integrated model across adolescence. We explored their temporal sequencing in a normative sample of 612 Canadian adolescents (54% girls) assessed annually over 5 years (Grade 7 to Grade 11). Potential confounders such as biological sex, ethnicity/race, and parent income and education were statistically controlled. We found evidence for the vulnerability model (self-esteem predicting depression) and the symptoms-driven model (depression predicting peer victimization). Our findings also supported the integration of these pathways into a self-perception driven model characterized by the indirect effect of self-esteem on later peer victimization via depressive symptoms. Specifically, poor self-esteem initiated a developmental cascade that led to poor mood and poor peer relations. These results highlight the importance of helping youth form a healthy identity that promotes positive mental health and peer relations, and the need to intervene with depressed, victimized, and at-risk adolescents to instill positive self-regard. Our results also emphasize the central role that self-perceptions play in the onset and maintenance of poor outcomes.

This study examined the interplay between a polygenic composite and cortisol activity as moderators of the mediational pathway among family adversity, youth negative emotional reactivity to family conflict, and their psychological problems. The longitudinal design contained three annual measurement occasions with 279 adolescents (Mean age = 13.0 years) and their parents. Latent difference score analyses indicated that observational ratings of adversity in interparental and parent–child interactions at Wave 1 predicted increases in a multimethod, multi-informant assessment of youth negative emotional reactivity to family conflict from Waves 1 to 2. Changes in youth negative emotional reactivity, in turn, predicted increases in a multi-informant (i.e., parents, adolescent, and teacher) assessment of psychological problems from Waves 1 to 3. Consistent with differential susceptibility theory, the association between family adversity and negative emotional reactivity was stronger for adolescents who carried more sensitivity alleles in a polygenic composite consisting of 5-HTTLPR, DRD4 VNTR, and BDNF polymorphisms. Analyses of adolescent cortisol in the period surrounding a family disagreement task at Wave 1 revealed that overall cortisol output, rather than cortisol reactivity, served as an endophenotype of the polygenic composite. Overall cortisol output was specifically associated with polygenic plasticity and moderated the association between family adversity and youth negative emotional reactivity in the same for better or for worse manner as the genetic composite. Finally, moderator-mediated-moderation analyses indicated that the moderating role of the polygenic plasticity composite was mediated by the moderating role of adolescent cortisol output in the association between family adversity and their emotional reactivity.