Relationships with parents and peers are crucial for children's socialization, but how parent–child and peer relationships mutually affect each other is not well understood. Guided by spillover theory, we zoomed in on the bidirectional interplay between parental rejection and warmth on the one hand and peer victimization on the other, and examined whether children's maladjustment symptoms mediated hypothesized cross-domain spillover effects. Data stem from five waves of the longitudinal KiVa study among 9,770 children (50% boys; mean age = 9.16, standard deviation = 1.29). Results from random intercept cross-lagged panel models showed that higher parental rejection and lower parental warmth predicted increases in peer victimization and vice versa across waves, thus supporting the bidirectional model. Moreover, spillover from parent–child rejection and warmth to peer victimization was partially driven by children's depressive symptoms and bullying perpetration. Vice versa, spillover from peer victimization to parent–child rejection and warmth was partially driven by children's social anxiety, depressive symptoms, conduct problems, and bullying perpetration. Thus, children might get caught in persistent problems in two important social domains, and these two domains influence each other through children's maladjustment. Family and school interventions should be integrated to prevent a downwards spiral.

Communication deviance (CD) reflects features of the content or manner of a person's speech that may confuse the listener and inhibit the establishment of a shared focus of attention. The construct was developed in the context of the study of familial risks for psychosis based on hypotheses regarding its effects during childhood. It is not known whether parental CD is associated with nonverbal parental behaviors that may be important in early development. This study explored the association between CD in a cohort of mothers (n = 287) at 32 weeks gestation and maternal sensitivity with infants at 29 weeks in a standard play procedure. Maternal CD predicted lower overall maternal sensitivity (B = –.385; p < .001), and the effect was somewhat greater for sensitivity to infant distress (B = –.514; p < .001) than for sensitivity to nondistress (B = –.311; p < .01). After controlling for maternal age, IQ and depression, and for socioeconomic deprivation, the associations with overall sensitivity and sensitivity to distress remained significant. The findings provide new pointers to intergenerational transmission of vulnerability involving processes implicated in both verbal and nonverbal parental behaviors.

Recent proposals suggest early adversity sets in motion particularly chronic and neurobiologically distinct trajectories of internalizing symptoms. However, few prospective studies in high-risk samples delineate distinct trajectories of internalizing symptoms from preschool age onward. We examined trajectories in a high-risk cohort, oversampled for internalizing symptoms, several preschool risk/maintenance factors, and school-age outcomes. Parents of 325 children completed the Strengths and Difficulties Questionnaire on up to four waves of data collection from preschool (3–5 years) to school age (8–9 years) and Preschool Age Psychiatric Assessment interviews at both ages. Multi-informant data were collected on risk factors and symptoms. Growth mixture modelling identified four trajectory classes of internalizing symptoms with stable low, rising low-to-moderate, stable moderate, and stable high symptoms. Children in the stable high symptom trajectory manifested clinically relevant internalizing symptoms, mainly diagnosed with anxiety disorders/depression at preschool and school age. Trajectories differed regarding loss/separation experience, maltreatment, maternal psychopathology, temperament, and stress-hormone regulation with loss/separation, temperament, maternal psychopathology, and stress-hormone regulation (trend) significantly contributing to explained variance. At school age, trajectories continued to differ on symptoms, disorders, and impairment. Our study is among the first to show that severe early adversity may trigger a chronic and neurobiologically distinct internalizing trajectory from preschool age onward.

This review summarizes current knowledge and outlines future directions relevant to questions concerning environmental epigenetics and the processes that contribute to temperament development. Links between prenatal adversity, epigenetic programming, and early manifestations of temperament are important in their own right, also informing our understanding of biological foundations for social–emotional development. In addition, infant temperament attributes represent key etiological factors in the onset of developmental psychopathology, and studies elucidating their prenatal foundations expand our understanding of developmental origins of health and disease. Prenatal adversity can take many forms, and this overview is focused on the environmental effects of stress, toxicants, substance use/psychotropic medication, and nutrition. Dysregulation associated with attention-deficit/hyperactivity–disruptive disorders was noted in the context of maternal substance use and toxicant exposures during gestation, as well as stress. Although these links can be made based on the existing literature, currently few studies directly connect environmental influences, epigenetic programming, and changes in brain development/behavior. The chain of events starting with environmental inputs and resulting in alterations to gene expression, physiology, and behavior of the organism is driven by epigenetics. Epigenetics provides the molecular mechanism of how environmental factors impact development and subsequent health and disease, including early brain and temperament development.

Alterations in reinforcement-based decision making may be associated with increased psychiatric vulnerability in children who have experienced maltreatment. A probabilistic passive avoidance task and a model-based functional magnetic resonance imaging analytic approach were implemented to assess the neurocomputational components underlying decision making: (a) reinforcement expectancies (the representation of the outcomes associated with a stimulus) and (b) prediction error signaling (the ability to detect the differences between expected and actual outcomes). There were three main findings. First, the maltreated group (n = 18; mean age = 13), relative to nonmaltreated peers (n = 19; mean age = 13), showed decreased activity during expected value processing in a widespread network commonly associated with reinforcement expectancies representation, including the striatum (especially the caudate), the orbitofrontal cortex, and medial temporal structures including the hippocampus and insula. Second, consistent with previously reported hyperresponsiveness to negative cues in the context of childhood abuse, the maltreated group showed increased prediction error signaling in the middle cingulate gyrus, somatosensory cortex, superior temporal gyrus, and thalamus. Third, the maltreated group showed increased activity in frontodorsal regions and in the putamen during expected value representation. These findings suggest that early adverse environments disrupt the development of decision-making processes, which in turn may compromise psychosocial functioning in ways that increase latent vulnerability to psychiatric disorder.

Early identification of problems with psychosocial stress regulation is important for supporting mental and physical health. However, we currently lack knowledge about when reliable individual differences in stress-responsive physiology emerge and which aspects of maternal behavior determine the unfolding of infants' stress responses. Knowledge of these processes is further limited by analytic approaches that do not account for multiple levels of within- and between-family effects. In a low-risk sample (n = 100 dyads), we observed infant cortisol and mother/infant behavior during regular play and stress sessions longitudinally from age 1 to 3, and used a three-level model to separately examine variability in infant cortisol trajectories within sessions, across years, and across infants. Stable individual differences in hypothalamus–pituitary–adrenal axis regulation were observed in the first 3 years of life. Infants of less sensitive and more intrusive mothers manifested stress sensitization, that is, elevated cortisol levels during and following stress exposure, a profile related to behavioral distress. These findings have important practical implications, suggesting that children at risk for long-term stress dysregulation may be identified in the earliest years of life.

We investigate the role of distal, proximal, and child risk factors as predictors of reading readiness and attention and behavior in children at risk of dyslexia. The parents of a longitudinal sample of 251 preschool children, including children at family risk of dyslexia and children with preschool language difficulties, provided measures of socioeconomic status, home literacy environment, family stresses, and child health via interviews and questionnaires. Assessments of children's reading-related skills, behavior, and attention were used to define their readiness for learning at school entry. Children at family risk of dyslexia and children with preschool language difficulties experienced more environmental adversities and health risks than controls. The risks associated with family risk of dyslexia and with language status were additive. Both home literacy environment and child health predicted reading readiness while home literacy environment and family stresses predicted attention and behavior. Family risk of dyslexia did not predict readiness to learn once other risks were controlled and so seems likely to be best conceptualized as representing gene–environment correlations. Pooling across risks defined a cumulative risk index, which was a significant predictor of reading readiness and, together with nonverbal ability, accounted for 31% of the variance between children.

Adolescent internalizing and externalizing psychopathology is strongly associated with adult psychiatric morbidity, including psychotic disorders. This study examined whether internalizing or externalizing trajectories (continuity/discontinuity of symptoms) from middle childhood were associated with adolescent psychotic-like experiences (PLEs). Prospective data were collected from a community sample of 553 children (mean age = 10.4 years; 50% male) and their primary caregivers. Participants completed questionnaire reports of internalizing and externalizing psychopathology and PLEs at baseline, and again approximately 2 years later. Logistic regression was used to examine the association of adolescent PLEs with four trajectories of internalizing and externalizing psychopathology (persistent, incident, remitting, and none), controlling for a range of potential confounders and sampling bias. Significant associations were identified between adolescent PLEs and the incident internalizing (adjusted odds ratio [adj. OR] = 2.96; 95% confidence interval [CI] = 1.60–5.49) and externalizing psychopathology (adj. OR = 2.14; 95% CI = 1.11–4.14) trajectories, as well as the persistent internalizing (adj. OR = 1.90; 95% CI = 1.13–3.18) and externalizing (adj. OR = 1.81, 95% CI = 1.02–3.19) trajectories. Children with remitting psychopathology trajectories were no more likely to present later PLEs than those who never experienced psychopathology. While for many individuals symptoms and illness remit during development without intervention, this study provides important insights regarding potential targets and timing for delivery of early intervention and prevention programs.

This paper presents multilevel findings on adolescents' victimization exposure from a large longitudinal cohort of twins. Data were obtained from the Environmental Risk (E-Risk) Longitudinal Twin Study, an epidemiological study of 2,232 children (1,116 twin pairs) followed to 18 years of age (with 93% retention). To assess adolescent victimization, we combined best practices in survey research on victimization with optimal approaches to measuring life stress and traumatic experiences, and introduce a reliable system for coding severity of victimization. One in three children experienced at least one type of severe victimization during adolescence (crime victimization, peer/sibling victimization, Internet/mobile phone victimization, sexual victimization, family violence, maltreatment, or neglect), and most types of victimization were more prevalent among children from low socioeconomic backgrounds. Exposure to multiple victimization types was common, as was revictimization; over half of those physically maltreated in childhood were also exposed to severe physical violence in adolescence. Biometric twin analyses revealed that environmental factors had the greatest influence on most types of victimization, while severe physical maltreatment from caregivers during adolescence was predominantly influenced by heritable factors. The findings from this study showcase how distinct levels of victimization measurement can be harmonized in large-scale studies of health and development.

Resilience and adaptation in the face of early genetic or environmental risk has become a major interest in child psychiatry over recent years. However, we still remain far from an understanding of how developing human brains as a whole adapt to the diffuse and widespread atypical synaptic function that may be characteristic of some common developmental disorders. The first part of this paper discusses four types of whole-brain adaptation in the face of early risk: redundancy, reorganization, niche construction, and adjustment of developmental rate. The second part of the paper applies these adaptation processes specifically to autism. We speculate that key features of autism may be the end result of processes of early brain adaptation, rather than the direct consequences of ongoing neural pathology.

Within a longitudinal study of 1,005 adolescents, we investigated how exposure to childhood psychosocial adversities was associated with the emergence of depressive symptoms between 14 and 17 years of age. The cohort was classified into four empirically determined adversity subtypes for two age periods in childhood (0–5 and 6–11 years). One subtype reflects normative/optimal family environments (n = 692, 69%), while the other three subtypes reflect differential suboptimal family environments (aberrant parenting: n = 71, 7%; discordant: n = 185, 18%; and hazardous: n = 57, 6%). Parent-rated child temperament at 14 years and adolescent self-reported recent negative life events in early and late adolescence were included in models implementing path analysis. There were gender-differentiated associations between childhood adversity subtypes and adolescent depressive symptoms. The discordant and hazardous subtypes were associated with elevated depressive symptoms in both genders but the aberrant parenting subtype only so in girls. Across adolescence the associations between early childhood adversity and depressive symptoms diminished for boys but remained for girls. Emotional temperament was also associated with depressive symptoms in both genders, while proximal negative life events related to depressive symptoms in girls only. There may be neurodevelopmental factors that emerge in adolescence that reduce depressogenic symptoms in boys but increase such formation in girls.

A randomized clinical trial was conducted to evaluate the efficacy of interpersonal psychotherapy (IPT) for ethnically and racially diverse, economically disadvantaged women with major depressive disorder. Non-treatment-seeking urban women (N = 128; M age = 25.40, SD = 4.98) with infants were recruited from the community. Participants were at or below the poverty level: 59.4% were Black and 21.1% were Hispanic. Women were screened for depressive symptoms using the Center for Epidemiologic Studies Depression Scale; the Diagnostic Interview Schedule was used to confirm major depressive disorder diagnosis. Participants were randomized to individual IPT or enhanced community standard. Depressive symptoms were assessed before, after, and 8 months posttreatment with the Beck Depression Inventory—II and the Revised Hamilton Rating Scale for Depression. The Social Support Behaviors Scale, the Social Adjustment Scale—Self-Report, and the Perceived Stress Scale were administered to examine mediators of outcome at follow-up. Treatment effects were evaluated with a growth mixture model for randomized trials using complier-average causal effect estimation. Depressive symptoms trajectories from baseline through postintervention to follow-up showed significant decreases among the IPT group compared to the enhanced community standard group. Changes on the Perceived Stress Scale and the Social Support Behaviors Scale mediated sustained treatment outcome.