This study examined the mediating role of maternal unsupportive parenting in explaining associations between family instability and children's externalizing symptoms during the transition to formal schooling in early childhood. Participants included 243 preschool children (M age = 4.60 years) and their parents. Findings from cross-lagged autoregressive models conducted with multimethod (survey and observations), multi-informant (parent, teacher, and observer), longitudinal (three annual waves of data collection) data indicated that experiences with heightened family instability predicted decreases in supportive parenting, which in turn predicted increases in children's externalizing symptoms. Analyses also revealed a bidirectional association between parenting and family instability over time, such that higher levels of instability predicted decreases in supportive parenting, which in turn predicted increases in family instability.

Classrooms are key social settings that impact children's mental health, though individual differences in physiological reactivity may render children more or less susceptible to classroom environments. In a diverse sample of children from 19 kindergarten classrooms (N = 338, 48% female, M age = 5.32 years), we examined whether children's parasympathetic reactivity moderated the association between classroom climate and externalizing symptoms. Independent observers coded teachers’ use of child-centered and teacher-directed instructional practices across classroom social and management domains. Children's respiratory sinus arrhythmia reactivity to challenge tasks was assessed in fall and a multi-informant measure of externalizing was collected in fall and spring. Both the social and the management domains of classroom climate significantly interacted with children's respiratory sinus arrhythmia reactivity to predict spring externalizing symptoms, controlling for fall symptoms. For more reactive children, as classrooms shifted toward greater proportional use of child-centered methods, externalizing symptoms declined, whereas greater use of teacher-dominated practices was associated with increased symptoms. Conversely, among less reactive children, exposure to more teacher-dominated classroom management practices was associated with lower externalizing. Consistent with the theory of biological sensitivity to context, considering variability in children's physiological reactivity aids understanding of the salience of the classroom environment for children's mental health.

The mediational sequence from body dissatisfaction through dieting to bulimia—often referred to as the “restraint pathway”—has been validated in numerous samples of adolescent girls, but the prevalence rate of bulimic pathology pales in comparison to rates of body dissatisfaction and dieting in this risk group. This discrepancy indicates that the restraint pathway may only apply to adolescent girls possessing certain characteristics or experiencing certain circumstances. Accordingly, the current study examined the moderating roles of thin-ideal internalization, interoceptive deficits, and age by using self-report data from a community sample of 353 middle school (n = 115), high school (n = 112), and college girls (n = 126). We found that (a) body-dissatisfied girls who reported high, versus low, thin-ideal internalization engaged in greater dietary restraint; (b) only dieters who reported high interoceptive deficits and were of college age expressed bulimic symptoms; and (c) the mediating effect pertained only to college girls with high interoceptive deficits, but was strongest for those who reported high, versus low, thin-ideal internalization. These results suggest that the restraint pathway's precision may be fine-tuned through greater sensitivity to potentiating factors and developmental context. Theoretical, empirical, and practical implications are discussed.

A considerable body of research has linked parenting to the development of children's self-regulation. However, few studies have considered different domains of self-regulation, the effects of early caregiving behaviors, and whether or not parenting influences children equally. Towards this, the present investigation tested how early maternal insensitivity was associated with difficulties in children's effortful control in early childhood and their regulation of negative emotions during the early school years. Further, we tested whether children's resting vagal tone may operate as a susceptibility factor, consistent with differential susceptibility models. The sample included 220 pairs of mothers and their children who were assessed at 18 months, 3.5 years and 5 years of age. Laboratory visits consisted of observational paradigms and survey assessments. Early maternal insensitivity at 18 months of age forecasted difficulties with effortful control at age 3.5. Moreover, effortful control at age 3.5 was associated with greater anger, but not sadness, regulation at age 5. Consistent with differential susceptibility, children's resting vagal tone at 18 months of age moderated the role of early caregiving on children's effortful control. The findings suggest that low resting vagal tone may operate as a differential susceptibility factor in process models testing associations between early caregiving environments and children's self-regulation.

Utilizing a large (N = 739), ancestrally homogenous sample, the current study aimed to better understand biological risk processes involved in the development of depressive symptoms in maltreated, African American children age 8-12 years. Maltreatment was independently coded from Child Protective Services records and maternal report. Self-reported depressive symptoms were attained in the context of a week-long, summer research camp. DNA was acquired from buccal cell or saliva samples and genotyped for nine polymorphisms in four hypothalamic-pituitary-adrenal (HPA)-axis-related genes: FKBP5, NR3C1, NR3C2, and CRHR1. Salivary cortisol samples were collected each morning (9 a.m.) and late afternoon (4 p.m.) throughout the week to assess HPA functioning. Results revealed that experiences of maltreatment beginning prior to age 5 were most predictive of depressive symptoms, whereas maltreatment onset after age 5 was most predictive of HPA axis dysregulation (blunted daytime cortisol patterns). Multigenic risk did not relate to HPA functioning, nor did it moderate the relationship between maltreatment and HPA activity. There was no mediation of the relationship between maltreatment and depressive symptoms by HPA dysfunction. Results are interpreted through a developmental psychopathology lens, emphasizing the principle of equifinality while carefully appraising racial differences. Implications for future research, particularly the need for longitudinal studies, and important methodological considerations are discussed.

Pubertal timing matters for psychological development. Early maturation in girls is linked to risk for depression and externalizing problems in adolescence and possibly adulthood, and early and late maturation in boys are linked to depression. It is unclear whether pubertal timing uniquely predicts problems; it might instead mediate the continuity of behavior problems from childhood to adolescence or create psychological risk specifically in youth with existing problems, thus moderating the link. We investigated these issues in 534 girls and 550 boys, measuring pubertal timing by a logistic model fit to annual self-report measures of development and, in girls, age at menarche. Prepuberty internalizing and externalizing behavior problems were reported by parents. Adolescent behavior problems were reported by parents and youth. As expected, behavior problems were moderately stable. Pubertal timing was not predicted by childhood problems, so it did not mediate the continuity of behavior problems from childhood to adolescence. Pubertal timing did not moderate links between early and later problems for girls. For boys, early maturation accentuated the link between childhood problems and adolescent substance use. Overall, the replicated links between puberty and behavior problems appear to reflect the unique effects of puberty and child behavior problems on the development of adolescent behavior problems.

Emotional distress during pregnancy is likely influenced by both maternal history of adversity and concurrent prenatal stressors, but prospective longitudinal studies are lacking. Guided by a life span model of pregnancy health and stress sensitization theories, this study investigated the influence of intimate partner violence (IPV) during pregnancy on the association between childhood adversity and prenatal emotional distress. Participants included an urban, community-based sample of 200 pregnant women (aged 18–24) assessed annually from ages 8 to 17 for a range of adversity domains, including traumatic violence, harsh parenting, caregiver loss, and compromised parenting. Models tested both linear and nonlinear effects of adversity as well as their interactions with IPV on prenatal anxiety and depression symptoms, controlling for potential confounds such as poverty and childhood anxiety and depression. Results showed that the associations between childhood adversity and pregnancy emotional distress were moderated by prenatal IPV, supporting a life span conceptualization of pregnancy health. Patterns of interactions were nonlinear, consistent with theories conceptualizing stress sensitization through an “adaptive calibration” lens. Furthermore, results diverged based on adversity subdomain and type of prenatal IPV (physical vs. emotional abuse). Findings are discussed in the context of existing stress sensitization theories and highlight important avenues for future research and practice.

Megan Gunnar's pubertal stress recalibration hypothesis was supported in a recent study of previously institutionalized (PI) youth such that increases in pubertal stage were associated with increases in cortisol stress reactivity. This work provides evidence that puberty may open up a window of recalibration for PI youth, resulting in a shift from a blunted to a more typical cortisol stress response. Using the same sample (N = 132), the current study aimed to elucidate whether increases in cortisol are associated with increases in adaptive functioning or whether they further underlie potential links to developmental psychopathology. Specifically, we examined the bidirectional associations between cortisol stress reactivity and both internalizing and externalizing symptoms across three timepoints during the pubertal period. Youth reported on their own internalizing symptoms and parents reported on youths’ externalizing symptoms. Cortisol reactivity was assessed during the Trier social stress test. Analyses revealed no associations between cortisol reactivity and externalizing symptoms across puberty for PI youth. However, longitudinal bidirectional associations did emerge for internalizing symptoms such that increases in cortisol reactivity predicted increases in internalizing symptoms and increases in internalizing symptoms predicted increases in cortisol reactivity. Findings suggest that recalibrating to more normative levels of cortisol reactivity may not always be associated with adaptive outcomes for PI youth.

At multiple developmental periods spanning from middle childhood through adolescence, we investigated the development of aggressive-victims. Multiple-informant data collected across four grade levels (1, 5, 8, and 11; N = 482; 50% females) was used to perform person-centered analyses including latent profile and latent transition analyses in order to examine the co-occurring development of multiple forms (i.e., physical, verbal, and relational) of aggression and peer victimization. Results indicated that there were two distinct subgroups of aggressive-victims, one of which was more relational in form (i.e., relational aggressive-victims), and children in these two subgroups were distinguishable with respect to their individual characteristics (emotion dysregulation, withdrawn behaviors, and moral disengagement) and relational experiences (peer rejection and friendships). Furthermore, the findings elucidated the mechanisms by which developmental continuity and change (i.e., transitions) among the subgroups occurred across childhood and adolescence.

To understand how exposure to victimization during adolescence and the presence of comorbid psychological conditions influence substance use treatment entry and substance use disorder diagnosis from 14 to 25 years old among serious juvenile offenders, this study included 1,354 serious juvenile offenders who were prospectively followed over 7 years. Growth mixture modeling was used to assess profiles of early victimization during adolescence (14–17 years). Discrete time survival mixture analysis was used to assess time to treatment entry and substance use disorder diagnosis. Posttraumatic stress disorder (PTSD) and major depressive disorder (MDD) were used as predictors of survival time. Mixture models revealed three profiles of victimization: sustained poly-victimization, moderate/decreasing victimization, and low victimization. Youth in the sustained poly-victimization class were more likely to enter treatment earlier and have a substance use diagnosis earlier than other classes. PTSD was a significant predictor of treatment entry for youth in the sustained poly-victimization class, and MDD was a significant predictor of substance use disorder diagnosis for youth in the moderate/decreasing victimization class. Therefore, substance use prevention programming targeted at youth experiencing poly-victimization in early adolescence—especially those who have PTSD or MDD—is needed.

Psychosocial acceleration theory suggests that pubertal maturation is accelerated in response to adversity. In addition, suboptimal caregiving accelerates development of the amygdala–medial prefrontal cortex circuit. These findings may be related. Here, we assess whether associations between family environment and measures of the amygdala–medial prefrontal cortex circuit are mediated by pubertal development in more than 2000 9- and 10-year-old children from the Adolescent Brain Cognitive Development Study (http://dx.doi.org/10.15154/1412097). Using structural equation modeling, demographic, child-reported, and parent-reported data on family dynamics were compiled into a higher level family environment latent variable. Magnetic resonance imaging preprocessing and compilations were performed by the Adolescent Brain Cognitive Development Study's data analysis core. Anterior cingulate cortex (ACC) thickness, area, white matter fractional anisotropy, amygdala volume, and cingulo-opercular network–amygdala resting-state functional connectivity were assessed. For ACC cortical thickness and ACC fractional anisotropy, significant indirect effects indicated that a stressful family environment relates to more advanced pubertal stage and more mature brain structure. For cingulo-opercular network–amygdala functional connectivity, results indicated a trend in the expected direction. For ACC area, evidence for quadratic mediation by pubertal stage was found. Sex-stratified analyses suggest stronger results for girls. Despite small effect sizes, structural measures of circuits important for emotional behavior are associated with family environment and show initial evidence of accelerated pubertal development.

A large and growing body of research suggests that maternal depressive symptoms and child externalizing behaviors are strongly associated. Theoretical arguments supported by these findings led to the question of whether maternal depressive symptoms are transactionally associated with child externalizing behaviors. Using 5-year nationally representative longitudinal data from Turkey (N = 1,052), we estimated a transactional bivariate autoregressive latent trajectory model addressing this question. This model disaggregated the association of the two processes into two components: (a) the association of the interindividual differences in the trajectories; and (b) the intradyad association of the changes in maternal depressive symptoms with the changes in child externalizing behaviors. Although maternal depressive symptoms were robustly associated with child externalizing behaviors at age 3, the transactional associations of the two processes were small prior to age 5 and absent at ages 5 to 7. Furthermore, maternal harsh parenting did not have a mediating role in the limited transactional association of maternal depressive symptoms with child externalizing behaviors.

Early neglect or maltreatment has been associated with changes in children's processing of emotional facial expressions, including a hypersensitivity to the emotion of anger. This may facilitate the avoidance of danger in a maltreating environment. However, few studies have examined whether experiences of early life stress (ELS) are associated with atypical avoidance responses towards emotional facial expressions, or whether the effects of ELS can be observed in adult participants. The present study therefore examined the effects of ELS on adults’ approach-avoidance tendencies towards angry, happy, and neutral facial expressions. Surprisingly, higher levels of ELS were associated with reduced avoidance of angry facial expressions among individuals with no evidence of mental illness. In contrast, there was no evidence of a relationship between ELS and avoidance of angry facial expressions among individuals with experience of mental illness. These novel findings suggest that ELS-related changes in social cognition can be observed years after the ELS itself occurred.

Maltreatment during development is associated with epigenetic changes to the genome. Enhancing caregiving may mitigate these effects. Attachment and Biobehavioral Catch-Up (ABC) is an intervention that has been shown to improve parent–child relationships and a variety of biological and behavioral outcomes among children that are involved in Child Protective Services. This preliminary study, using a small sample size, explored whether children who received ABC exhibit different methylation patterns than those who received a control intervention. The participants included 23 children aged 6–21 months who were randomized to receive ABC (n = 12) or a control intervention (n = 11). While the children displayed similar methylation patterns preintervention, DNA methylation varied between the ABC and control groups at 14,828 sites postintervention. Functional pathway analyses indicated that these differences were associated with gene pathways that are involved in cell signaling, metabolism, and neuronal development. This study is one of the first to explore parenting intervention effects on children's DNA methylation at the whole genome level in infancy. These preliminary findings provide a basis for hypothesis generation in further research with larger-scale studies regarding the malleability of epigenetic states that are associated with maltreatment.

Greater psychosocial risk in childhood and adolescence predicts poorer cardiometabolic outcomes in adulthood. We assessed whether the timing of psychosocial risk from infancy through adolescence predicts cardiometabolic outcomes in young adulthood. Young adults and their mothers participated in a longitudinal study beginning in infancy in Santiago, Chile (N = 1040). At infancy, 5 years, 10 years, and adolescence, mothers reported on depressive symptoms, stressful experiences, support for child development in the home, father absence, parental education, and socioeconomic status (SES) to create a psychosocial risk composite at each time point. Young adults (52.1% female; 21–27 years) provided fasting serum samples and participated in anthropometric and blood pressure (BP) assessments, including a dual-energy X-ray absorptiometry (DXA) scan for measuring body fat. Greater infant psychosocial risk was associated with a greater young adult metabolic syndrome score (β = 0.07, 95% confidence intervals (CI): 0.01 to 0.13, p = 0.02), a higher body mass index and waist circumference composite (β = 0.08, 95% CI: 0.03 to 0.13, p = 0.002), and a higher body fat (DXA) composite (β = 0.07, 95% CI: 0.01 to 0.12, p = 0.02). No psychosocial risk measure from any time point was associated with BP. Infant psychosocial risk predicted cardiometabolic outcomes in young adulthood better than psychosocial risk at 5 years, 10 years, or adolescence, mean of psychosocial risk from infancy through adolescence, and maximum of psychosocial risk at any one time. Consistent with the Developmental Origins of Health and Disease model, findings suggest that infancy is a sensitive period for psychosocial risk leading to poorer cardiometabolic outcomes in young adulthood.

The study examined (a) whether alcohol use subgroups could be identified among African Americans assessed from adolescence through early adulthood, and (b) whether subgroup membership was associated with the interaction between internalizing symptoms and antisocial behavior polygenic risk scores (PRSs) and environmental characteristics (i.e., parental monitoring, community disadvantage). Participants (N = 436) were initially recruited for an elementary school-based prevention trial in a Mid-Atlantic city. Youths reported on the frequency of their past year alcohol use from ages 14–26. DNA was obtained from participants at age 21. Internalizing symptoms and antisocial behavior PRSs were created based on a genome-wide association study (GWAS) conducted by Benke et al. (2014) and Tielbeek et al. (2017), respectively. Parental monitoring and community disadvantage were assessed at age 12. Four classes of past year alcohol use were identified: (a) early-onset, increasing; (b) late-onset, moderate use; (c) low steady; and (d) early-onset, decreasing. In high community disadvantaged settings, participants with a higher internalizing symptoms PRS were more likely to be in the early-onset, decreasing class than the low steady class. When exposed to elevated community disadvantage, participants with a higher antisocial behavior PRS were more likely to be in the early-onset, increasing class than the early-onset, decreasing and late-onset, moderate use classes.

Gastrointestinal and mental disorders are highly comorbid, and animal models have shown that both can be caused by early adversity (e.g., parental deprivation). Interactions between the brain and bacteria that live within the gastrointestinal system (the microbiome) underlie adversity–gastrointestinal–anxiety interactions, but these links have not been investigated during human development. In this study, we utilized data from a population of 344 youth (3–18 years old) who were raised with their biological parents or were exposed to early adverse caregiving experiences (i.e., institutional or foster care followed by international adoption) to explore adversity–gastrointestinal–anxiety associations. In Study 1, we demonstrated that previous adverse care experiences were associated with increased incidence of gastrointestinal symptoms in youth. Gastrointestinal symptoms were also associated with concurrent and future anxiety (measured across 5 years), and those gastrointestinal symptoms mediated the adversity–anxiety association at Time 1. In a subsample of children who provided both stool samples and functional magnetic resonance imaging of the brain (Study 2, which was a “proof-of-principle”), adversity was associated with changes in diversity (both alpha and beta) of microbial communities, and bacteria levels (adversity-associated and adversity-independent) were correlated with prefrontal cortex activation to emotional faces. Implications of these data for supporting youth mental health are discussed.

The hypothalamic–pituitary–adrenal (HPA) axis is sensitive to early life stress, with enduring consequences for biological stress vulnerability and health (Gunnar & Talge, 2008). Low socioeconomic status (SES) is associated with dysregulation of the stress hormone cortisol in early childhood. However, a mechanistic understanding of this association is lacking. Multidimensional assessment of both SES and cortisol is needed to characterize the intricate relations between SES and cortisol function in early childhood. We assessed parent-reported family income, parent education, occupational prestige, neighborhood risk, food insecurity, and household chaos for 12-month-old infants (N = 90) and 3.5-year-old children (N = 91). Hair cortisol concentration (HCC) was obtained from parent and child, indexing chronic biological stress, and diurnal salivary cortisol was measured in the children. Controlling for parent HCC, parent education uniquely predicted infant and child HCC and, in addition, neighborhood risk uniquely predicted infant HCC. Household chaos predicted bedtime salivary cortisol concentration (SCC) for both infants and children, and infant daily cortisol output. Food insecurity was associated with flattened cortisol slope in 3.5-year-old children. Parental sensitivity did not mediate relations between SES and cortisol. Results highlight the utility of SES measures that index unpredictable and unsafe contexts, such as neighborhood risk, food insecurity, and household chaos.

Moral reasoning and decision making help guide behavior and facilitate interpersonal relationships. Accounts of morality that position commonsense psychology as the foundation of moral development, (i.e., rationalist theories) have dominated research in morality in autism spectrum disorder (ASD). Given the well-documented differences in commonsense psychology among autistic individuals, researchers have investigated whether the development and execution of moral judgement and reasoning differs in this population compared with neurotypical individuals. In light of the diverse findings of investigations of moral development and reasoning in ASD, a summation and critical evaluation of the literature could help make sense of what is known about this important social-cognitive skill in ASD. To that end, we conducted a systematic review of the literature investigating moral decision making among autistic children and adults. Our search identified 29 studies. In this review, we synthesize the research in the area and provide suggestions for future research. Such research could include the application of an alternative theoretical framework to studying morality in autism spectrum disorder that does not assume a deficits-based perspective.

Belonging to a social group is one of the most important factors contributing to well-being. The Belonging Regulation model proposes that humans possess a social monitoring system (SMS) that evaluates social inclusion and monitors belonging needs. Here, we used a prospective longitudinal design to examine links between peer victimization experienced across 7 years and social monitoring at the behavioral and neural level in adolescent girls (n = 38, Mage = 15.43 years, SD = .33). Participants completed a social evaluation task during a functional magnetic resonance imaging (fMRI) scan. More severe peer victimization was associated with increased activation to in-group versus out-group peers in the amygdala, ventral striatum, fusiform gyrus, and temporoparietal junction. Moreover, participants who displayed increased activation in these regions reported lower social self esteem and higher levels of internalizing and externalizing symptoms. These results suggest that exposure to peer victimization across the school years is associated with heightened social monitoring at the neural level during adolescence, which has potential adverse implications for girls’ adjustment and well-being.