Although infants less than 18 months old are capable of engaging in self-regulatory behavior (e.g., avoidance, withdrawal, and orienting to other aspects of their environment), the use of self-regulatory strategies at this age (as opposed to relying on caregivers) is associated with elevated behavioral and physiological distress. This study investigated infant dopamine-related genotypes (dopamine receptor D2 [DRD2], dopamine transporter solute carrier family C6, member 4 [SLC6A3], and catechol-O-methyltransferase [COMT]) as they interact with maternal self-reported history of maltreatment to predict observed infant independent emotion regulation behavior. A community sample (N = 193) of mother–infant dyads participated in a toy frustration challenge at infant age 15 months, and infant emotion regulation behavior was coded. Buccal cells were collected for genotyping. Maternal maltreatment history significantly interacted with infant SLC6A3 and COMT genotypes, such that infants with more 10-repeat and valine alleles of SLC6A3 and COMT, respectively, relative to infants with fewer or no 10-repeat and valine alleles, utilized more independent (i.e., maladaptive) regulatory behavior if mother reported a more extensive maltreatment history, as opposed to less. The findings indicate that child genetic factors moderate the intergenerational impact of maternal maltreatment history. The results are discussed in terms of potential mechanism of Gene × Environment interaction.

Prenatal experience is both a formative and a regulatory force in the process of development. As a result, birth is not an adequate starting point for explanations of behavioral development. However, surprisingly little is currently known regarding the role of prenatal experience in the emergence and facilitation of perceptual, cognitive, or social development. Our lack of knowledge in this area is due in part to the very restricted experimental manipulations possible with human fetuses. A comparative approach utilizing animal models provides an essential step in addressing this gap in our knowledge and providing testable predictions for studies with human fetuses, infants, and children. Further, animal-based comparative research serves to minimize the amount of exploratory research undertaken with human subjects and hone in on issues and research directions worthy of further research investment. In this article, I review selected animal-based research exploring how developmental influences during the prenatal period can guide and constrain subsequent behavioral and social development. I then discuss the importance of linking the prenatal environment to postnatal outcomes in terms of how psychologists conceptualize “innate” biases, preferences, and skills in the study of human development.

Among children exposed to elevated maternal depression symptoms (MDS), recent studies have demonstrated reduced internalizing and externalizing problems for those who have attended formal childcare (i.e., center-based, family-based childcare). However, these studies did not consider whether childcare attendance is associated with benefits for the child only or also with reduced MDS. Using a four-wave longitudinal cross-lagged model, we evaluated whether formal childcare attendance was associated with MDS or child behavior problems and whether it moderated longitudinal associations between MDS and child behavior problems and between child behavior problems and MDS. The sample was drawn from a population-based cohort study and consisted of 908 biologically related mother–child dyads, followed from 5 months to 5 years. Attending formal childcare was not associated with MDS or child behavior problems but moderated the association between MDS at 3.5 years and child internalizing and externalizing problems at 5 years as well as between girls’ externalizing problems at 3.5 years and MDS at 5 years. No other moderation of formal childcare was found. Findings suggest that attending formal childcare reduces the risks of behavior problems in the context of MDS but also the risk of MDS in the context of girls’ externalizing problems.

Research on Gene × Environment interactions typically focuses on maladaptive contexts and outcomes. However, the same genetic factors may also impact susceptibility to positive social contexts, leading to adaptive behavior. This paper examines whether the GABA receptor subunit alpha-2 (GABRA2) single nucleotide polymorphism rs279858 moderates the influence of positive peer affiliation on externalizing behavior and various forms of competence. Regions of significance were calculated to determine whether the form of the interaction supported differential susceptibility (increased sensitivity to both low and high positive peer affiliation) or vantage sensitivity (increased sensitivity to high positive peer affiliation). It was hypothesized that those carrying the homozygous minor allele (GG) would be more susceptible to peer effects. A sample (n = 300) of primarily male (69.7%) and White (93.0%) adolescents from the Michigan Longitudinal Study was assessed from ages 12 to 17. There was evidence for prospective Gene × Environment interactions in three of the four models. At low levels of positive peer involvement, those with the GG genotype were rated as having fewer adaptive outcomes, while at high levels they were rated as having greater adaptive outcomes. This supports differential susceptibility. Conceptualizing GABRA2 variants as purely risk factors may be inaccurate. Genetic differences in susceptibility to adaptive environmental exposures warrants further investigation.

Young children's disregard for conduct rules (failing to experience discomfort following transgressions and violating adults' prohibitions) often foreshadows future antisocial trajectories, perhaps in part because it elicits more power-assertive parental discipline, which in turn promotes children's antisocial behavior. This process may be particularly likely for children with low skin conductance level (SCL). In 102 two-parent community families, we tested a model in which children's SCL, assessed at 8 years, was posed as a moderator of the cascade from children's disregard for conduct rules at 4.5 years to parents' power assertion at 5.5 and 6.5 years to antisocial behavior at 10 and 12 years. Children's disregard for conduct rules was observed in scripted laboratory paradigms, parents' power assertion was observed in discipline contexts, and children's antisocial behavior was rated by parents. Conditional process analyses revealed that the developmental cascade from early disregard for rules to future parental power assertion to antisocial outcomes occurred only for the children with low SCL (below median), but not their high-SCL (above median) peers. By elucidating the specific interplay among children's disregard for rules, the parenting they receive, and their psychophysiology, this study represents a developmentally informed, multilevel approach to early etiology of antisocial behavior.

Individuals with Williams syndrome and those with Down syndrome are both characterized by heightened social interest, although the manifestation is not always similar. Using a dot-probe task, we examined one possible source of difference: allocation of attention to facial expressions of emotion. Thirteen individuals with Williams syndrome (mean age = 19.2 years, range = 10–28.6), 20 with Down syndrome (mean age = 18.8 years, range = 12.1–26.3), and 19 typically developing children participated. The groups were matched for mental age (mean = 5.8 years). None of the groups displayed a bias to angry faces. The participants with Williams syndrome showed a selective bias toward happy faces, whereas the participants with Down syndrome behaved similarly to the typically developing participants with no such bias. Homogeneity in the direction of bias was markedly highest in the Williams syndrome group whose bias appeared to result from enhanced attention capture. They appeared to rapidly and selectively allocate attention toward positive facial expressions. The complexity of social approach behavior and the need to explore other aspects of cognition that may be implicated in this behavior in both syndromes is discussed.

An association has been found between receipt of harsh parenting in childhood and adult health problems. However, this research has been principally retrospective, has treated children as passive recipients of parental behavior, and has overlooked individual differences in youth responsivity to harsh parenting. In a 10-year multiple-wave prospective study of African American families, we addressed these issues by focusing on the influence of polymorphisms in the oxytocin receptor gene (OXTR), variants of which appear to buffer or amplify responses to environmental stress. The participants were 303 youths, with a mean age of 11.2 at the first assessment, and their parents, all of whom were genotyped for variations in the rs53576 (A/G) polymorphism. Teachers rated preadolescent (ages 11 to 13) emotionally intense and distractible temperaments, and adolescents (ages 15 and 16) reported receipt of harsh parenting. Allostatic load was assessed during young adulthood (ages 20 and 21). Difficult preadolescent temperament forecast elevated receipt of harsh parenting in adolescence, and adolescents who experienced harsh parenting evinced high allostatic load during young adulthood. However, these associations emerged only among children and parents who carried A alleles of the OXTR genotype. The results suggest the oxytocin system operates along with temperament and parenting to forecast young adults’ allostatic load.

Dysregulated physiological stress reactivity has been suggested to impact the development of children and adolescents with important health consequences throughout the life span. Both environmental adversity and genetic predispositions can lead to physiological imbalances in stress systems, which in turn lead to developmental differences. We investigated genetic and environmental contributions to autonomic nervous system reactivity to a psychosocial stressor. Furthermore, we tested whether these effects were consistent with the differential susceptibility framework. Composite measures of adverse life events combined with socioeconomic status were constructed. Effects of these adversity scores in interaction with a polygenic score summarizing six genetic variants, which were hypothesized to work as susceptibility factors, were tested on autonomic nervous system measures as indexed by heart rate and heart rate variability. Results showed that carriers of more genetic variants and exposed to high adversity manifested enhanced heart rate variability reactivity to a psychosocial stressor compared to carriers of fewer genetic variants. Conversely, the stress procedure elicited a more moderate response in these individuals compared to carriers of fewer variants when adversity was low.

The etiology of psychopathology is multifaceted and warrants consideration of factors at multiple levels and across developmental time. Although experiences of adversity in early life have been associated with increased risk of developing psychopathology, pathways toward maladaptation or resilience are complex and depend upon a variety of factors, including individuals’ physiological regulation and cognitive functioning. Therefore, in a longitudinal cohort of 113 mother–child dyads, we explored associations from early adverse experiences to physiological coregulation across multiple systems and subsequent variations in executive functioning. Latent profile analysis derived multisystem profiles based on children's heart rate, respiratory sinus arrhythmia, pre-ejection period, and cortisol measured during periods of rest and reactivity throughout a developmentally challenging protocol. Three distinct profiles of multisystem regulation emerged: heightened multisystem baseline activity (anticipatory arousal/ autonomic nervous system [ANS] responder), typically adaptive patterns across all systems (active copers/mobilizers), and heightened hypothalamic–pituitary–adrenal (HPA) axis activity (HPA axis responders). Path models revealed that children exposed to adversity before 18 months were more likely to evidence an anticipatory arousal/ANS responders response at 36 months, and children in this profile had lower executive functioning scores than the active copers/mobilizers. In sum, these findings provide important information about potential physiological associations linking early adversity to variations in children's task-based executive functioning.

Youth's academic and emotional functioning are closely related, yet little is known about the timing and direction of relationships involving internalizing problems, which are characterized by over control of emotions, anxiety, and depression as well as multiple aspects of academic achievement. This study addresses these gaps using data from the Study of Early Child Care and Youth Development (N = 1,048) to examine the processes by which problems in one domain of functioning lead to problems in another, known as a “cascade effect.” Results of longitudinal structural equation modeling indicate (a) a direct and indirect negative cascade effect from girls’ internalizing problems to their school achievement in high school, (b) a positive contemporaneous association of 9th grade boys’ internalizing problems with their cognitive achievement; and (c) ways in which demographic characteristics and adolescent social and maturational processes account for variation in functioning yet do not alter the processes by which the emotional and academic functioning interact. Results are discussed with regard to identifiying adolescents’ internalizing problems, gender differences in the effects of internalizing problems on academic functioning, timing of evidence-based interventions, and implications for mental health promotion among girls.

Exposure to childhood adversity is a powerful risk factor for psychopathology. Despite extensive efforts, we have not yet identified effective or scalable interventions that prevent the emergence of mental health problems in children who have experienced adversity. In this modified Delphi study, we identified intervention strategies for effectively targeting both the neurodevelopmental mechanisms linking childhood adversity and psychopathology – including heightened emotional reactivity, difficulties with emotion regulation, blunted reward processing, and social information processing biases, as well as a range of psychopathology symptoms. We iteratively synthesized information from experts in the field and relevant meta-analyses through three surveys, first with experts in intervention development, prevention, and childhood adversity (n = 32), and then within our study team (n = 8). The results produced increasing stability and good consensus on intervention strategy recommendations for specific neurodevelopmental mechanisms and symptom presentations and on strength of evidence ratings of intervention strategies targeting youth and parents. More broadly, our findings highlight how intervention decision making can be informed by meta-analyses, enhanced by aggregate group feedback, saturated before consensus, and persistently subjective or even contradictory. Ultimately, the results converged on several promising intervention strategies for prevention programming with adversity-exposed youth, which will be tested in an upcoming clinical trial.

The ability to regulate stress is a critical developmental milestone of early childhood that involves a set of interconnected behavioral and physiological processes and is influenced by genetic and environmental stimuli. Prenatal exposure to traumatic stress and trauma, including intimate partner violence (IPV), increases risk for offspring biobehavioral regulation problems during childhood and adolescence. Although individual differences in susceptibility to prenatal stress have been largely unexplored, a handful of studies suggest children with specific genetic characteristics are most vulnerable to prenatal stress. We evaluated the brain-derived neurotrophic factor Val66Met gene (BDNF) as a moderator of the effect of prenatal IPV exposure on infant temperamental and cortisol regulation in response to a psychosocial challenge. Ninety-nine mother–infant dyads recruited from the community were assessed when infants (51% female) were 11 to 14 months. Maternal reports of IPV during pregnancy and infant temperament were obtained, and infant saliva was collected for genotyping and to assess cortisol reactivity (before and after the Strange Situation Task). Significant genetic moderation effects were found. Among infants with the BDNF Met allele, prenatal IPV predicted worse temperamental regulation and mobilization of the cortisol response, while controlling for infant postnatal exposure to IPV, other maternal traumatic experiences, and infant sex. However, prenatal IPV exposure was not associated with temperamental or cortisol outcomes among infant carriers of the Val/Val genotype. Findings are discussed in relation to prenatal programming and biological susceptibility to stress.

Whether men's and women's reciprocation of their intimate partners’ negative and positive affect during conflictual topic discussions accounted for the association between their trait hostility and perpetration of physical intimate partner violence (IPV) was examined within a dyadic model, using concurrent measurement. The work builds on that of Dr. Tom Dishion regarding hostile and coercive interactions in key relationships on risk outcomes and the importance of moment-by-moment influences in social interactions. Using dynamic development systems theory and a community sample of at-risk men (N = 156) and their female partners, the hypothesis that quicker negative and slower positive affect reactivity would account for physical IPV perpetration beyond trait hostility was tested. Results suggest that, for women, quicker negative affect reactivity partially explains the hostility IPV association, whereas for men, trait hostility of both partners best explained their perpetration of physical IPV. No support was found for positive affect reactivity as a protective relationship process for IPV involvement. Findings are in line with other studies indicating men were less likely to engage in negative reciprocity relative to women. Furthermore, findings highlight how both partners’ individual characteristics, communication patterns, and emotion regulation processes germane to the romantic relationship impact the likelihood of experiencing physical IPV.

Given the equivocal literature on the relationship between internalizing symptoms and early adolescent alcohol use (AU) and AU disorder (AUD), the present study took a developmental perspective to understand how internalizing and externalizing symptoms may operate together in the etiology of AU and AUD. We pit the delayed onset and rapid escalation hypothesis (Hussong et al., 2011) against a synthesis of the dual failure model and the stable co-occurring hypothesis (Capaldi, 1992; Colder et al., 2013, 2018) to test competing developmental pathways to adolescent AU and AUD involving problem behavior, peer delinquency, and early initiation of AU. A latent transactional and mediational framework was used to test pathways to AUD spanning developmental periods before AU initiation (Mage = 11) to early and high risk for AUD (Mage = 14–15 and Mage = 17–18). The results supported three pathways to AUD. The first started with “pure” externalizing symptoms in early childhood and involved multiple mediators, including the subsequent development of co-occurring symptoms and peer delinquency. The second pathway involved stable co-occurring symptoms. Interestingly, chronically elevated pure internalizing symptoms did not figure prominently in pathways to AUD. Selection and socialization effects between early AU and peer delinquency constituted a third pathway.

Adolescent association with deviant and delinquent friends was examined for its roots in coercive parent–teen interactions and its links to functional difficulties extending beyond delinquent behavior and into adulthood. A community sample of 184 adolescents was followed from age 13 to age 27, with collateral data obtained from close friends, classmates, and parents. Even after accounting for adolescent levels of delinquent and deviant behavior, association with deviant friends was predicted by coercive parent–teen interactions and then linked to declining functioning with peers during adolescence and greater internalizing and externalizing symptoms and poorer overall adjustment in adulthood. Results are interpreted as suggesting that association with deviant friends may disrupt a core developmental task—establishing positive relationships with peers—with implications that extend well beyond deviancy-training effects.

Violence exposure during childhood is common and associated with poor cognitive and academic functioning. However, little is known about how violence exposure influences cognitive processes that might contribute to these disparities, such as working memory, or their neural underpinnings, particularly for cognitive processes that occur in emotionally salient contexts. We address this gap in a sample of 54 participants aged 8 to 19 years (50% female), half with exposure to interpersonal violence. Participants completed a delayed match to sample task for emotional faces while undergoing functional magnetic resonance imaging scanning. Violence-exposed youth performed worse than controls on happy and neutral, but not angry, trials. In whole-brain analysis, violence-exposed youth had reduced activation in the left middle frontal gyrus and right intraparietal sulcus during encoding and the left superior temporal sulcus and temporal–parietal junction during retrieval compared to control youth. Reduced activation in the left middle frontal gyrus during encoding and the left superior temporal sulcus during retrieval mediated the association between violence exposure and task performance. Violence exposure influences the frontoparietal network that supports working memory as well as regions involved in facial processing during working memory for emotional stimuli. Reduced neural recruitment in these regions may explain atypical patterns of cognitive processing seen among violence-exposed youth, particularly within emotional contexts.

The current longitudinal study examined how between-person (BP) differences and within-person (WP) fluctuations in adolescents’ peer victimization and schooling format across ninth grade related to changes in their internalizing symptoms during the COVID-19 pandemic. Participants were 388 adolescents (61% female; Mage = 14.02) who completed three online surveys, administered 3 months apart, from November 2020 to May 2021. Multilevel modeling revealed BP (time-invariant) and WP (time-varying) effects of peer victimization and school instructional format (i.e., in-person; hybrid; online) on internalizing symptoms while accounting for potentially confounding demographic (e.g., gender) and contextual (e.g., COVID-19 positivity rates) factors. Results indicated that adolescents who experienced higher overall levels of peer victimization across the school year, compared to those who experienced lower victimization, reported more severe internalizing symptoms. Whereas relative WP increases in peer victimization predicted corresponding increases in adolescents’ depressive and somatic symptoms regardless of schooling format, WP increases in peer victimization only predicted elevated anxiety during months when students attended fully in-person, but not online, school. Adolescents who spent a greater proportion of their school year attending online school also reported less peer victimization across the year. Findings highlight WP fluctuations in the effects of peer victimization on internalizing and contextual variations depending on schooling format.

Despite the important social functions of moral emotions, they are understudied in the autism spectrum disorder (ASD) population. This three-wave longitudinal study is among the first to examine the development of moral emotions and their associations with theory of mind in 3- to 7-year-old children with ASD, using observational tasks. One hundred and forty-two children (52 with ASD) were followed over a period of 2 years. We found that while the expressions of shame and guilt remained stable in non-ASD children, they decreased with age in children with ASD. No group differences were found in the levels or the developmental trajectories of pride. Besides, better false-belief understanding was uniquely related to the expressions of pride in children with ASD. Our findings highlight the importance of enhancing understanding of moral emotion development and related factors in children with ASD.

Children of adolescent mothers are a high-risk group for negative child development. Previous findings suggest that early interventions may enhance child development by improving mother–child interaction. The purpose of the current study was to evaluate a mother–child intervention (STEEP-b) program in high-risk adolescent mother–infant dyads (N = 56) within a randomized controlled trial (RCT). Mother–child interaction was assessed at baseline (T1), postintervention (T2), and follow-up (T3). The primary outcome was the change in maternal sensitivity and child responsiveness from T1 to T2 that was measured by blinded ratings of videotaped mother–child-interaction with the Emotional Availability Scales. A modified intention-to-treat analysis was performed to examine the data. No intervention effect was found for maternal sensitivity, 95% CI [-0.59–0.60], p = .99, and child responsiveness, 95% CI [-0.51–0.62], p = .84. Maternal sensitivity and child responsiveness did not change over time in both groups (all ps > .05). A statistically nonsignificant, but potentially clinically meaningful difference emerged between rates of serious adverse events, SC: 4 (14.8%), STEEP-b: 1 (3.4%), possibly driven by different intensity of surveillance of dyads in the treatment groups. The current findings question the effectiveness of STEEP-b for high-risk adolescent mothers and do not justify the broad implementation of this approach.

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.