Effortful control has been demonstrated to have important ramifications for children's self-regulation and social–emotional adjustment. However, there are wide socioeconomic disparities in children's effortful control, with impoverished children displaying heightened difficulties. The current study was designed to demonstrate how instability within the proximal rearing context of young children may serve as a key operant on the development of children's effortful control in the context of poverty. Two separate studies were conducted that included samples of children living within homes characterized by heightened economic risk. In Study 1, we tested the differential prediction of family instability on two domains of children's effortful control: cool effortful control and delay control. Consistent with hypotheses, elevated instability was associated with decreased hot effortful control but not cool effortful control over the span of 2 years. In Study 2, we examined how children's basal cortisol activity may account for associations between heightened instability and effortful control in reward tasks. The results were consistent with sensitization models, suggesting that elevated cortisol activity arising from increased uncertainty and unpredictability in rearing contexts may influence children's hot effortful control. The findings are interpreted within emerging evolutionary–developmental frameworks of child development.

The present study investigated the associations of mothers' and fathers' lifetime depression and anxiety symptoms, and of infants' negative temperament with parents' and infants' gaze, facial expressions of emotion, and synchrony. We observed infants' (age between 3.5 and 5.5 months, N = 101) and parents' gaze and facial expressions during 4-min naturalistic face-to-face interactions. Parents' lifetime symptoms of depression and anxiety were assessed with clinical interviews, and infants' negative temperament was measured with standardized observations. Parents with more depressive symptoms and their infants expressed less positive and more neutral affect. Parents' lifetime anxiety symptoms were not significantly related to parents' expressions of affect, while they were linked to longer durations of gaze to parent, and to more positive and negative affect in infants. Parents' lifetime depression or anxiety was not related to synchrony. Infants' temperament did not predict infants' or parents' interactive behavior. The study reveals that more depression symptoms in parents are linked to more neutral affect from parents and from infants during face-to-face interactions, while parents' anxiety symptoms are related to more attention to parent and less neutral affect from infants (but not from parents).

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.

Building upon various lines of research, we posited that methylation of the oxytocin receptor gene (OXTR) would mediate the effect of adult adversity on increased commitment to negative schemas and in turn the development of depression. We tested our model using structural equation modeling and longitudinal data from a sample of 100 middle-aged, African American women. The results provided strong support for the model. Analysis of the 12 CpG sites available for the promoter region of the OXTR gene identified four factors. One of these factors was related to the study variables, whereas the others were not. This factor mediated the effect of adult adversity on schemas relating to pessimism and distrust, and these schemas, in turn, mediated the impact of OXTR methylation on depression. All indirect effects were statistically significant, and they remained significant after controlling for childhood trauma, age, romantic relationship status, individual differences in cell types, and average level of genome-wide methylation. These finding suggest that epigenetic regulation of the oxytocin system may be a mechanism whereby the negative cognitions central to depression become biologically embedded.

Childhood abuse and neglect (CAN) is considered as a risk factor for substance use disorder (SUD). Based on the drinking to cope model, this study investigated the association of two trauma-relevant emotions (shame and sadness) and substance use. Using ecological momentary assessment we compared real-time emotion regulation in situations with high and low intensity of shame and sadness in currently abstinent patients with CAN and lifetime SUD (traumaSUD group), healthy controls with CAN (traumaHC group), and without CAN (nontraumaHC group). Multilevel analysis showed a positive linear relationship between high intensity of both emotions and substance use for all groups. The traumaSUD group showed heightened substance use in low, as well as in high, intensity of shame and sadness. In addition, we found an interaction between type of emotion, intensity, and group: the traumaHC group exhibited a fourfold increased risk for substance use in high intense shame situations relative to the traumaSUD group. Our findings provide evidence for the drinking to cope model. The traumaSUD group showed a reduced distress tolerance for variable intensity of negative emotions. The differential effect of intense shame for the traumaHC group emphazises its potential role in the development of SUD following CAN. In addition, shame can be considered a relevant focus for therapeutic preinterventions and interventions for SUD after CAN.

There are multiple recent reports of an association between anxious/depressed (A/D) symptomatology and the rate of cerebral cortical thickness maturation in typically developing youths. We investigated the degree to which anxious/depressed symptoms are tied to age-related microstructural changes in cerebral fiber pathways. The participants were part of the NIH MRI Study of Normal Brain Development. Child Behavior Checklist A/D scores and diffusion imaging were available for 175 youths (84 males, 91 females; 241 magnetic resonance imagings) at up to three visits. The participants ranged from 5.7 to 18.4 years of age at the time of the scan. Alignment of fractional anisotropy data was implemented using FSL/Tract-Based Spatial Statistics, and linear mixed model regression was carried out using SPSS. Child Behavior Checklist A/D was associated with the rate of microstructural development in several white matter pathways, including the bilateral anterior thalamic radiation, bilateral inferior longitudinal fasciculus, left superior longitudinal fasciculus, and right cingulum. Across these pathways, greater age-related fractional anisotropy increases were observed at lower levels of A/D. The results suggest that subclinical A/D symptoms are associated with the rate of microstructural development within several white matter pathways that have been implicated in affect regulation, as well as mood and anxiety psychopathology.

This study examined whether risk status and cumulative risk were associated with autonomic nervous system reactivity and recovery, and emotion regulation in infants. The sample included 121 6-month-old infants. Classification of risk status was based on World Health Organization criteria (e.g., presence of maternal psychopathology, substance use, and social adversity). Heart rate, parasympathetic respiratory sinus arrhythmia, and sympathetic preejection period were examined at baseline and across the still face paradigm. Infant emotion regulation was coded during the still face paradigm. Infants in the high-risk group showed increased heart rate, parasympathetic withdrawal, and sympathetic activation during recovery from the still face episode. Higher levels of cumulative risk were associated with increased sympathetic nervous system activation. Moreover, increased heart rate during recovery in the high-risk group was mediated by both parasympathetic and sympathetic activity, indicating mobilization of sympathetic resources when confronted with socioemotional challenge. Distinct indirect pathways were observed from maternal risk to infant emotion regulation during the still face paradigm through parasympathetic and sympathetic regulation. These findings underline the importance of specific measures of parasympathetic and sympathetic response and recovery, and indicate that maternal risk is associated with maladaptive regulation of stress early in life reflecting increased risk for later psychopathology.

Informed by developmental ecological and epigenetic theory, the current study examined three aims concerning adolescent marijuana use with a large community sample (N = 755; gender = 53% female) and six annual assessments that spanned 11–18 years of age. First, the natural history of adolescent marijuana use was modeled using a two-part latent growth curve analysis. Second, the validity of the mixtures was examined with a broad array of known correlates of adolescent marijuana use. Third, temperament (e.g., surgency, effortful control, and negative affect) was tested as individual differences that would enter into statistical interactions with peer substance use and prior alcohol and cigarette use to distinguish trajectories of marijuana use. The results suggested that escalations in marijuana use were observed for some youth who initiated marijuana use early in adolescence. Youth whose marijuana use did escalate substantially (10%) were distinguished on temperament, conduct disorder, peer delinquency, and pubertal development at baseline. Furthermore, hypothesized interactions between surgency and both peer substance use and prior substance use discriminated different patterns of marijuana use. The findings are discussed with respect to strategies for timing and content of preventive interventions.

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.

In utero exposure to maternal psychological distress is a risk factor for developmental psychopathology, and these effects are believed to partially occur via dysregulation of the maternal and fetal hypothalamus–adrenal–pituitary axes. Nevertheless, only a few human studies have directly assessed the effects of prenatal cortisol exposure on infant cortisol reactivity, and none have investigated sex differences or potential interactions between prenatal cortisol and psychological distress. Here we report on a prospective longitudinal investigation (N = 236) of in utero exposure to maternal cortisol and distress in a relatively high socioeconomic status and low-risk population to determine whether these exposures interact in their effects on infant (M age = 3.0 months, range = 2.3–5.0 months, 51.9% male) cortisol reactivity and whether there are sex differences in these effects. Results revealed both sexually dimorphic and interactive effects of prenatal cortisol and distress, even after controlling for postnatal distress. In general, blunted reactivity in females was associated with exposure to high maternal distress and flattened patterns of diurnal maternal cortisol, whereas blunted reactivity in males was associated with exposure to steeper morning increases and daytime decreases in maternal cortisol. The findings suggest that sex differences in the effects of prenatal cortisol and distress on infant cortisol reactivity are a plausible mechanism by which maternal experiences during pregnancy contribute to sex differences in the development of psychopathology.

Longitudinal investigations that have applied Moffitt's dual taxonomic framework to criminal offending have provided support for the existence of adolescent-limited and life-course persistent antisocial individuals, but have also identified additional trajectories. For instance, rather than a single persistent trajectory, studies have found both high-level and moderate-level persistent offenders. To inform theory and progress our understanding of chronic antisocial behavior, the present study used a sample of serious adolescent offenders (N =1,088) followed from middle adolescence to early adulthood (14–25 years), and examined how moderate-level persistent offenders differed from low-rate, desisting, and high-level persistent offenders. Results indicated that moderate-level persisters' etiology and criminal offense patterns were most similar to high-level persisters, but there were notable differences. Specifically, increasing levels of contextual adversity characterized both moderate-level and high-level persisting trajectories, but moderate-level persisters reported consistently lower levels of environmental risk. While both high- and moderate-level persisters committed more drug-related offenses in early adulthood compared to adolescence, moderate-level persisters engaged in lower levels of antisocial behavior across all types of criminal offenses. Taken cumulatively, the findings of this study suggest that sociocontextual interventions may be powerful in reducing both moderate- and high-level persistence in crime.

Extremely low birth weight (ELBW; <1000 g) infants have been exposed to stressful intrauterine and early postnatal environments. Even greater early adversity has been experienced by ELBW survivors who were also born small for gestational age (SGA; <10th percentile for GA) compared to those born appropriate for GA (AGA). ELBW survivors, particularly those born SGA, face increased risk for internalizing problems compared to normal BW (NBW; ≥2500 g) controls. Internalizing problems are related to allelic variations in the promoter region of the serotonin transporter linked polymorphic region gene (5-HTTLPR). We followed the oldest longitudinal cohort of ELBW survivors to adulthood. Participants provided buccal cells and reported on internalizing problems, using the Young Adult Self-Report when they were in their mid-20s (ELBW/SGA, N = 28; ELBW/AGA, N = 60; NBW, N = 81) and mid-30s (ELBW/SGA, N = 27; ELBW/AGA, N = 58; NBW, N = 76). The findings indicate that ELBW/SGAs carrying the 5-HTTLPR short allele reported increased internalizing problems, particularly depression, during the third and fourth decades of life. This is the first known report on gene–environment interactions predicting psychopathology among ELBW survivors. Our findings elucidate putative neurobiological pathways that underlie risk for psychopathology.

The current study examined a stage-based alcohol use trajectory model to test for potential causal effects of earlier drinking milestones on later drinking milestones in a combined sample of two cohorts of Australian monozygotic and same-sex dizygotic twins (N = 7,398, age M = 30.46, SD = 2.61, 61% male, 56% monozygotic twins). Ages of drinking, drunkenness, regular drinking, tolerance, first nontolerance alcohol use disorder symptom, and alcohol use disorder symptom onsets were assessed retrospectively. Ages of milestone attainment (i.e., age-of-onset) and time between milestones (i.e., time-to-event) were examined via frailty models within a multilevel discordant twin design. For age-of-onset models, earlier ages of onset of antecedent drinking milestones increased hazards for earlier ages of onset for more proximal subsequent drinking milestones. For the time-to-event models, however, earlier ages of onset for the “starting” milestone decreased risk for a shorter time period between the starting and the “ending” milestone. Earlier age of onset of intermediate milestones between starting and ending drinking milestones had the opposite effect, increasing risk for a shorter time period between the starting and ending milestones. These results are consistent with a causal effect of an earlier age of drinking milestone onset on temporally proximal subsequent drinking milestones.

Relations between restricted and repetitive behavior at age 26 months and children's concurrent (N = 203) and later (n = 161) social cognition and language development were investigated. Restricted and repetitive behavior was assessed using two scales: sensory and motor repetitive behaviors and rigidity/routines/restricted interests. Language was assessed at ages 26 and 51 months; social cognition was assessed at ages 26 (symbolic play) and 51 and 61 months (theory of mind). Sensory and motor repetitive behavior was negatively related to children's (a) language performance at 26 and 51 months, (b) instructed symbolic play at 26 months, and (c) theory of mind performance at 51 and 61 months. Path analyses showed that children's sensory and motor repetitive behavior at age 26 months was related to lower receptive verbal ability and theory of mind at 51 months, which led to lower theory of mind at 61 months. Rigidity/routines/restricted interests at 26 months were unrelated to concurrent and later social cognition and language. These results are discussed in terms of the pathways via which sensory and motor repetitive behavior might impact negatively on development.

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.

Studies have demonstrated that the effects of two well-known predictors of adolescent substance use, family monitoring and antisocial peers, are not static but change over the course of adolescence. Moreover, these effects may differ for different groups of youth. The current study uses time-varying effect modeling to examine the changes in the association between family monitoring and antisocial peers and marijuana use from ages 11 to 19, and to compare these associations by gender and levels of behavioral disinhibition. Data are drawn from the Raising Healthy Children study, a longitudinal panel of 1,040 youth. The strength of association between family monitoring and antisocial peers and marijuana use was mostly steady over adolescence, and was greater for girls than for boys. Differences in the strength of the association were also evident by levels of behavioral disinhibition: youth with lower levels of disinhibition were more susceptible to the influence of parents and peers. Stronger influence of family monitoring on girls and less disinhibited youth was most evident in middle adolescence, whereas the stronger effect of antisocial peers was significant during middle and late adolescence. Implications for the timing and targeting of marijuana preventive interventions are discussed.

Prenatal maternal depression and a multilocus genetic profile of two susceptibility genes implicated in the stress response were examined in an interaction model predicting negative emotionality in the first 3 years. In 179 mother–infant dyads from the Maternal Adversity, Vulnerability, and Neurodevelopment cohort, prenatal depression (Center for Epidemiologic Studies Depressions Scale) was assessed at 24 to 36 weeks. The multilocus genetic profile score consisted of the number of susceptibility alleles from the serotonin transporter linked polymorphic region gene (5-HTTLPR): no long-rs25531(A) (LA: short/short, short/long-rs25531(G) [LG], or LG/LG] vs. any LA) and the dopamine receptor D4 gene (six to eight repeats vs. two to five repeats). Negative emotionality was extracted from the Infant Behaviour Questionnaire—Revised at 3 and 6 months and the Early Child Behavior Questionnaire at 18 and 36 months. Mixed and confirmatory regression analyses indicated that prenatal depression and the multilocus genetic profile interacted to predict negative emotionality from 3 to 36 months. The results were characterized by a differential susceptibility model at 3 and 6 months and by a diathesis–stress model at 36 months.

This study sought to identify trajectories of DSM-IV based internalizing (INT) and externalizing (EXT) problem scores across childhood and adolescence and to provide insight into the comorbidity by modeling the co-occurrence of INT and EXT trajectories. INT and EXT were measured repeatedly between age 7 and age 15 years in over 7,000 children and analyzed using growth mixture models. Five trajectories were identified for both INT and EXT, including very low, low, decreasing, and increasing trajectories. In addition, an adolescent onset trajectory was identified for INT and a stable high trajectory was identified for EXT. Multinomial regression showed that similar EXT and INT trajectories were associated. However, the adolescent onset INT trajectory was independent of high EXT trajectories, and persisting EXT was mainly associated with decreasing INT. Sex and early life environmental risk factors predicted EXT and, to a lesser extent, INT trajectories. The association between trajectories indicates the need to consider comorbidity when a child presents with INT or EXT disorders, particularly when symptoms start early. This is less necessary when INT symptoms start at adolescence. Future studies should investigate the etiology of co-occurring INT and EXT and the specific treatment needs of these severely affected children.

Research on childhood adversity has traditionally focused on single types of adversity, which is limited because of high co-occurrence, or on the total number of adverse experiences, which assumes that diverse experiences influence development similarly. Identifying dimensions of environmental experience that are common to multiple types of adversity may be a more effective strategy. We examined the unique associations of two such dimensions (threat and cognitive deprivation) with automatic emotion regulation and cognitive control using a multivariate approach that simultaneously examined both dimensions of adversity. Data were drawn from a community sample of adolescents (N = 287) with variability in exposure to violence, an indicator of threat, and poverty, which is associated with cognitive deprivation. Adolescents completed tasks measuring automatic emotion regulation and cognitive control in neutral and emotional contexts. Violence was associated with automatic emotion regulation deficits, but not cognitive control; poverty was associated with poor cognitive control, but not automatic emotion regulation. Both violence and poverty predicted poor inhibition in an emotional context. Utilizing an approach focused on either single types of adversity or cumulative risk obscured specificity in the associations of violence and poverty with emotional and cognitive outcomes. These findings suggest that different dimensions of childhood adversity have distinct influences on development and highlight the utility of a differentiated multivariate approach.

In contrast to victimization, prior research on the antecedents and outcomes of bullying perpetration has provided little conclusive knowledge. Some adolescent bullies may be well adjusted and popular among peers, while other bullies are rejected and lack self-control. There is also great variation in the outcomes, with a number of studies (but not all) showing increased risk for externalizing and internalizing problems. We used a developmental framework and data from 2,230 participants of the Dutch Tracking Adolescents’ Individual Lives Survey (TRAILS) to examine bullying perpetration across adolescence, to test the links with various antecedents in preadolescence, and to elucidate the outcomes in early adulthood. Latent growth models indicated significant variance in initial bullying perpetration levels and an overall decrease between pre- and late adolescence. Individual, family, and peer factors were associated with initial levels and partially associated with bullying development over time. Bullying perpetration was linked to later maladjustment and substance use, although only in girls. Finally, bullying perpetration appears to function as an intermediate variable between preadolescent individual, family, and peer risk and substance use more than 10 years later. These results have important implications for understanding the gender-specific nature of bullying perpetration and its outcomes and for demonstrating that bullying carries early risk into adulthood.