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.

We examined whether adolescents’ genetic sensitivity, measured by a polygenic index score, moderated the longitudinal associations between parenting and adolescents’ psychological adjustment. The sample included 323 mothers, fathers, and adolescents (177 female, 146 male; Time 1 [T1] average age = 12.61 years, SD = 0.54 years; Time 2 [T2] average age = 13.59 years, SD = 0.59 years). Parents’ warmth and hostility were rated by trained, independent observers using videotapes of family discussions. Adolescents reported their symptoms of anxiety, depressed mood, and hostility at T1 and T2. The results from autoregressive linear regression models showed that adolescents’ genetic sensitivity moderated associations between observations of both mothers’ and fathers’ T1 parenting and adolescents’ T2 composite maladjustment, depression, anxiety, and hostility. Compared to adolescents with low genetic sensitivity, adolescents with high genetic sensitivity had worse adjustment outcomes when parenting was low on warmth and high on hostility. When parenting was characterized by high warmth and low hostility, adolescents with high genetic sensitivity had better adjustment outcomes than their counterparts with low genetic sensitivity. The results support the differential susceptibility model and highlight the complex ways that genes and environment interact to influence development.

The parent–child attachment relationship plays an important role in the development of the infant's stress regulation system. However, genetic and epigenetic factors such as FK506 binding protein 51 (FKBP5) genotype and DNA methylation have also been associated with hypothalamus–pituitary–adrenal axis functioning. In the current study, we examined how parent–child dyadic regulation works in concert with genetic and epigenetic aspects of stress regulation. We study the associations of attachment, extreme maternal insensitivity, FKBP5 single nucleotide polymorphism 1360780, and FKBP5 methylation, with cortisol reactivity to the Strange Situation Procedure in 298 14-month-old infants. The results indicate that FKBP5 methylation moderates the associations of FKBP5 genotype and resistant attachment with cortisol reactivity. We conclude that the inclusion of epigenetics in the field of developmental psychopathology may lead to a more precise picture of the interplay between genetic makeup and parenting in shaping stress reactivity.

Velocardiofacial syndrome, also known as 22q11.2 deletion syndrome (22q11DS), is associated with an increased risk of major psychiatric disorders, including schizophrenia. The emergence of psychotic symptoms in individuals with schizophrenia in the general population is often preceded by a premorbid period of poor or worsening social and/or academic functioning. Our current study evaluated premorbid adjustment (via the Cannon–Spoor Premorbid Adjustment Scale [PAS]) and psychotic symptoms (via the Structured Interview for Prodromal Symptoms and the Kiddie Schedule for Affective Disorders and Schizophrenia for School-Age Children—Present and Lifetime Version) in youth with 22q11DS (N = 96), unaffected siblings (N = 40), and community controls (N = 50). The PAS scores indicated greater maladjustment during all developmental periods in individuals with 22q11DS compared to the controls. Many participants with 22q11DS had chronically poor (n = 33) or deteriorating (n = 6) PAS scores. In 22q11DS, chronically poor PAS trajectories and poor childhood and early adolescence academic domain and total PAS scores significantly increased the risk of prodromal symptoms or overt psychosis. Taking into account the catechol-O-methyltransferase (COMT) genotype, the best predictor of (prodromal) psychosis was the early adolescence academic domain score, which yielded higher sensitivity and specificity in the subgroup of youth with 22q11DS and the high-activity (valine) allele. PAS scores may help identify individuals at higher risk for psychosis.

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.

Previous research suggests that mothers’ and fathers’ parenting may be differentially influenced by marital and child factors within the family. Some research indicates that marital stress is more influential in fathers’ than mothers’ parenting, whereas other research shows that children's difficult behavior preferentially affects mothers’ parenting. The present study examined marital stress and children's externalizing behavior in middle childhood as predictors of mothers’ versus fathers’ consistency, monitoring, and support and care in early adolescence, and the subsequent associations of these parenting behaviors with externalizing behavior 1.5 years later. Pathways were examined within a longitudinal mediation model testing for moderation by parent gender (N = 276 mothers, N = 229 fathers). Children's externalizing behavior in middle childhood was found to more strongly inversely predict mothers’ versus fathers’ monitoring in early adolescence. In contrast, marital stress more strongly predicted low monitoring for fathers than for mothers. Regardless of parent gender, marital stress predicted lower levels of parental consistency, and children's externalizing behavior predicted lower levels of parental support. Mothers’ monitoring and fathers’ support in early adolescence predicted lower levels of externalizing behavior 1.5 years later. The results are discussed with respect to family transactions relative to parent gender and implications for intervention.

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.

This study examined whether the association between age and amygdala–medial prefrontal cortex (mPFC) connectivity in typically developing 6- to 10-year-old children is correlated with parental care. Resting-state functional magnetic resonance imaging scans were acquired from 124 children of the Generation R Study who at 4 years old had been observed interacting with their parents to assess maternal and paternal sensitivity. Amygdala functional connectivity was assessed using a general linear model with the amygdalae time series as explanatory variables. Higher level analyses assessing Sensitivity × Age as well as exploratory Sensitivity × Age × Gender interaction effects were performed restricted to voxels in the mPFC. We found significant Sensitivity × Age interaction effects on amygdala–mPFC connectivity. Age was related to stronger amygdala–mPFC connectivity in children with a lower combined parental sensitivity score (b = 0.11, p = .004, b = 0.06, p = .06, right and left amygdala, respectively), but not in children with a higher parental sensitivity score, (b = –0.07, p = .12, b = –0.06, p = .12, right and left amygdala, respectively). A similar effect was found for maternal sensitivity, with stronger amygdala–mPFC connectivity in children with less sensitive mothers. Exploratory (parental, maternal, paternal) Sensitivity × Age × Gender interaction analyses suggested that this effect was especially pronounced in girls. Amygdala-mPFC resting-state functional connectivity has been shown to increase from age 10.5 years onward, implying that the positive association between age and amygdala–mPFC connectivity in 6- to 10-year-old children of less sensitive parents represents accelerated development of the amygdala–mPFC circuit.

Maternal trauma is a complex risk factor that has been linked to adverse child outcomes, yet the mechanisms underlying this association are not well understood. This study, which included adoptive and biological families, examined the heritable and environmental mechanisms by which maternal trauma and associated depressive symptoms are linked to child internalizing and externalizing behaviors. Path analyses were used to analyze data from 541 adoptive mother–adopted child (AM–AC) dyads and 126 biological mother–biological child (BM–BC) dyads; the two family types were linked through the same biological mother. Rearing mother's trauma was associated with child internalizing and externalizing behaviors in AM–AC and BM–BC dyads, and this association was mediated by rearing mothers’ depressive symptoms, with the exception of biological child externalizing behavior, for which biological mother trauma had a direct influence only. Significant associations between maternal trauma and child behavior in dyads that share only environment (i.e., AM–AC dyads) suggest an environmental mechanism of influence for maternal trauma. Significant associations were also observed between maternal depressive symptoms and child internalizing and externalizing behavior in dyads that were only genetically related, with no shared environment (i.e., BM–AC dyads), suggesting a heritable pathway of influence via maternal depressive symptoms.

This study tested the prospective association between observational indicators of temperament, which were obtained across multiple assessments when children were 6–36 months of age, and parent and teacher reports of children's attention-deficit/hyperactivity disorder (ADHD) behaviors, when children were in first grade. Data were drawn from the Family Life Project and included 1,074 children for whom temperament and either parent- or teacher-reported ADHD behavioral data were available. The results of variable-centered regression models indicated that individual differences in temperament regulation, but not temperamental reactivity, was uniquely predictive of parent- and teacher-reported ADHD behaviors. Latent profile analyses were used to characterize configurations of temperamental reactivity and regulation. Person-centered regression models were subsequently estimated in which temperamental profile membership replaced continuous indicators of temperamental reactivity and regulation as predictors. The results of person-centered regression models indicated that temperamental reactivity and regulation both contributed (both alone and in combination) to the prediction of subsequent ADHD behaviors. In general, the predictive associations from early temperament to later ADHD were of modest magnitude (R2 = .10–.17). Results are discussed with respect to interest in the early identification of children who are at elevated risk for later ADHD.

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.

Little is known about the role of stress reactivity in the emergence of psychopathology across early childhood. In this longitudinal study, we tested the hypothesis that child cortisol reactivity at age 3 moderates associations between early parenting and children's internalizing and externalizing symptoms from age 3 to age 6. One hundred and sixty children were assessed at age 3, and 135 children were reassessed at age 6. At age 3, we exposed children to stress-inducing laboratory tasks, during which we obtained four salivary cortisol samples, and parental hostility was assessed using an observational parent–child interaction task. At ages 3 and 6, child psychiatric symptoms were assessed using a clinical interview with parents. The results indicated that the combination of high child cortisol reactivity and high observed parental hostility at age 3 was associated with greater concurrent externalizing symptoms at age 3 and predicted increases in internalizing and externalizing symptoms from age 3 to age 6. Findings highlight that increased stress reactivity, within the context of hostile parenting, plays a role in the emergence of psychopathology from preschool to school entry.

Institutional caregiving is associated with significant deviations from species-expected caregiving, altering the normative sequence of attachment formation and placing children at risk for long-term emotional difficulties. However, little is known about factors that can promote resilience following early institutional caregiving. In the current study, we investigated how adaptations in affective processing (i.e., positive valence bias) and family-level protective factors (i.e., secure parent–child relationships) moderate risk for internalizing symptoms in previously institutionalized (PI) youth. Children and adolescents with and without a history of institutional care performed a laboratory-based affective processing task and self-reported measures of parent–child relationship security. PI youth were more likely than comparison youth to show positive valence biases when interpreting ambiguous facial expressions. Both positive valence bias and parent–child relationship security moderated the association between institutional care and parent-reported internalizing symptoms, such that greater positive valence bias and more secure parent–child relationships predicted fewer symptoms in PI youth. However, when both factors were tested concurrently, parent–child relationship security more strongly moderated the link between PI status and internalizing symptoms. These findings suggest that both individual-level adaptations in affective processing and family-level factors of secure parent–child relationships may ameliorate risk for internalizing psychopathology following early institutional caregiving.

The present study utilizes longitudinal data from a high-risk community sample to examine the unique effects of genetic risk, parental knowledge about the daily activities of adolescents, and peer substance use on emerging adult substance use disorders (SUDs). These effects are examined over and above a polygenic risk score. In addition, this polygenic risk score is used to examine gene–environment correlation and interaction. The results show that during older adolescence, higher adolescent genetic risk for SUDs predicts less parental knowledge, but this relation is nonsignificant in younger adolescence. Parental knowledge (using mother report) mediates the effects of parental alcohol use disorder (AUD) and adolescent genetic risk on risk for SUD, and peer substance use mediates the effect of parent AUD on offspring SUD. Finally, there are significant gene–environment interactions such that, for those at the highest levels of genetic risk, less parental knowledge and more peer substance use confers greater risk for SUDs. However, for those at medium and low genetic risk, these effects are attenuated. These findings suggest that the evocative effects of adolescent genetic risk on parenting increase with age across adolescence. They also suggest that some of the most important environmental risk factors for SUDs exert effects that vary across level of genetic propensity.

A quarter of the global population meets diagnostic criteria for metabolic syndrome (MetS). MetS prevalence stratifies by socioeconomic status (SES), such that low SES is associated with higher MetS risk starting in childhood. Despite this trend, some low-SES children maintain good metabolic health across the life span, but the factors responsible for their resilience are not well understood. This study examined the role of threat vigilance as either a moderator or a mediator of the effects of low early life SES on adult metabolic risk. Three hundred twenty-five Canadians aged 15–55 participated (M = 36.4 years, SD = 10.7; 55.4% female). We coded parental occupational status between the ages of 0 and 5 to index early life SES. We used the International Diabetes Federation case definition for MetS based on waist circumference, blood pressure, triglyceride levels, HDL cholesterol, and glycosylated hemoglobin measures. Threat vigilance was assessed using the Weapons Identification Procedure, a visual discrimination paradigm that captures implicit perceptions of threat. Analyses supported the moderator hypothesis: low early life SES was associated with MetS diagnosis exclusively among those with high levels of threat vigilance. This suggests that low early life SES environments that heighten vigilance to threat might be particularly detrimental for metabolic health. Conversely, low threat vigilance may buffer against the metabolic risks associated with socioeconomic disadvantage.

Limbic white matter pathways link emotion, cognition, and behavior and are potentially malleable to the influences of traumatic events throughout development. However, the impact of interactions between childhood and later life trauma on limbic white matter pathways has yet to be examined. Here, we examined whether childhood maltreatment moderated the effect of combat exposure on diffusion tensor imaging measures within a sample of military veterans (N = 28). We examined five limbic tracts of interest: two components of the cingulum (cingulum, cingulate gyrus, and cingulum hippocampus [CGH]), the uncinate fasciculus, the fornix/stria terminalis, and the anterior limb of the internal capsule. Using effect sizes, clinically meaningful moderator effects were found only within the CGH. Greater combat exposure was associated with decreased CGH fractional anisotropy (overall structural integrity) and increased CGH radial diffusivity (perpendicular water diffusivity) among individuals with more severe childhood maltreatment. Our findings provide preliminary evidence of the moderating effect of childhood maltreatment on the relationship between combat exposure and CGH structural integrity. These differences in CGH structural integrity could have maladaptive implications for emotion and memory, as well as provide a potential mechanism by which childhood maltreatment induces vulnerability to later life trauma exposure.

This study aimed to specify the neural mechanisms underlying the link between low household income and diminished executive control in the preschool period. Specifically, we examined whether individual differences in the neural processes associated with executive attention and inhibitory control accounted for income differences observed in performance on a neuropsychological battery of executive control tasks. The study utilized a sample of preschool-aged children (N = 118) whose families represented the full range of income, with 32% of families at/near poverty, 32% lower income, and 36% middle to upper income. Children completed a neuropsychological battery of executive control tasks and then completed two computerized executive control tasks while EEG data were collected. We predicted that differences in the event-related potential (ERP) correlates of executive attention and inhibitory control would account for income differences observed on the executive control battery. Income and ERP measures were related to performance on the executive control battery. However, income was unrelated to ERP measures. The findings suggest that income differences observed in executive control during the preschool period might relate to processes other than executive attention and inhibitory control.

Parental responses to their children are crucially influenced by stress. However, brain-based mechanistic understanding of the adverse effects of parenting stress and benefits of therapeutic interventions is lacking. We studied maternal brain responses to salient child signals as a function of Mom Power (MP), an attachment-based parenting intervention established to decrease maternal distress. Twenty-nine mothers underwent two functional magnetic resonance imaging brain scans during a baby-cry task designed to solicit maternal responses to child's or self's distress signals. Between scans, mothers were pseudorandomly assigned to either MP (n = 14) or control (n = 15) with groups balanced for depression. Compared to control, MP decreased parenting stress and increased child-focused responses in social brain areas highlighted by the precuneus and its functional connectivity with subgenual anterior cingulate cortex, which are key components of reflective self-awareness and decision-making neurocircuitry. Furthermore, over 13 weeks, reduction in parenting stress was related to increasing child- versus self-focused baby-cry responses in amygdala–temporal pole functional connectivity, which may mediate maternal ability to take her child's perspective. Although replication in larger samples is needed, the results of this first parental-brain intervention study demonstrate robust stress-related brain circuits for maternal care that can be modulated by psychotherapy.

Preventing problem behavior requires an understanding of earlier factors that are amenable to intervention. The main goals of our prospective longitudinal study were to trace trajectories of child externalizing behavior between ages 3 and 10 years, and to identify patterns of developmentally significant child and parenting risk factors that differentiated pathways of problem behavior. Participants were 218 3-year-old boys and girls who were reassessed following the transition to kindergarten (age 5–6 years) and during the late school-age years (age 10). Mothers contributed ratings of children's externalizing behavior at all three time points. Children's self-regulation abilities and theory of mind were assessed during a laboratory visit, and parenting risk (frequent corporal punishment and low maternal warmth) was assessed using interview-based and questionnaire measures. Four developmental trajectories of externalizing behavior yielded the best balance of parsimony and fit with our longitudinal data and latent class growth analysis. Most young children followed a pathway marked by relatively low levels of symptoms that continued to decrease across the school-age years. Atypical trajectories marked chronically high, increasing, and decreasing levels of externalizing problems across early and middle childhood. Three-year-old children with low levels of effortful control were far more likely to show the chronic pattern of elevated externalizing problems than changing or low patterns. Early parental corporal punishment and maternal warmth, respectively, differentiated preschoolers who showed increasing and decreasing patterns of problem behavior compared to the majority of children. The fact that children's poor effortful regulation skills predicted chronic early onset problems reinforces the need for early childhood screening and intervention services.

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.