Individual differences in two inhibitory temperament systems have been implicated as key in the development of early disruptive behaviors. The reactive inhibition system, behavioral inhibition (BI) entails fearfulness, shyness, timidity, and caution. The active inhibition system, or effortful control (EC) entails a capacity to deliberately suppress, modify, or regulate a predominant behavior. Lower scores in each system have been associated with more disruptive behaviors. We examined how the two systems interact, and whether one can alleviate or exacerbate risks due to the other. In two community samples (Study 1, N = 112, ages 2.5 to 4, and Study 2, N = 102, ages 2 to 6.5), we assessed early BI and EC, and future disruptive behaviors (observed disregard for rules in Study 1 and parent-rated externalizing problems in Study 2). Robustly replicated interactions revealed that for children with low BI (relatively fearless), better EC was associated with less disruptive behavior; for children with low EC, more BI was associated with less disruptive behavior. This research extends the investigation of Temperament × Temperament interactions in developmental psychology and psychopathology, and it suggests that reactive and active inhibition systems may play mutually compensatory roles. Those effects emerged after age 2.

Recent neurodevelopmental and evolutionary theories offer strong theoretical rationales and some empirical evidence to support the importance of specific dimensions of early adversity. However, studies have often been limited by omission of other adversity dimensions, singular outcomes, and short follow up durations. 1,420 participants in the community, Great Smoky Mountains Study, were assessed up to eight times between age 9 and 16 for four dimensions of early adversity: Threat, Material Deprivation, Unpredictability, and Loss (as well as a Cumulative Adversity measure). Participants were followed up to four times in adulthood (ages 19, 21, 25, and 30) to measure psychiatric disorders, substance disorder, and “real-world” functioning. Every childhood adversity dimension was associated with multiple adult psychiatric, substance, or functional outcomes when tested simultaneously in a multivariable analysis that accounted for other childhood adversities. There was evidence of differential impact of dimensions of adversity exposure on proximal outcomes (e.g., material deprivation and IQ) and even on distal outcomes (e.g., threat and emotional functioning). There were similar levels of prediction between the best set of individual adversity scales and a single cumulative adversity measure when considering distal outcomes. All dimensions of childhood adversity have lasting, pleiotropic effects, on adult health and functioning, but these dimensions may act via distinct proximal pathways.

The present study examined putative environmental predictors of adolescent substance use, using a prospective adoption design to distinguish between environmental mediation (i.e., parenting influencing adolescent substance use), passive gene–environment correlation (i.e., parental genetic predisposition influencing the association between parenting characteristics and adolescent substance use), and evocative gene–environment correlation (i.e., children’s genetic predisposition influencing parenting). Longitudinal data from the Colorado Adoption Project (395 adoptees, 491 nonadoptees, 485 adoptive parents, and 490 biological parents) were examined. Children (48% girls) were assessed at ages 1 to 17 years. Over 90% of the sample were non-Hispanic White. Associations between parenting and adolescent substance use were compared between adoptive and nonadoptive families. Positive, negative, and inconsistent parenting measures in early childhood through adolescence were not consistently associated with adolescent substance use, with only 6% of correlations being statistically significant (r = −0.152 to .207). However, parent–child relationship quality assessed from childhood to adolescence and orientation to parents assessed during adolescence were significantly, negatively associated with adolescent substance use, with 71% of correlations being statistically significant (r = −0.88 to −0.11). There was little evidence of sex differences in the associations. Environmental mediation, rather than passive or evocative gene–environment correlation, explained most associations.

Individual differences in temperament have been well-described, but individual differences in temperament trajectories require elaboration. Specifically, it is unknown if subgroups of infants display different developmental patterns and if these patterns relate to later behavioral problems. The aims were to identify distinct developmental patterns in broad dimensions of temperament among typically developing infants, to determine whether these developmental patterns differ by sex, to evaluate how developmental patterns within each dimension of temperament relate to developmental patterns within other dimensions of temperament, and to determine whether developmental patterns of infant temperament are associated with internalizing and externalizing behavior at 2 years of age. Data from the longitudinal Alberta Pregnancy Outcomes and Nutrition study (n = 1,819) were used to model latent class trajectories of parent-reported infant temperament at 3, 6, and 12 months. Four to five unique latent trajectories were identified within each temperament dimension. Sex was not associated with trajectory groups. Developmental coordination was observed between trajectories of negative emotionality and regulatory capacity, and between regulatory capacity and positive affect, but not between positive affect and negative emotionality. Negative emotionality and regulatory capacity predicted internalizing and externalizing behavior. Patterns of development in infant temperament, and not just intensity of temperament, contribute toward later problem behavior.

Exposure to childhood maltreatment (CM) may disrupt typical development of neural systems underlying impulse control and emotion regulation. Yet resilient outcomes are observed in some individuals exposed to CM. Individual differences in adult functioning may result from variation in inhibitory control in the context of emotional distractions, underpinned by cognitive–affective brain circuits. Thirty-eight healthy adults with a history of substantiated CM and 34 nonmaltreated adults from the same longitudinal sample performed a Go/No-Go task in which task-relevant stimuli (letters) were presented at the center of task-irrelevant, negative, or neutral images, while undergoing functional magnetic resonance imaging. The comparison group, but not the maltreated group, made increased inhibitory control errors in the context of negative, but not neutral, distractor images. In addition, the comparison group had greater right inferior frontal gyrus and bilateral frontal pole activation during inhibitory control blocks with negative compared to neutral background images relative to the CM group. Across the full sample, greater adaptive functioning in everyday contexts was associated with superior inhibitory control and greater right frontal pole activation. Results suggest that resilience following early adversity is associated with enhanced attention and behavioral regulation in the context of task-irrelevant negative emotional stimuli in a laboratory setting.

The present study examined the effect of early life stress (ELS) on the glucocorticoid receptor gene (NR3C1) methylation, the associations between NR3C1 methylation and behavior problems, and the effect of the program Parents as Teachers (PAT) on NR3C1 methylation. Participants included 132 children, 72 assigned to the PAT intervention group and 60 to the PAT control group. Children were aged 3 years, and were living in psychosocially at-risk families. We assessed NR3C1 methylation of the NGFI-A binding regions of exon 1F via sodium bisulfite sequencing from saliva DNA. Results indicated that (a) children living in families receiving PAT had decreased methylation at one single cytosine–guanine dinucleotides (CpG) site; (b) current maternal depressive symptoms and parental disagreement were predictive of increased methylation of mean NGFI-A and three single CpG sites; and (c) increased methylation of mean NGFI-A and one single CpG site was significantly associated with increased internalizing and externalizing symptoms. In addition, mean NGFI-A was a mediator of the association between parental disagreement and a child's affective problems. These results suggest that PAT may contribute to preventing NR3C1 methylation in preschool children living in psychosocially at-risk situations, and confirm previous findings on the associations between ELS, NR3C1 methylation, and behavior problems.

Much research indicates that exposure to early life adversity (ELA) predicts chronic inflammatory activity, increasing one’s risk of developing diseases of aging later in life. Despite its costs, researchers have proposed that chronic inflammation may be favored in this context because it would help promote immunological vigilance in environments with an elevated risk of infection and injury. Although intuitively appealing, the assumption that exaggerated inflammatory activity predicts favorable immunological outcomes among those exposed to ELA has not been tested. Here, we seek to address this gap, examining the links between exposure to ELA, inflammation, and immune function. Consistent with others’ work, results revealed that those from low socioeconomic status (SES) childhood environments exhibited exaggerated unstimulated inflammatory activity relative to what was observed among those from higher SES childhood environments. Further, results revealed that – although levels of inflammation predicted the magnitude of immunological responses in those from higher SES backgrounds – for those who grew up in low SES environments, higher levels of inflammation were unrelated to the magnitude of immunological responses. Results suggest that exaggerated inflammatory activity in the context of ELA may not predict improved ability to manage acute immunological threats.

Identifying the potential pathways linking childhood abuse to depression and suicidal ideation is critical for developing effective interventions. This study investigated implicit self-esteem—unconscious valenced self-evaluation—as a potential pathway linking childhood abuse with depression and suicidal ideation. A sample of youth aged 8–16 years (N = 240) completed a self-esteem Implicit Association Test (IAT) and assessments of abuse exposure, and psychopathology symptoms, including depression, suicidal ideation, anxiety, and externalizing symptoms. Psychopathology symptoms were re-assessed 1–3 years later. Childhood abuse was positively associated with baseline and follow-up depression symptoms and suicidal ideation severity, and negatively associated with implicit self-esteem. Lower implicit self-esteem was associated with both depression and suicidal ideation assessed concurrently and predicted significant increases in depression and suicidal ideation over the longitudinal follow-up period. Lower implicit self-esteem was also associated with baseline anxiety, externalizing symptoms, and a general psychopathology factor (i.e. p-factor). We found an indirect effect of childhood abuse on baseline and follow-up depression symptoms and baseline suicidal ideation through implicit self-esteem. These findings point to implicit self-esteem as a potential mechanism linking childhood abuse to depression and suicidal ideation.

An impairment in recognizing distress is implicated in the development and severity of antisocial behavior. It has been hypothesized that a lack of attention to the eyes plays a role, but supporting evidence is limited. We developed a computerized training to improve emotion recognition in children and examined the role of eye gaze before and after training. Children referred into an intervention program to prevent antisocial outcomes completed an emotion recognition task with concurrent eye tracking. Those with emotion recognition impairments (n = 54, mean age: 8.72 years, 78% male) completed the training, while others (n = 38, mean age: 8.95 years, 84% male) continued with their usual interventions. Emotion recognition and eye gaze were reassessed in all children 8 weeks later. Impaired negative emotion recognition was significantly related to severity of behavioral problems at pretest. Children who completed the training significantly improved in emotion recognition; eye gaze did not contribute to impairment or improvement in emotion recognition. This study confirms the role of emotion recognition in severity of disruptive behavior and shows that a targeted intervention can quickly improve emotion impairments. The training works by improving children's ability to appraise emotional stimuli rather than by influencing their visual attention.

Some children are more affected by specific family environments than others, as a function of differences in their genetic make-up. However, longitudinal studies of genetic moderation of parenting effects during early childhood have not been conducted. We examined developmental profiles of child behavior problems between 18 months and age 8 in a longitudinal parent–offspring sample of 361 adopted children. In toddlerhood (18 months), observed structured parenting indexed parental guidance in service of task goals. Biological parent psychopathology served as an index of genetic influences on children’s behavior problems. Four profiles of child behavior problems were identified: low stable (11%), average stable (50%), higher stable (29%), and high increasing (11%). A multinominal logistic regression analysis indicated a genetically moderated effect of structured parenting, such that for children whose biological mother had higher psychopathology, the odds of the child being in the low stable group increased as structured parenting increased. Conversely, for children whose biological mother had lower psychopathology, the odds of being in the low stable group was reduced when structured parenting increased. Results suggest that increasing structured parenting is an effective strategy for children at higher genetic risk for psychopathology, but may be detrimental for those at lower genetic risk.

Different dimensions of adversity may affect mental health through distinct neurobiological mechanisms, though current supporting evidence consists largely of cross-sectional associations between threat or deprivation and fronto-limbic circuitry. In this exploratory three-wave longitudinal study spanning ages 9–19 years, we examined the associations between experiences of unpredictability, threat, and deprivation with the development of functional connectivity within and between three brain networks implicated in psychopathology: the salience (SAL), default mode (DMN), and fronto-parietal (FPN) networks, and tested whether network trajectories moderated associations between adversity and changes in internalizing symptoms. Connectivity decreased with age on average; these changes differed by dimension of adversity. Whereas family-level deprivation was associated with lower initial levels and more stability across most networks, unpredictability was associated with stability only in SAL connectivity, and threat was associated with stability in FPN and DMN-SAL connectivity. In youth exposed to higher levels of any adversity, lower initial levels and more stability in connectivity were related to smaller increases in internalizing symptoms. Our findings suggest that whereas deprivation is associated with widespread neurodevelopmental differences in cognitive and emotion processing networks, unpredictability is related selectively to salience detection circuitry. Studies with wider developmental windows should examine whether these neurodevelopmental alterations are adaptive or serve to maintain internalizing symptoms.

Difficult infants are commonly considered at risk for maladaptive developmental cascades, but evidence is mixed, prompting efforts to elucidate moderators of effects of difficulty. We examined features of parents’ representations of their infants – adaptive (appropriate mind-mindedness, MM) and dysfunctional (low reflective functioning, RF, hostile attributions) – as potential moderators. In Family Study (N = 102), we tested parents’ appropriate MM comments to their infants as moderating a path from infants’ observed difficulty (negative affect, unresponsiveness) to parents’ observed power assertion at ages 2–4.5 to children's observed and parent-rated (dis)regard for conduct rules at age 5.5. In father–child relationships, MM moderated that path: for fathers with low MM, the infants’ increasing difficulty was associated with fathers’ greater power assertion, which in turn was associated with children's more disregard for rules. The path was absent for fathers with average or high MM. In Children and Parents Study (N = 200), dysfunctional representations (low RF, hostile attributions) moderated the link between child objective difficulty, observed as anger in laboratory episodes, and difficulty as described by the parent. Reports of mothers with highly dysfunctional representations were unrelated to children's observed anger. Reports of mothers with average or low dysfunctional representations aligned with laboratory observations.

Although early-life adversity can undermine healthy development, children growing up in harsh environments may develop intact, or even enhanced, skills for solving problems in high-adversity contexts (i.e., “hidden talents”). Here we situate the hidden talents model within a larger interdisciplinary framework. Summarizing theory and research on hidden talents, we propose that stress-adapted skills represent a form of adaptive intelligence that enables individuals to function within the constraints of harsh, unpredictable environments. We discuss the alignment of the hidden talents model with current knowledge about human brain development following early adversity; examine potential applications of this perspective to multiple sectors concerned with youth from harsh environments, including education, social services, and juvenile justice; and compare the hidden talents model with contemporary developmental resilience models. We conclude that the hidden talents approach offers exciting new directions for research on developmental adaptations to childhood adversity, with translational implications for leveraging stress-adapted skills to more effectively tailor education, jobs, and interventions to fit the needs and potentials of individuals from a diverse range of life circumstances. This approach affords a well-rounded view of people who live with adversity that avoids stigma and communicates a novel, distinctive, and strength-based message.

Deficits in executive functioning both run in families and serve as a transdiagnostic risk factor for psychopathology. The present study employed twin modeling to examine parenting as an environmental pathway underlying the intergenerational transmission of executive functioning in an at-risk community sample of children and adolescents (N = 354 pairs, 167 monozygotic). Using structural equation modeling of multi-informant reports of parenting and a multi-method measure of child executive functioning, we found that better parent executive functioning related to less harsh, warmer parenting, which in turn related to better child executive functioning. Second, we assessed the etiology of executive functioning via the nuclear twin family model, finding large non-shared environmental effects (E = .69) and low-to-moderate heritability (A = .22). We did not find evidence of shared environmental effects or passive genotype–environment correlation. Third, a bivariate twin model revealed significant shared environmental overlap between both warm and harsh parenting and child executive functioning (which may indicate either passive genotype–environment correlation or environmental mediation), and non-shared environmental overlap between only harsh parenting and child executive functioning (indicating an effect of harsh parenting separable from genetic confounds). In summary, genetics contribute to the intergenerational transmission of executive functioning, with environmental mechanisms, including harsh parenting, also making unique contributions.

Contamination, when members of a comparison or control condition are exposed to the event or intervention under scientific investigation, is a methodological phenomenon that downwardly biases the magnitude of effect size estimates. This study tested a novel approach for controlling contamination in observational child maltreatment research. Data from The Longitudinal Studies of Child Abuse and Neglect (LONGSCAN; N = 1354) were obtained to estimate the risk of confirmed child maltreatment on trajectories of internalizing and externalizing behaviors before and after controlling contamination. Baseline models, where contamination was uncontrolled, demonstrated a risk for greater internalizing (b = .29, p < .001, d = .40) and externalizing (b = .14, p = .040, d = .19) behavior trajectories. Final models, where contamination was controlled by separating the comparison condition into subgroups that did or did not self-report maltreatment, also demonstrated risks for greater internalizing (b = .37, p < .001, d = .51) and externalizing (b = .22, p = .028, d = .29) behavior trajectories. However, effect size estimates in final models were 27.5%–52.6% larger compared to baseline models. Controlling contamination in child maltreatment research can strengthen effect size estimates for child behavior problems, aiding future child maltreatment research design and analysis.

Twin studies demonstrate significant environmental influences and a lack of genetic effects on disordered eating before puberty in girls. However, genetic factors could act indirectly through passive gene–environment correlations (rGE; correlations between parents’ genes and an environment shaped by those genes) that inflate environmental (but not genetic) estimates. The only study to explore passive rGE did not find significant effects, but the full range of parental phenotypes (e.g., internalizing symptoms) that could impact daughters’ disordered eating was not examined. We addressed this gap by exploring whether parents’ internalizing symptoms (e.g., anxiety, depressive symptoms) contribute to daughters’ eating pathology through passive rGE. Participants were female twin pairs (aged 8–14 years; M = 10.44) in pre-early puberty and their biological parents (n = 279 families) from the Michigan State University Twin Registry. Nuclear twin family models explored passive rGE for parents’ internalizing traits/symptoms and twins’ overall eating disorder symptoms. No evidence for passive rGE was found. Instead, environmental factors that create similarities between co-twins (but not with their parents) and unique environmental factors were important. In pre-early puberty, genetic factors do not influence daughters’ disordered eating, even indirectly through passive rGE. Future research should explore sibling-specific and unique environmental factors during this critical developmental period.

This study tested the independent effects and interactions of sympathetic nervous system reactivity and hostile attribution biases (HAB) in predicting change in pure and co-occurring relational bullying and victimization experiences over one year. Co-occurring and pure relational bullying and victimization experiences were measured using a dimensional bifactor model, aiming to address methodological limitations of categorical approaches, using data from 300 preschoolers (Mage = 44.70 months, SD = 4.38). Factor scores were then saved and used in nested path analyses with a subset of participants (n = 81) to test main study hypotheses regarding effects of HAB and skin conductance level reactivity (SCL-R). Bifactor models provided good fit to the data at two independent time points. HAB and SCL-R interacted to predict increases in co-occurring relational bullying/victimization with evidence for over- and underarousal pathways.

To identify sources of phenotypic heterogeneity in attention-deficit/hyperactivity disorder (ADHD) accounting for diversity in developmental/ pathogenic pathways, we examined, in a large sample of youth (N = 354), (a) associations between observed temperamental emotionality at age 3, an electrocortical index (i.e., reward positivity [RewP]) of initial responsiveness to reward at age 9, and ADHD symptoms at age 12, and (b) whether the association between emotionality and ADHD symptoms is mediated by initial responsiveness to reward. Bivariate analyses indicated greater positive emotionality (PE) was associated with enhanced RewP, lower age-9ADHD and lower age-12 inattention (IA). Negative emotionality (NE) was not associated with RewP or ADHD. Mediation analyses revealed the association between PE and hyperactivity/impulsivity (H/I) was mediated by RewP; enhanced RewP was associated with greater H/I. Greater PE was associated with enhanced RewP at a trend level. These effects held accounting for age-9 ADHD, age-12 IA and age-12 oppositional defiant and conduct disorder symptoms. As such, preschool emotionality is associated with adolescent ADHD-H/I symptoms through late childhood initial responsiveness to reward. These relations indicate that individual differences in emotionality and reward responsiveness may be informative for personalizing ADHD interventions.

Child maltreatment gives rise to atypical patterns of social functioning with peers which might be particularly pronounced in early adolescence when peer influence typically peaks. Yet, few neuroimaging studies in adolescents use peer interaction paradigms to parse neural correlates of distinct maltreatment exposures. This fMRI study examines effects of abuse, neglect, and emotional maltreatment (EM) among 98 youth (n = 58 maltreated; n = 40 matched controls) using an event-related Cyberball paradigm affording assessment of both social exclusion and inclusion across early and mid-adolescence (≤13.5 years, n = 50; >13.5 years, n = 48). Younger adolescents showed increased activation to social exclusion versus inclusion in regions implicated in mentalizing (e.g., superior temporal gyrus). Individual exposure-specific analyses suggested that neglect and EM coincided with less reduction of activation to social exclusion relative to inclusion in the dorsal anterior cingulate cortex/pre-supplementary motor area (dACC/pre-SMA) among younger versus older adolescents. Integrative follow-up analyses showed that EM accounted for this dACC/pre-SMA activation pattern over and above other exposures. Moreover, age-independent results within respective exposure groups revealed that greater magnitude of neglect predicted blunted exclusion-related activity in the parahippocampal gyrus, while EM predicted increased activation to social exclusion in the precuneus/posterior cingulate cortex.

Research has supported a link between insecure attachment and disordered eating in adolescents; however, how this influence is exerted remains unclear. This study explored whether depressive symptoms constitute a pathway through which insecure attachment to parents predicts subsequent development of disordered eating in the transition from childhood to adolescence. The study also examines whether there are differential effects regarding the attachment figure, child's gender, or reciprocity between variables. A community-based sample of Spanish youth (n = 904; 49.4% girls) was followed biennially from age 10 to 16 years. Attachment, depressive symptoms, and disordered eating were measured using the Inventory of Parental and Peer Attachment, Children's Depression Inventory, and Children's Eating Attitudes Test, respectively. Prospective data were analyzed using a dynamic panel model, which accounts for unmeasured time-invariant factors. Whereas insecure attachment to the father did not predict later depression or disordered eating, higher insecure attachment to the mother at ages 10 and 12 years predicted more disordered eating at ages 14 and 16 years via increased depressive symptoms at ages 12 and 14 years. No child's gender-specific or reverse mediational effects were found. This study suggests that an increase in depressive symptoms might be one mechanism by which insecure attachment exerts its influence on the development of eating disorders symptomatology in adolescence. Intervention efforts aimed at strengthening particularly the mother–child attachment relationship may reduce the vulnerability to develop depressive symptoms and disordered eating.