If performance goals (i.e., motivation to prove ability) increase children's vulnerability to depression (Dykman, 1998), why are they overlooked in the psychopathology literature? Evidence has relied on self-report or observational methods and has yet to articulate how this vulnerability unfolds across levels of analysis implicated in stress–depression linkages; for example, hypothalamic–pituitaryadrenal axis (HPA), sympathetic nervous system (SNS). Utilizing a multiple-levels-of-analysis approach (Cicchetti, 2010), this experimental study tested Dykman's goal orientation model of depression vulnerability in a community sample of preadolescents (N = 121, Mage = 10.60 years, Range = 9.08–12.00 years, 51.6% male). Self-reports of performance goals, attachment security, and subjective experience of internalizing difficulties were obtained in addition to objective behavioral (i.e., task persistence) and physiologic arousal (i.e., salivary cortisol, skin conductance level) responses to the Trier Social Stress Test (TSST) and two randomly assigned coping conditions: avoidance, distraction. Children with performance goals reported greater internalizing difficulties and exhibited more dysregulated TSST physiologic responses (i.e., HPA hyperreactivity, SNS protracted recovery), yet unexpectedly displayed greater TSST task persistence and more efficient physiologic recovery during avoidance relative to distraction. These associations were stronger and nonsignificant in the context of insecure and secure attachment, respectively. Findings illustrate a complex matrix of in-the-moment, integrative psychobiological relationships linking performance goals to depression vulnerability.

We expand upon prior work (Gibbons et al., 2012) relating childhood stressor effects, particularly harsh childhood environments, to risky behavior and ultimately physical health by adding longer-term outcomes – deoxyribonucleic acid (DNA) methylation-based measures of accelerated aging (DNAm-aging). Further, following work on the effects of early exposure to danger (McLaughlin et al., 2014), we also identify an additional pathway from harsh childhood environments to DNAm-aging that we label the danger/FKBP5 pathway, which includes early exposure to dangerous community conditions that are thought to impact glucocorticoid regulation and pro-inflammatory mechanisms. Because different DNAm-aging indices provide different windows on accelerated aging, we contrast effects on early indices of DNAm-aging based on chronological age with later indices that focused on predicting biological outcomes. We utilize data from Family and Community Health Study participants (N = 449) from age 10 to 29. We find that harshness influences parenting, which, in turn, influences accelerated DNAm-aging through the risky cognitions and substance use (i.e., behavioral) pathway outlined by Gibbons et al. (2012). Harshness is also associated with increased exposure to threat/danger, which, in turn, leads to accelerated DNAm-aging through effects on FKBP5 activity and enhanced pro-inflammatory tendencies (i.e., the danger/FKBP5 pathway).

This study examined children's duration of attention to negative emotions (i.e., anger, sadness, fear) as a mediator of associations among maternal and paternal unsupportive parenting and children's externalizing symptoms in a sample of 240 mothers, fathers, and their preschool children (Mage = 4.64 years). The multimethod, multi-informant design consisted of three annual measurement occasions. Analysis of maternal and paternal unsupportive parenting as predictors in latent difference changes in children's affect-biased attention and behavior problems indicated that children's attention to negative emotions mediated the specific association between maternal unsupportive parenting and children's subsequent increases in externalizing symptoms. Maternal unsupportive parenting at Wave 1 predicted decreases in children's attention to negative facial expressions of adults from Wave 1 to 2. Reductions in children's attention to negative emotion, in turn, predicted increases in their externalizing symptoms from Wave 1 to 3. Additional tests of children's fearful distress and hostile responses to parental conflict as explanatory mechanisms revealed that increases in children's fearful distress reactivity from Wave 1 to 2 accounted for the association between maternal unsupportive parenting and concomitant decreases in their attention to negative emotions. Results are discussed in the context of information processing models of family adversity and developmental psychopathology.

Impaired facial emotion recognition is a transdiagnostic risk factor for a range of psychiatric disorders. Childhood behavioral difficulties and parental emotional environment have been independently associated with impaired emotion recognition; however, no study has examined the contribution of these factors in conjunction. We measured recognition of negative (sad, fear, anger), neutral, and happy facial expressions in 135 children aged 5–7 years referred by their teachers for behavioral problems. Parental emotional environment was assessed for parental expressed emotion (EE) – characterized by negative comments, reduced positive comments, low warmth, and negativity towards their child – using the 5-minute speech sample. Child behavioral problems were measured using the teacher-informant Strengths and Difficulties Questionnaire (SDQ). Child behavioral problems and parental EE were independently associated with impaired recognition of negative facial expressions specifically. An interactive effect revealed that the combination of both factors was associated with the greatest risk for impaired recognition of negative faces, and in particular sad facial expressions. No relationships emerged for the identification of happy facial expressions. This study furthers our understanding of multidimensional processes associated with the development of facial emotion recognition and supports the importance of early interventions that target this domain.

The purpose of this study was to examine possible pathways by which genetic risk associated with externalizing is transmitted in families. We used molecular data to disentangle the genetic and environmental pathways contributing to adolescent externalizing behavior in a sample of 1,111 adolescents (50% female; 719 European and 392 African ancestry) and their parents from the Collaborative Study on the Genetics of Alcoholism. We found evidence for genetic nurture such that parental externalizing polygenic scores were associated with adolescent externalizing behavior, over and above the effect of adolescents’ own externalizing polygenic scores. Mediation analysis indicated that parental externalizing psychopathology partly explained the effect of parental genotype on children’s externalizing behavior. We also found evidence for evocative gene-environment correlation, whereby adolescent externalizing polygenic scores were associated with lower parent–child communication, less parent–child closeness, and lower parental knowledge, controlling for parental genotype. These effects were observed among participants of European ancestry but not African ancestry, likely due to the limited predictive power of polygenic scores across ancestral background. These results demonstrate that in addition to genetic transmission, genes influence offspring behavior through the influence of parental genotypes on their children’s environmental experiences, and the role of children’s genotypes in shaping parent–child relationships.

Several aspects of mother–child relationships are associated with children's internalizing problems. We examined longitudinal associations between mother–child conflict and children's internalizing problems in middle childhood. Specifically, we examined whether conflict and children's internalizing problems predict each other longitudinally in a sample of children from 3rd through 6th grade (N = 1,364) and their mothers using a cross-lagged panel model with random intercepts. In line with expectations, we found stable between-family differences in both mother–child conflict and children's internalizing problems. Contrary to expectations, we did not find that mother–child conflict and children's internalizing problems showed significant cross-lagged associations. However, mother–child conflict and children's internalizing problems had correlated errors at each wave, indicating that these two constructs covary with each other concurrently at multiple times across development, independent of stable between-family associations (i.e., as one increases, so does the other, and vice versa). The results of this study point to the importance of using statistical approaches that can disentangle between-family differences from within-family processes. In future studies, shorter time scales (e.g., weeks or months) may better capture dynamic associations between parent–child conflict and internalizing problems.

Despite broad evidence suggesting that adversity-exposed youth experience an impaired ability to recognize emotion in others, the underlying biological mechanisms remains elusive. This study uses a multimethod approach to target the neurological substrates of this phenomenon in a well-phenotyped sample of youth meeting diagnostic criteria for posttraumatic stress disorder (PTSD). Twenty-one PTSD-afflicted youth and 23 typically developing (TD) controls completed clinical interview schedules, an emotion recognition task with eye-tracking, and an implicit emotion processing task during functional magnetic resonance imaging )fMRI). PTSD was associated with decreased accuracy in identification of angry, disgust, and neutral faces as compared to TD youth. Of note, these impairments occurred despite the normal deployment of visual attention in youth with PTSD relative to TD youth. Correlation with a related fMRI task revealed a group by accuracy interaction for amygdala–hippocampus functional connectivity (FC) for angry expressions, where TD youth showed a positive relationship between anger accuracy and amygdala–hippocampus FC; this relationship was reversed in youth with PTSD. These findings are a novel characterization of impaired threat recognition within a well-phenotyped population of severe pediatric PTSD. Further, the differential amygdala–hippocampus FC identified in youth with PTSD may imply aberrant efficiency of emotional contextualization circuits.

Parents share half of their genes with their children, but they also share background social factors and actively help shape their child’s environment – making it difficult to disentangle genetic and environmental causes of parent–offspring similarity. While adoption and extended twin family designs have been extremely useful for distinguishing genetic and nongenetic parental influences, these designs entail stringent assumptions about phenotypic similarity between relatives and require samples that are difficult to collect and therefore are typically small and not publicly shared. Here, we describe these traditional designs, as well as modern approaches that use large, publicly available genome-wide data sets to estimate parental effects. We focus in particular on an approach we recently developed, structural equation modeling (SEM)-polygenic score (PGS), that instantiates the logic of modern PGS-based methods within the flexible SEM framework used in traditional designs. Genetically informative designs such as SEM-PGS rely on different and, in some cases, less rigid assumptions than traditional approaches; thus, they allow researchers to capitalize on new data sources and answer questions that could not previously be investigated. We believe that SEM-PGS and similar approaches can lead to improved insight into how nature and nurture combine to create the incredible diversity underlying human behavior.

The relation between peer victimization and depressive symptoms is complex, requiring the use of methodologically rigorous designs to examine these relations and potential mediating factors. The current study used a random intercepts cross-lagged panel model (RI-CLPM) to investigate both between-person and within-person associations in peer victimization, depressive symptoms, and family cohesion across five waves in a sample of adolescents (N = 801, ages 13–15 years at recruitment) in the Northeast. We also investigated the moderating effects of sex and victimization status (i.e., bullying victimization vs. peer victimization). Overall, findings revealed a reciprocal relation between peer victimization and depressive symptoms for females, but no relation for males. A reciprocal relation between peer victimization and family cohesion was found for males. No significant differences were found by victimization status. Future research on peer victimization and associated outcomes and the role of family should account for both between-person and within-person variance.

Guided by principles from life-history theory, theories of adaptive calibration provide an overarching theoretical framework for understanding the developmental roots of impulsivity and externalizing psychopathology. The current research provides evidence for robust associations between perceptions of childhood unpredictability, delay discounting (Studies 1a and 1b), and adult externalizing traits and behaviors (Study 2). Both associations were observed while controlling for perceptions of the harshness of childhood environments, as well as a range of demographic characteristics. The association with externalizing traits and behavior was observed over and above current mood and depressive symptoms. Study 2 also replicated a previously documented association between changes in maternal employment, residence, and cohabitation during childhood and externalizing behavior and, furthermore, suggested that this association was mediated by perceptions of unpredictability. These studies provided no evidence for links between perceived childhood unpredictability and basic forms of risk-taking (Studies 1a and 1c). This research adds to a growing body of work leveraging principles from life-history theory to demonstrate links between childhood experiences, impulsivity, and potentially debilitating forms of mental illness. This work also highlights the value of assessing people’s perceptions of their childhood environments.

Despite public sentiment to the contrary, recreational marijuana use is deleterious to adolescent health and development. Prospective studies of marijuana use trajectories and their predictors are needed to differentiate risk profiles and inform intervention strategies. Using data on 15,960 participants in the National Longitudinal Study of Adolescent to Adult Health, variable-centered approaches were used to examine the impact of childhood polyvictimization on marijuana onset, marijuana use from age 15 to 24 years, and marijuana dependence symptoms. Zero-Inflated Poisson latent class growth analysis (ZIP-LCGA) was used to identify marijuana use subgroups, and their associations with childhood polyvictimization were tested via multinomial logit regression within ZIP-LCGA. Results showed that the overall probability and frequency of marijuana use increased throughout adolescence, peaked in early adulthood, and diminished gradually thereafter. Polyvictimization was associated with earlier onset and greater overall use, frequency of use, and dependence symptoms. ZIP-LCGA uncovered four subgroups, including non-users and three classes of users: adolescence-limited users, escalators, and chronic users. Polyvictimization distinguished non-users from all classes of marijuana users. The findings underscore the lasting developmental implications of significant childhood trauma. Children who experience polyvictimization represent a group that may benefit from selective interventions aimed at preventing early, frequent, chronic, and dependent marijuana use.

Context-appropriate infant physiological functioning may support emotion regulation and mother–infant emotion coregulation. Among a sample of 210 low-income Mexican-origin mothers and their 24-week-old infants, dynamic structural equation modeling (DSEM) was used to examine whether within-infant vagal functioning accounted for between-dyad differences in within-dyad second-by-second emotion regulation and coregulation during free play. Vagal functioning was captured by within-infant mean and variability (standard deviation) of respiratory sinus arrhythmia (RSA) during free play. Infant emotion regulation was quantified as emotional equilibria (within-person mean), volatility (within-person deviation from equilibrium), carryover (how quickly equilibrium is restored following a disturbance), and feedback loops (the extent to which prior affect dampens or amplifies subsequent affect) in positive and negative affect during free play; coregulation was quantified as the influence of one partner's affect on the other's subsequent affect. Among infants with lower RSA variability, positive affect fluctuated around a higher equilibrium, and negative affect fluctuated around a lower equilibrium; these infants exhibited feedback loops where their positive affect dampened their subsequent negative affect. As expected, infants with higher mean RSA exhibited more volatility in positive affect, feedback loops between their positive and negative affect, and stronger mother-driven emotion coregulation. The results highlight differences in simultaneously occurring biological and emotion regulation.

Childhood adversity and anxiety have been associated with increased risk for internalizing disorders later in life and with a range of brain structural abnormalities. However, few studies have examined the link between harsh parenting practices and brain anatomy, outside of severe maltreatment or psychopathology. Moreover, to our knowledge, there has been no research on parenting and subclinical anxiety symptoms which remain persistent over time during childhood (i.e., between 2.5 and 9 years old). Here, we examined data in 94 youth, divided into four cells based on their levels of coercive parenting (high / low) and of anxiety (high / low) between 2.5 and 9 years old. Anatomical images were analyzed using voxel-based morphometry (VBM) and FreeSurfer. Smaller gray matter volumes in the prefrontal cortex regions and in the amygdala were observed in youth with high versus low levels of harsh parenting over time. In addition, we observed significant interaction effects between parenting practices and subclinical anxiety symptoms in rostral anterior cingulate cortical thickness and in amygdala volume. These youth should be followed further in time to identify which youth will or will not go on to develop an anxiety disorder, and to understand factors associated with the development of sustained anxiety psychopathology.

Adolescent risk for self-injurious thoughts and behaviors (STBs) involves disturbance across multiple systems (e.g., affective valence, arousal regulatory, cognitive and social processes). However, research integrating information across these systems is lacking. Utilizing a multiple-levels-of-analysis approach, this person-centered study identified psychobiological stress response profiles and linked them to cognitive processes, interpersonal behaviors, and STBs. At baseline, adolescent girls (N = 241, Mage = 14.68 years, Range = 12–17) at risk for STBs completed the Trier Social Stress Test (TSST), questionnaires, and STB interviews. Positive affect (PA), negative affect (NA), and salivary cortisol (SC) were assessed before and after the TSST. STBs were assessed again during 3, 6, and 9 month follow-up interviews. Multitrajectory modeling of girls’ PA, NA, and SC revealed four profiles, which were compared on cognitive and behavioral correlates as well as STB outcomes. Relative to normative, girls in the affective distress, hyperresponsive, and hyporesponsive subgroups were more likely to report negative cognitive style (all three groups) and excessive reassurance seeking (hyporesponsive only) at baseline, as well as nonsuicidal self-injury (all three groups) and suicidal ideation and attempt (hyporesponsive only) at follow-up. Girls’ close friendship characteristics moderated several profile–STB links. A synthesis of the findings is presented alongside implications for person-centered tailoring of intervention efforts.

Extrinsic mortality risks calibrating fast life history (LH) represent a species-general principle that applies to almost all animals including humans. However, empirical research also finds exceptions to the LH principle. The present study proposes a maternal socialization hypothesis, whereby we argue that the more human-relevant attachment system adds to the LH principle by up- and down-regulating environmental harshness and unpredictability and their calibration of LH strategies. Based on a longitudinal sample of 259 rural Chinese adolescents and their primary caregivers, the results support the statistical moderating effect of caregiver–child attachment on the relation between childhood environmental adversities (harshness and unpredictability) and LH strategies. Our theorizing and findings point to an additional mechanism likely involved in the organization and possibly the slowdown of human LH.

Studies have long observed the bidirectional nature of mother–infant relationships. While behavioral studies have shown that mothers high in social avoidance tendencies can influence the development of these traits in their offspring, the neurophysiological mechanisms underlying this phenomenon, and the role that the infants play, are not well understood. Here we acquired frontal electroencephalogram asymmetry (FA) data simultaneously in 40 mother–infant dyads (Mage mother = 31.6 years; Mage infant = 9 months). Using an actor–partner interdependence model, we examined whether mother (or infant) resting-state FA predicted infant (or mother) FA during two subsequent emotion-eliciting conditions (happy and fear). Maternal social approach versus avoidance traits were assessed as moderators to examine the impact of maternal characteristics on these mother–infant FA relations. In dyads led by mothers with high social avoidance/low social approach characteristics, maternal resting-state FA predicted infant FA during both emotion-eliciting conditions. We did not observe any effects of infant FA on mothers. Therefore, we speculate that individual differences in FA patterns might be a putative brain mechanism through which socially avoidant mothers transfer affective/behavioral information to their infants.

While substantial research supports the role of parent–child interactions on the emergence of psychiatric symptoms, few studies have explored biological mechanisms for this association. The current study explored behavioral and neural parent–child synchronization during frustration and play as predictors of internalizing and externalizing behaviors across a span of 1.5 years. Parent–child dyads first came to the laboratory when the child was 4–5 years old and completed the Disruptive Behavior Diagnostic Observation Schedule: Biological Synchrony (DB-DOS: BioSync) task while functional near-infrared spectroscopy (fNIRS) data were recorded. Parents reported on their child's internalizing and externalizing behaviors using the Child Behavior Checklist (CBCL) four times over 1.5 years. Latent growth curve (LGC) modeling was conducted to assess neural and behavioral synchrony as predictors of internalizing and externalizing trajectories. Consistent with previous investigations in this age range, on average, internalizing and externalizing behaviors decreased over the four time points. Parent–child neural synchrony during a period of play predicted rate of change in internalizing but not externalizing behaviors such that higher parent–child neural synchrony was associated with a more rapid decrease in internalizing behaviors. Our results suggest that a parent–child dyad's ability to coordinate neural activation during positive interactions might serve as a protective mechanism in the context of internalizing behaviors.

Although there is increasing attention for the interrelationship between obsessive–compulsive personality disorder (OCPD) and obsessive–compulsive disorder (OCD), their shared characteristics in terms of childhood trait antecedents remain understudied. Perfectionism may be a viable candidate trait antecedent, given its role in the clinical manifestation of both OCPD and OCD in adulthood, and the evidence that perfectionism reflects a dispositional tendency observable from childhood onwards. However, little is known about childhood trajectories of perfectionism with prospective links to later OCPD versus OCD. Using latent growth curve modeling, this study explored the baseline and growth of childhood perfectionism in 485 community and referred children (55.5% girls, 7.17–14.78 years old, Mage = 10.74, SD = 1.50) across three waves. Adolescent OCPD traits and OCD symptoms were measured in Wave 4. An overall decreasing trend of perfectionism from childhood through adolescence appeared, without inter-individual differences in growth. Individual differences in baseline levels of childhood perfectionism were significant, and equally predicting adolescent OCPD and OCD outcomes. At a more specific level, childhood perfectionism predicted most strongly the rigid perfectionism component of OCPD, and the orderliness/cleanliness/perfectionism and obsession domain of OCD. This demonstrates the value of childhood perfectionism for understanding differential outcomes of adolescent OCPD traits and OCD symptoms.

Background: Negative body image predicts many adverse outcomes. The current study prospectively examined patterns of body esteem development in early adolescence and identified predictors of developmental subtypes. Methods: 328 girls and 429 boys reported annually across a 4-year period (Mage at baseline = 11.14, SD = 0.35) on body esteem, appearance ideal internalization, perceived sociocultural pressures, appearance comparisons, appearance-related teasing, self-esteem, positive and negative affect, and dietary restraint. We performed latent class growth analyses to identify the most common trajectories of body esteem development and examine risk and protective factors for body image development. Results: Three developmental subgroups were identified: (a) high body esteem (39.1%); (b) moderate body esteem (46.1%); and (c) low body esteem (14.8%). Body esteem was stable within the low trajectory and there were minor fluctuations in the high and moderate trajectories. Greater appearance-related teasing, lower self-esteem, less positive affect, and higher dietary restraint predicted the low trajectory, whereas higher self-esteem and lower dietary restraint best predicted the high trajectory. Conclusions: Low body esteem appears to be largely stable from age 11 years. Prevention programming may be enhanced by incorporating components to address transdiagnostic resilience factors such as self-esteem and positive affect.

Recent developments in the application life history theory to human development indicate two fundamental dimension of the early environment – harshness and unpredictability – are key regulators life history strategies. Few studies have examined the manner with which these dimensions influence development, though age at menarche (AAM) and age at first sexual intercourse have been proposed as possible mechanisms among women. Data from the Avon Longitudinal Study of Parents and Children (N = 3,645) were used to examine direct and indirect effects of harshness (financial difficulties) and unpredictability (paternal transitions) on lifetime and past year sexual partners during adolescence and young adulthood. Genetic confounding was addressed using an AAM polygenic score (PGS) and potential gene-by-environment interactions were also evaluated using the PGS. Path model results showed only harshness was directly related to AAM. Harshness, unpredictability, and AAM were indirectly related to lifetime and past year sexual partner number via age at first sexual intercourse. The PGS did not account for any of the associations and no significant interactions were detected. Implications of these results for developmental models derived from life history theory are discussed as well as the role of PGSs in gene–environment interplay research.