Resilience is a dynamic process depicted by better than expected levels of functioning in response to significant adversity. This can be assessed statistically, by taking the residuals from a model of psychological functioning regressed onto negative life events. We report the first study to investigate multiple cognitive factors in relation to this depiction of resilient functioning. Life events, internalizing symptoms, and a range of cognitive risk and protective factors were assessed in a large sample of adolescents (N = 504) across three waves spaced 12–18 months apart. Adolescents who displayed fewer symptoms than expected, relative to negative life events, were considered more resilient. Adolescents who displayed more symptoms than expected, relative to negative life events, were considered less resilient. All cognitive factors were associated with resilient functioning to differing degrees. These included memory bias, interpretation bias, worry, rumination, self-esteem, and self-reported trait resilience. Regression models showed that memory bias was a key factor explaining unique variance in prospective resilient functioning. In a subsequent cross-lagged panel model, memory bias and resilient functioning were reinforcing mechanisms across time points, supporting cognitive models of emotional resilience. This study adds to the literature, by highlighting key cognitive mechanisms as potential intervention targets

A recent suicidal drive hypothesis posits that psychotic experiences (PEs) may serve to externalize internally generated and self-directed threat (i.e., self-injurious/suicidal behavior [SIB]) in order to optimize survival; however, it must first be demonstrated that such internal threat can both precede and inform PEs. The current study conducted the first known bidirectional analysis of SIB and PEs to test whether SIB could be considered as a plausible antecedent for PEs. Prospective data were utilized from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative birth cohort of 2232 twins, that captured SIB (any self-harm or suicidal attempt) and PEs at ages 12 and 18 years. Cross-lagged panel models demonstrated that the association between SIB at age 12 and PEs at age 18 was as strong as the association between PEs at age 12 and SIB at age 18. Indeed, the best representation of the data was a model where these paths were constrained to be equal (OR = 2.48, 95% CI = 1.63–3.79). Clinical interview case notes for those who reported both SIB and PEs at age 18, revealed that PEs were explicitly characterized by SIB/threat/death-related content for 39% of cases. These findings justify further investigation of the suicidal drive hypothesis.

The COVID-19 pandemic is a unique period of stress, uncertainty, and adversity that will have significant implications for adolescent mental health. Nevertheless, stress and adversity related to COVID-19 may be more consequential for some adolescents’ mental health than for others. We examined whether heart rate variability (HRV) indicated differential susceptibility to mental health difficulties associated with COVID-19 stress and COVID-19 family adversity. Approximately 4 years prior to the pandemic, we assessed resting HRV and HRV reactivity to a well-validated stress paradigm in 87 adolescents. During the pandemic, these adolescents (ages 13–19) reported on their health-related stress and concerns about COVID-19, family adversity related to COVID-19, and their recent emotional problems. The association between COVID-19 stress and emotional problems was significantly stronger for adolescents who previously exhibited higher resting HRV or higher HRV reactivity. For adolescents who exhibited lower resting HRV or HRV augmentation, COVID-19 stress was not associated with emotional problems. Conversely, lower resting HRV indicated vulnerability to the effect of COVID-19 family adversity on emotional problems. Different patterns of parasympathetic functioning may reflect differential susceptibility to the effects of COVID-19 stress versus vulnerability to the effects of COVID-19 family adversity on mental health during the pandemic.

We examined whether adolescents’ loneliness and social withdrawal mediated the association between maternal depressive symptoms and adolescent suicidality. Secondary analyses on the Québec Longitudinal Study of Child Development data were conducted (n = 1,623). Each mother completed the Centre for Epidemiologic Studies Depression Scale (at child ages 5 months, 1.5, 3.5, 5, and 7 years). Adolescent's social withdrawal (adolescent, father, and teacher reported at 10, 12, and 13 years) and loneliness (adolescent reported at 10, 12, and 13 years), were assessed using items from the Social Behavior Questionnaire and the Loneliness and Social Satisfaction Questionnaire, respectively. Adolescents completed self-reports to assess suicidal thoughts and attempts at 13, 15, 17, and 20 years. Children of mothers with higher levels of maternal depressive symptoms had an increased risk for suicidality (OR = 1.15, 95% CI: 1.03–1.28). Loneliness explained 16% of the total effect of maternal depressive symptoms on adolescent suicidality (indirect effect OR = 1.02, 95% CI: 1.00–1.04). There was no indirect effect of maternal depressive symptoms on adolescent suicidal outcomes via social withdrawal (indirect effect OR = 1.00, 95% CI: 0.99–1.02). Interventions that target loneliness may be beneficial for decreasing the risk for suicidality among adolescents of mothers with depressive symptoms.

Father absence has a small but robust association with earlier age at menarche (AAM), likely reflecting both genetic confounding and an environmental influence on life history strategy development. Studies that have attempted to disambiguate genetic versus environmental contributions to this association have shown conflicting findings, though genomic-based studies have begun to establish the role of gene–environment interplay in the father absence/AAM literature. The purpose of this study was to replicate and extend prior genomic work using the Avon Longitudinal Study of Parents and Children (ALSPAC), a prospective longitudinal cohort study (N = 2,685), by (a) testing if an AAM polygenic score (PGS) could account for the father absence/AAM association, (b) replicating G×E research on lin-28 homolog B (LIN28B) variation and father absence, and (c) testing the G×E hypothesis using the PGS. Results showed that the PGS could not explain the father absence/AAM association and there was no interaction between father absence and the PGS. Findings using LIN28B largely replicated prior work that showed LIN28B variants predicted later AAM in father-present girls, but this AAM-delaying effect was absent or reversed in father-absent girls. Findings are discussed in terms genetic confounding, the unique biological role of LIN28B, and using PGSs for G×E tests.

Intensity in adolescent romantic relationships was examined as a long-term predictor of higher adult blood pressure in a community sample followed from age 17 to 31 years. Romantic intensity in adolescence – measured via the amount of time spent alone with a partner and the duration of the relationship – was predicted by parents’ psychologically controlling behavior and was in turn found to predict higher resting adult systolic and diastolic blood pressure even after accounting for relevant covariates. The prediction to adult blood pressure was partially mediated via conflict in nonromantic adult friendships and intensity in adult romantic relationships. Even after accounting for these mediators, however, a direct path from adolescent romantic intensity to higher adult blood pressure remained. Neither family income in adolescence nor trait measures of personality assessed in adulthood accounted for these findings. The results of this study are interpreted both as providing further support for the view that adolescent social relationship qualities have substantial long-term implications for adult health, as well as suggesting a potential physiological mechanism by which adolescent relationships may be linked to adult health outcomes.

Life course theorists posit that sensitive periods exist during life span development where risk and protective factors may be particularly predictive of psychological outcomes relative to other periods in life. While there have been between-cohort studies trying to examine differences in discrimination and depressive symptoms, these studies have not been designed to identify these sensitive periods, which are best modeled by examining intra-individual change across time. To identify sensitive periods where discrimination and shift-&-persist (S&P) – a coping strategy that may protect against the negative impact of discrimination – are most strongly predictive of depressive symptoms, we employed latent growth curve modeling using an accelerated longitudinal design to track intra-individual change in depressive symptoms from ages 20–69. Participants were 3,685 adults measured at three time points ~10 years apart from the Midlife in the United States study (Mage = 37.93, SD = 6.948 at Wave I). Results identified two sensitive periods in development where high levels of S&P interacted with discrimination to protect against depressive symptoms; during the 30s and a lagged effect where 40's S&P protected against depressive symptoms when participants were in their 50s. Implications for the life course study of discrimination, coping, and depression are discussed.

Early adverse experiences are believed to have a profound effect on inhibitory control and the underlying neural regions. In the current study, behavioral and event-related potential (ERP) data were collected during a go/no-go task from adolescents who were involved with the child welfare system due to child maltreatment (n = 129) and low-income, nonmaltreated adolescents (n = 102). The nonmaltreated adolescents were more accurate than the maltreated adolescents on the go/no-go task, particularly on the no-go trials. Paralleling the results with typically developing populations, the nonmaltreated adolescents displayed a more pronounced amplitude of the N2 during the no-go trials than during the go trials. However, the maltreated adolescents demonstrated a more pronounced amplitude of the N2 during the go trials than during the no-go trials. Furthermore, while the groups did not differ during the go trials, the nonmaltreated adolescents displayed a more negative amplitude of the N2 than the maltreated adolescents during no-go trials. In contrast, there was not a significant group difference in amplitude of the P3. Taken together, these results provide evidence that the early adverse experiences encountered by maltreated populations impact inhibitory control and the underlying neural activity in early adolescence.

Justice sensitivity (JS), the tendency to perceive and negatively respond to alleged injustice, has been associated with a range of internalizing and externalizing problems and peer victimization; however, it remains unclear if it has an association with self-victimization. Participants (N = 769) reported on their JS longitudinally at 9–19 (T1), 11–21 (T2), and 14–22 years of age (T3). They further reported on nonsuicidal self-injury (NSSI) and illegal substance use as indicators of self-victimization as well as victimization by peers at T2 and T3. A cross-lagged latent model revealed that victim JS at T1 was positively associated with NSSI, substance use, and peer victimization at T2, and victim JS at T2 was positively associated with substance use at T3. Higher observer JS at T2 predicted higher illegal substance use at T3 and higher illegal substance use at T2 predicted higher observer JS at T3. Finally, higher peer victimization at T2 predicted less perpetrator JS at T3 in the total group. Multigroup models further revealed sex-specific effects. Our findings highlight that being sensitive to injustice, particularly the tendency to feel unfairly treated or being taken advantage of, contributes to individuals’ vulnerability to both engaging in behaviors reflecting self-victimization and being a target of peer victimization, which in turn have influences on JS.

In this three-generation longitudinal study of familial depression, we investigated the continuity of parenting styles, and major depressive disorder (MDD), temperament, and social support during childrearing as potential mechanisms. Each generation independently completed the Parental Bonding Instrument (PBI), measuring individuals’ experiences of care and overprotection received from parents during childhood. MDD was assessed prospectively, up to 38 years, using the semi-structured Schedule for Affective Disorders and Schizophrenia (SADS). Social support and temperament were assessed using the Social Adjustment Scale – Self-Report (SAS-SR) and Dimensions of Temperament Scales – Revised, respectively. We first assessed transmission of parenting styles in the generation 1 to generation 2 cycle (G1→G2), including 133 G1 and their 229 G2 children (367 pairs), and found continuity of both care and overprotection. G1 MDD accounted for the association between G1→G2 experiences of care, and G1 social support and temperament moderated the transmission of overprotection. The findings were largely similar when examining these psychosocial mechanisms in 111 G2 and their spouses (G2+S) and their 136 children (G3) (a total of 223 pairs). Finally, in a subsample of families with three successive generations (G1→G2→G3), G2 experiences of overprotection accounted for the association between G1→G3 experiences of overprotection. The results of this study highlight the roles of MDD, temperament, and social support in the intergenerational continuity of parenting, which should be considered in interventions to “break the cycle” of poor parenting practices across generations.

The present study used a longitudinal and discordant twin design to explore in depth the developmental associations between victimization and loneliness from mid-childhood to young adulthood. The data were drawn from the Environmental Risk (E-Risk) Longitudinal Twin Study, a birth cohort of 2,232 individuals born in England and Wales during 1994–1995. Diverse forms of victimization were considered, differing across context, perpetrator, and timing of exposure. The results indicated that exposure to different forms of victimization was associated with loneliness in a dose–response manner. In childhood, bullying victimization was uniquely associated with loneliness, over and above concurrent psychopathology, social isolation, and genetic risk. Moreover, childhood bullying victimization continued to predict loneliness in young adulthood, even in the absence of ongoing victimization. Within-twin pair analyses further indicated that this longitudinal association was explained by genetic confounds. In adolescence, varied forms of victimization were correlated with young adult loneliness, with maltreatment, neglect, and cybervictimization remaining robust to controls for genetic confounds. These findings indicate that vulnerability to loneliness in victimized young people varies according to the specific form of victimization in question, and also to the developmental period in which it was experienced.

Conduct disorder (CD), characterized by youth antisocial behavior, is associated with a variety of neurocognitive impairments. However, questions remain regarding the neural underpinnings of these impairments. To investigate novel neural mechanisms that may support these neurocognitive abnormalities, the present study applied a graph analysis to resting-state functional magnetic resonance imaging (fMRI) data collected from a national sample of 4,781 youth, ages 9–10, who participated in the baseline session of the Adolescent Brain Cognitive DevelopmentSM Study (ABCD Study®). Analyses were then conducted to examine the relationships among levels of CD symptomatology, metrics of global topology, node-level metrics for subcortical structures, and performance on neurocognitive assessments. Youth higher on CD displayed higher global clustering (β = .039, 95% CIcorrected [.0027 .0771]), but lower Degreesubcortical (β = −.052, 95% CIcorrected [−.0916 −.0152]). Youth higher on CD had worse performance on a general neurocognitive assessment (β = −.104, 95% CI [−.1328 −.0763]) and an emotion recognition memory assessment (β = −.061, 95% CI [−.0919 −.0290]). Finally, global clustering mediated the relationship between CD and general neurocognitive functioning (indirect β = −.002, 95% CI [−.0044 −.0002]), and Degreesubcortical mediated the relationship between CD and emotion recognition memory performance (indirect β = −.002, 95% CI [−.0046 −.0005]). CD appears associated with neuro-topological abnormalities and these abnormalities may represent neural mechanisms supporting CD-related neurocognitive disruptions.

Adolescent females are at elevated risk for the development of depression. In this study, we addressed two questions: Are pubertal hormones associated with adolescent mental health? Might this association depend on pubertal development? We tested the hypothesis that estradiol, which has been associated with adolescent social sensitivity, might interact with pubertal stage to predict depression risk at three time points in ninth and tenth grade. Hormones and pubertal development were measured ninth-grade females. Linear regression analyses were used to predict fall ninth-grade (N = 79), spring ninth-grade (N = 76), and spring tenth-grade (N = 67) Children's Depression Inventory (CDI) scores. The hypothesized model was not statistically significant, but exploratory analyses revealed that two- and three-way interactions incorporating estradiol, puberty (stage and perceived onset), and cortisol predicted current and future CDI scores. Our exploratory model did not predict changes in CDI but did account for future (spring of ninth grade) CDI scores. Specifically, estradiol was positively correlated with fall and spring ninth-grade depressive symptoms in participants with high cortisol who also reported earlier stages and later perceived onset of pubertal development. These findings suggest that hormones associated with sensitivity to the social environment deserve consideration in models of adolescent depression risk.

The generalist genes specialist environment model, when applied to developmental psychopathology, predicts that genetic influences should explain variance that is shared across internalizing and externalizing problems, whereas environmental influences should explain variance that distinguishes the two overarching problem types. The present study is a direct test of this hypothesis, leveraging a sample of 708 twins and siblings (aged 10–18 years, 93% White) from the United States. Measures of severity of symptoms, regardless of type, and of directionality of symptoms – whether the adolescent tended to exhibit more externalizing or internalizing problems – were subjected to genetic (A), shared environmental (C), and nonshared environmental (E) (ACE) variance decompositions. As expected, severity of problems was under substantial genetic influence, but there were also significant shared and nonshared environmental influences. Contrary to the generalist genes specialist environment model, directionality of problem type was also under considerable genetic influence, with modest nonshared environmental influence. Findings corroborate existing evidence from other designs highlighting the role of familial influences (including generalist genes) in comorbidity of adolescent internalizing and externalizing problems, but suggest that the specialist environments hypothesis may not be the key factor in distinguishing problem type.

Neuropsychological evidence supports the developmental taxonomy theory of antisocial behavior, suggesting that abnormal brain development distinguishes life-course-persistent from adolescence-limited antisocial behavior. Recent neuroimaging work confirmed that prospectively-measured life-course-persistent antisocial behavior is associated with differences in cortical brain structure. Whether this extends to subcortical brain structures remains uninvestigated. This study compared subcortical gray-matter volumes between 672 members of the Dunedin Study previously defined as exhibiting life-course-persistent, adolescence-limited or low-level antisocial behavior based on repeated assessments at ages 7–26 years. Gray-matter volumes of 10 subcortical structures were compared across groups. The life-course-persistent group had lower volumes of amygdala, brain stem, cerebellum, hippocampus, pallidum, thalamus, and ventral diencephalon compared to the low-antisocial group. Differences between life-course-persistent and adolescence-limited individuals were comparable in effect size to differences between life-course-persistent and low-antisocial individuals, but were not statistically significant due to less statistical power. Gray-matter volumes in adolescence-limited individuals were near the norm in this population-representative cohort and similar to volumes in low-antisocial individuals. Although this study could not establish causal links between brain volume and antisocial behavior, it constitutes new biological evidence that all people with antisocial behavior are not the same, supporting a need for greater developmental and diagnostic precision in clinical, forensic, and policy-based interventions.

We aim to determine the correlation between parental rearing, personality traits, and obsessive–compulsive disorder (OCD) in different quantiles. In particular, we created an intermediary effect model in which parental rearing affects OCD through personality traits. All predictors were measured at the time of the survey, comprising parental rearing (paternal rearing and maternal rearing), demographics (grade and gender), and personality traits (neuroticism, extroversion, and psychoticism). These results suggest that (a) paternal emotional warmth was negatively correlated with OCD at the 0.40–0.80 quantile, while maternal emotional warmth was positively correlated with the OCD at the 0.45–0.69 quantile. (b) The correlation between negative parental rearing and OCD ranged from the 0.67 to 0.95 quantile for paternal punishment, 0.14–0.82 quantile for paternal overprotection, 0.05–0.36 and >0.50 quantile for maternal over-intervention and overprotection, and 0.08–0.88 quantile for maternal rejection. (c) Extroversion, neuroticism, and psychoticism were not only associated with OCD in a particular quantile but also mediated between parental rearing (namely parental emotional warmth, paternal punishment, paternal overprotection, maternal rejection, maternal over-intervention, and overprotection) and OCD. These findings provide targets for early interventions of OCD to improve the form of family education and personality traits and warrant validation.

Incremental prediction of aggression from callous–unemotional (CU) traits is well established, but cross-cultural replication and studies of young children are needed. Little is understood about the contribution of CU traits in children who are already aggressive. We addressed these issues in prospective studies in the United Kingdom and Colombia. In a UK epidemiological cohort, CU traits and aggression were assessed at age 3.5 years, and aggression at 5.0 years by mothers (N = 687) and partners (N = 397). In a Colombian general population sample, CU traits were assessed at age 3.5 years and aggression at 3.5 and 5.0 years by mother report (N = 220). Analyses consistently showed prediction of age-5.0 aggression by age-3.5 CU traits controlling for age-3.5 aggression. Associations between age-3.5 CU traits and age-5.0 aggression were moderated by aggression at 3.5 years, with UK interaction terms, same informant, β = .07 p = .014 cross-informant, β = .14 p = .002, and in Colombia, β = .09 p = .128. The interactions arose from stronger associations between CU traits and later aggression in those already aggressive. Our findings with preschoolers replicated across culturally diverse settings imply a major role for CU traits in the maintenance and amplification of already established aggression, and cast doubt on their contribution to its origins.

Although variable-oriented analyses are dominant in developmental psychopathology, researchers have championed a person-oriented approach that focuses on the individual as a totality. This view has methodological implications and various person-oriented methods have been developed to test person-oriented hypotheses. Configural frequency analysis (CFA) has been identified as a prime method for a person-oriented analysis of categorical data. CFA searches for configurations in cross-classifications and asks whether the number of observed cases is larger (CFA type) or smaller (CFA antitype) than expected under a probability model. The present study introduces a combination of CFA and model-based recursive partitioning (MOB) to test for type/antitype heterogeneity in the population. MOB CFA is well suited to detect complex moderation processes and can distinguish between subpopulation and population types/antitypes. Model specifications are discussed for first-order CFA and prediction CFA. Results from two simulation studies suggest that MOB CFA is able to detect moderation processes with high accuracy. Two empirical examples are given from school mental health research for illustrative purposes. The first example evaluates heterogeneity in student behavior types/antitypes, the second example focuses on the effect of a teacher classroom management intervention on student behavior. An implementation of the approach is provided in R.

The cognitive control system matures gradually with age and shows age-related sex differences. To gain knowledge concerning error adaptation in familial high-risk groups, investigating error adaptation among the offspring of parents with severe mental disorders is important and may contribute to the understanding of cognitive functioning in at-risk individuals. We identified an observational cohort through Danish registries and measured error adaptation using an Eriksen flanker paradigm. We tested 497 7-year-old children with a familial high risk of schizophrenia (N = 192) or bipolar disorder (N = 116) for deficits in error adaptation compared with a control group (N = 189). We investigated whether error adaptation differed between high-risk groups compared with controls and sex differences in the adaptation to errors, irrespective of high-risk status. Overall, children exhibited post-error slowing (PES), but the slowing of responses did not translate to significant improvements in accuracy. No differences were detected between either high-risk group compared with the controls. Boys showed less PES and PES after incongruent trials than girls. Our results suggest that familial high risk of severe mental disorders does not influence error adaptation at this early stage of cognitive control development. Error adaptation behavior at age 7 years shows specific sex differences.

The triarchic model was advanced as an integrative, trait-based framework for investigating psychopathy using different assessment methods and across developmental periods. Recent research has shown that the triarchic traits of boldness, meanness, and disinhibition can be operationalized effectively in youth, but longitudinal research is needed to realize the model's potential to advance developmental understanding of psychopathy. We report on the creation and validation of scale measures of the triarchic traits using questionnaire items available in the University of Southern California Risk Factors for Antisocial Behavior (RFAB) project, a large-scale longitudinal study of the development of antisocial behavior that includes measures from multiple modalities (self-report, informant rating, clinical-diagnostic, task-behavioral, physiological). Using a construct-rating and psychometric refinement approach, we developed triarchic scales that showed acceptable reliability, expected intercorrelations, and good temporal stability. The scales showed theory-consistent relations with external criteria including measures of psychopathy, internalizing/externalizing psychopathology, antisocial behavior, and substance use. Findings demonstrate the viability of measuring triarchic traits in the RFAB sample, extend the known nomological network of these traits into the developmental realm, and provide a foundation for follow-up studies examining the etiology of psychopathic traits and their relations with multimodal measures of cognitive-affective function and proneness to clinical problems.