We examined whether maltreatment experienced in childhood and/or adolescence prospectively predicts young adult functioning in a diverse and well-characterized sample of females with childhood-diagnosed attention-deficit/hyperactivity disorder (N = 140). Participants were part of a longitudinal study and carefully evaluated in childhood, adolescence, and young adulthood (Mage = 9.6, 14.3, and 19.7 years, respectively), with high retention rates across time. A thorough review of multisource data reliably established maltreatment status for each participant (Mκ = 0.78). Thirty-two (22.9%) participants experienced at least one maltreatment type (physical abuse, sexual abuse, or neglect). Criterion variables included a broad array of young adult measures of functioning gleaned from multiple-source, multiple-informant instruments. With stringent statistical control of demographic, prenatal, and family status characteristics as well as baseline levels of the criterion variable in question, maltreated participants were significantly more impaired than nonmaltreated participants with respect to self-harm (suicide attempts), internalizing symptomatology (anxiety and depression), eating disorder symptomatology, and well-being (lower overall self-worth). Effect sizes were medium. Comprising the first longitudinal evidence linking maltreatment with key young adult life impairments among a carefully diagnosed and followed sample of females with attention-deficit/hyperactivity disorder, these findings underscore the clinical importance of trauma experiences within this population.

Understanding factors increasing susceptibility to social contexts and predicting psychopathology can help identify targets for prevention. Persistently high externalizing behavior in adolescence is predictive of psychopathology in adulthood. Parental monitoring predicts low externalizing behavior, yet youth likely vary in the degree to which they are affected by parents. Genetic variants of GABA receptor subunit alpha-2 (GABRA2) may increase susceptibility to parental monitoring, thus impacting externalizing trajectories. We had several objectives: (a) to determine whether GABRA2 (rs279827, rs279826, rs279858) moderates the relationship between a component of parental monitoring, parental knowledge, and externalizing trajectories; (b) to test the form of this interaction to assess whether GABRA2 variants reflect risk (diathesis–stress) or susceptibility (differential susceptibility) factors; and (c) to clarify GABRA2 associations on the development of problem behavior. This prospective study (N = 504) identified three externalizing trajectory classes (i.e., low, decreasing, and high) across adolescence. A GABRA2 × Parental Monitoring effect on class membership was observed, such that A-carriers were largely unaffected by parental monitoring, whereas class membership for those with the GG genotype was affected by parental monitoring. Findings support differential susceptibility in GABRA2.

The genetic and environmental etiology of individual differences was examined in initial level and change in psychopathic personality from ages 9 to 18 years. A piecewise growth curve model, in which the first change score (G1) influenced all ages (9–10, 11–13, 14–15, and 16–18 years) and the second change score (G2) only influenced ages 14–15 and 16–18 years, fit the data better did than the standard single slope model, suggesting a turning point from childhood to adolescence. The results indicated that variations in levels and both change scores were mainly due to genetic (A) and nonshared environmental (E) influences (i.e., AE structure for G0, G1, and G2). No sex differences were found except on the mean values of level and change scores. Based on caregiver ratings, about 81% of variance in G0, 89% of variance in G1, and 94% of variance in G2 were explained by genetic factors, whereas for youth self-reports, these three proportions were 94%, 71%, and 66%, respectively. The larger contribution of genetic variance and covariance in caregiver ratings than in youth self-reports may suggest that caregivers considered the changes in their children to be more similar as compared to how the children viewed themselves.

Although the negative impact of marital conflict on children has been amply documented, few studies have examined the process of risk in a long-term, longitudinal design. We examined parent–child attachment security as a mechanism that may account for the impact of interparental conflict on children's long-term risk of internalizing problems. Sixty-two community mothers, fathers, and children were followed from ages 2 to 10. Parents reported on their conflicts when their children were 2. Trained observers produced parent–child attachment security scores (Attachment Q-Set, Waters, 1987), based on lengthy naturalistic observations of the child with each parent. Parents rated children's internalizing problems at age 10. A conditional process model and bootstrap approach were implemented to examine conditional indirect effects of conflict on child internalizing problems through attachment security for girls versus boys. Maladaptive marital conflict (destructive strategies, severity of arguments) increased internalizing problems 8 years later due to the undermined security for girls, whereas negative emotional aftermath of conflict (unresolved, lingering tension) increased internalizing problems for both boys and girls. The emotional aftermath of conflict is often overlooked, yet it appears to be a key dimension influencing emotional security in the family system, with significant consequences for children's development.

This prospective longitudinal study examines the long-term influence of intimate partner violence (IPV) exposure in utero. We hypothesized that (a) prenatal IPV increases risk for internalizing and externalizing problems as well as for a profile of dysregulated cortisol reactivity, and (b) patterns of cortisol hyper- and hyporeactivity are differentially associated with internalizing and externalizing problems. The participants were 119 10-year-old children. Their mothers reported their IPV experiences and distress during pregnancy. Child and maternal reports of internalizing and externalizing problems as well as lifetime IPV exposure were obtained. Salivary cortisol was assessed at baseline, 20 min, and 40 min after challenge. The results partially supported our hypotheses: Exposure to IPV during pregnancy predicted child-reported internalizing and externalizing problems, mother ratings of child externalizing problems, and a profile of high cortisol secretion before and after stress challenge. The results were significant above and beyond the influence of maternal distress during pregnancy and IPV that occurred during the child's life. In addition, a profile of high cortisol secretion was associated with maternal reports of child internalizing behaviors. Findings support the growing consensus that prenatal stress can lead to lasting disruptions in adaptation and highlight the need for more longitudinal examinations of prenatal IPV exposure.

Children entering out-of-home (OoH) care have often experienced multiple forms of maltreatment and are at risk of psychiatric disorder and poor long-term outcome. Recent evidence shows high rates of disinhibited attachment disorder (DAD) among maltreated adolescents in UK OoH care (Kay & Green, 2013). This study aimed to further understand the mechanisms of outcome in this group through investigation of social cognitive functioning. Patterns of theory of mind (ToM) and social information processing were assessed alongside DAD behavior and psychopathology in 63 adolescents in UK OoH care (mean age = 176 months, SD = 22; 48% male; 89% White British) and 69 low-risk comparison adolescents (mean age = 171 months, SD = 17; 46% male; 87% White British). Compared to low risk, OoH adolescents showed a hostile attribution bias and ToM deficit, but this was confounded by language ability. ToM was associated with reduced hostile attribution and responding biases and increased social competence, which was further associated with lower levels of externalizing psychopathology. There was no association between social cognition and core features of DAD. Social cognitive deficits and biases may play a role in the high rates of externalizing psychopathology and relationship functioning difficulties in maltreated samples. Future research should assess alternative cognitive mechanisms for DAD.

Affective family processes are associated with the development of depression during adolescence. However, empirical description of these processes is generally based on examining affect at the individual or dyadic level. The purpose of this study was to examine triadic patterns of affect during parent–adolescent interactions in families with or without a depressed adolescent. We used state space grid analysis to characterize the state of all three actors simultaneously. Compared to healthy controls, triads with depressed adolescents displayed a wider range of affect, demonstrated less predictability of triadic affective sequences, spent more time in and returned more quickly to discrepant affective states, and spent less time in and returned more slowly to matched affective states, particularly while engaged in a problem-solving interaction. Furthermore, we identified seven unique triadic states in which triads with depressed adolescents spent significantly more time than triads with healthy controls. The present study enhances understanding of family affective processes related to depression by taking a more systemic approach and revealing triadic patterns that go beyond individual and dyadic analyses.

Stress has been shown to have a causal effect on risk for depression. We investigated the role of cognitive ability as a moderator of the effect of stressful life events on depressive symptoms and whether this varied by gender. Data were analyzed in two adolescent data sets: one representative community sample aged 11–12 years (n = 460) and one at increased familial risk of depression aged 9–17 years (n = 335). In both data sets, a three-way interaction was found whereby for girls, but not boys, higher cognitive ability buffered the association between stress and greater depressive symptoms. The interaction was replicated when the outcome was a diagnosis of major depressive disorder. This buffering effect in girls was not attributable to coping efficacy. However, a small proportion of the variance was accounted for by sensitivity to environmental stressors. Results suggest that this moderating effect of cognitive ability in girls is largely attributable to greater available resources for cognitive operations that offer protection against stress-induced reductions in cognitive processing and cognitive control which in turn reduces the likelihood of depressive symptomatology.

Risk factors for the childhood development of co-occurring internalizing and externalizing symptoms are not well understood, despite a high prevalence and poor clinical outcomes associated with this co-occurring phenotype. We examined inherited and environmental risk factors for co-occurring symptoms in a sample of children adopted at birth and their birth mothers and adoptive mothers (N = 293). Inherited risk factors (i.e., birth mothers' processing speed and internalizing symptoms) and environmental risk factors (i.e., adoptive mothers' processing speed, internalizing symptoms, and uninvolved parenting) were examined as predictors for the development of internalizing-only, externalizing-only, or co-occurring symptoms using structural equation modeling. Results suggested a unique pattern of predictive factors for the co-occurring phenotype, with risk conferred by adoptive mothers' uninvolved parenting, birth mothers' slower processing speed, and the birth mothers' slower processing speed in tandem with adoptive mothers' higher internalizing symptoms. Additional analyses indicated that when co-occurring-symptom children were incorporated into internalizing and externalizing symptom groups, differential risk factors for externalizing and internalizing symptoms emerged. The findings suggest that spurious results may be found when children with co-occurring symptoms are not examined as a unique phenotypic group.

Researchers have identified cross-sectional links between interpersonal stress and inflammation. Little is known, however, about how these dynamics unfold over time, what underlying immune pathways might exist, or whether moderators such as race could alter the strength of the connection between interpersonal stress and inflammatory processes. We examined whether adolescent girls whose relationship trajectories were characterized by chronic stress would exhibit a proinflammatory phenotype marked by systemic inflammation, heightened cytokine responses to bacterial challenges, and resistance to the anti-inflammatory properties of cortisol. Significant Stress × Race interactions revealed that family stress trajectories predicted glucocorticoid sensitivity and peer stress trajectories predicted cytokine production for White but not Asian girls. Relationship stress trajectories were not associated with systemic inflammation, however. These findings suggest that particular subgroups of adolescent girls who face chronic and elevated stress in their close relationships may be at risk for disruptions to the immune system.

Four different models have been generally proposed as plausible etiological explanations for the relation between personality and psychopathology, namely, the vulnerability, complication, pathoplasty, and spectrum or continuity model. The current study entails a joint investigation of the continuity, pathoplasty, and complication models to explain the nature of the associations between early maladaptive traits and psychopathology over time in 717 referred and community children (54.4% girls), aged from 8 to 14 years. Across a 2-year time span, maladaptive traits and psychopathology were measured at three different time points, thereby relying on comprehensive and age-specific dimensional operationalizations of both personality symptoms and psychopathology. The results demonstrate overall compelling evidence for the continuity model, finding more focused support for pathoplasty and complication effects for particular combinations of personality symptoms and psychopathology dimensions. As expected, the continuity associations were found to be more robust for those personality–psychopathology associations that are conceptually closer, such as the emotional instability/introversion–internalizing problems association and the disagreeableness–externalizing problems association. Continuity associations were also stronger when personality was considered from a maladaptive rather than from a general trait perspective. The implication of the findings for the treatment of psychopathology and personality symptoms are briefly discussed.

We examined how genotype–environment correlation processes differ as a function of adolescent age. We tested whether adolescent age moderates genetic and environmental influences on positivity and negativity in mother–adolescent and father–adolescent relationships using parallel samples of twin parents from the Twin and Offspring Study in Sweden and twin/sibling adolescents from the Nonshared Environment in Adolescent Development Study. We inferred differences in the role of passive and nonpassive genotype–environment correlation based on biometric moderation findings. The findings indicated that nonpassive gene–environment correlation played a stronger role for positivity in mother– and father–adolescent relationships in families with older adolescents than in families with younger adolescents, and that passive gene–environment correlation played a stronger role for positivity in the mother–adolescent relationship in families with younger adolescents than in families with older adolescents. Implications of these findings for the timing and targeting of interventions on family relationships are discussed.

Cognitive impulsivity may increase children's risk of developing delinquent behavior. However, the influence of cognitive impulsivity may depend on social environmental risk factors. This study examined the moderating effect of late childhood parenting behaviors and peer relations on the influence of children's cognitive impulsivity on delinquency development across adolescence and early adulthood, while taking possible interactions with intelligence also into account. Delinquent behavior of 412 boys from the Pittsburgh Youth Study was measured annually from ages 13 to 29 years with official arrest records. Cognitive impulsivity (neurocognitive test scores) and intelligence were assessed at age 12–13. Parenting behaviors (persistence of discipline, positive reinforcement, and parental knowledge), peer delinquency, and peer conventional activities were assessed between ages 10 and 13 years. Results showed that, while controlling for intelligence, the influence of youths' cognitive impulsivity on delinquency depended on their parents' behaviors. An interaction was found among cognitive impulsivity, intelligence, and peer delinquency, but instead of cognitive impulsivity, the effect of intelligence on delinquency was particularly moderated. Overall, findings suggest that when there was moderation, high cognitive impulsivity and low intelligence were associated with an increased probability for engaging in delinquency predominantly among boys in a good social environment, but not in a poor social environment.

The present study examines whether heterogeneous groups of children identified based on their longitudinal scores on conduct problems (CP) and callous–unemotional (CU) traits differ on physiological and behavioral measures of fear. Specifically, it aims to test the hypothesis that children with high/stable CP differentiated on CU traits score on opposite directions on a fear–fearless continuum. Seventy-three participants (M age = 11.21; 45.2% female) were selected from a sample of 1,200 children. Children and their parents completed a battery of questionnaires assessing fearfulness, sensitivity to punishment, and behavioral inhibition. Children also participated in an experiment assessing their startle reactivity to fearful mental imagery, a well-established index of defensive motivation. The pattern of results verifies the hypothesis that fearlessness, assessed with physiological and behavioral measures, is a core characteristic of children high on both CP and CU traits (i.e., receiving the DSM-5 specifier of limited prosocial emotions). To the contrary, children with high/stable CP and low CU traits demonstrated high responsiveness to fear, high behavioral inhibition, and high sensitivity to punishment. The study is in accord with the principle of equifinality, in that different developmental mechanisms (i.e., extremes of high and low fear) may have the same behavioral outcome manifested as phenotypic antisocial behavior.

Children's observed effortful control (EC) at 30, 42, and 54 months (n = 145) was predicted from the interaction between mothers' observed parenting with their 30-month-olds and three variants of the solute carrier family C6, member 3 (SLC6A3) dopamine transporter gene (single nucleotide polymorphisms in intron8 and intron13, and a 40 base pair variable number tandem repeat [VNTR] in the 3′-untranslated region [UTR]), as well as haplotypes of these variants. Significant moderating effects were found. Children without the intron8-A/intron13-G, intron8-A/3′-UTR VNTR-10, or intron13-G/3′-UTR VNTR-10 haplotypes (i.e., haplotypes associated with the reduced SLC6A3 gene expression and thus lower dopamine functioning) appeared to demonstrate altered levels of EC as a function of maternal parenting quality, whereas children with these haplotypes demonstrated a similar EC level regardless of the parenting quality. Children with these haplotypes demonstrated a trade-off, such that they showed higher EC, relative to their counterparts without these haplotypes, when exposed to less supportive maternal parenting. The findings revealed a diathesis–stress pattern and suggested that different SLC6A3 haplotypes, but not single variants, might represent different levels of young children's sensitivity/responsivity to early parenting.

Negative emotionality is a distinguishing feature of borderline personality disorder (BPD). However, this person-level characteristic has not been examined as a marker of vulnerability in the development of this disorder. The current study utilized a multimethod approach to examine the interplay between negative emotional reactivity and cumulative exposure to family adversity on the development of BPD symptoms across 3 years (ages 16–18) in a diverse, at-risk sample of adolescent girls (N = 113). A latent variable of negative emotional reactivity was created from multiple assessments at age 16: self-report, emotion ratings to stressors from ecological assessments across 1 week, and observer-rated negative affectivity during a mother–daughter conflict discussion task. Exposure to family adversity was measured cumulatively between ages 5 and 16 from annual assessments of family poverty, single parent household, and difficult life circumstances. The results from latent growth curve models demonstrated a significant interaction between negative emotional reactivity and family adversity, such that exposure to adversity strengthened the association between negative emotional reactivity and BPD symptoms. In addition, family adversity predicted increasing BPD symptoms during late adolescence. These findings highlight negative emotional reactivity as a marker of vulnerability that ultimately increases risk for the development of BPD symptoms.

Internalizing symptoms during adolescence and beyond is a major public health concern, particularly because severe symptoms can lead to the diagnosis of a number of serious psychiatric conditions. This study utilizes a unique sample with a complex statistical method in order to explore Gene × Environment interactions found in internalizing symptoms during adolescence. Data for this study were drawn from a longitudinal prevention intervention study (n = 798) of Baltimore city school children. Internalizing symptom data were collected using self-report and blood or saliva samples genotyped using Affymetrix 6.0 microarrays. A major depression polygenic score was created for each individual using information from the major depressive disorder Psychiatric Genetics Consortium and used as a predictor in a latent trait–state–occasion model. The major depressive disorder polygenic score was a significant predictor of the stable latent trait variable, which captures time-independent phenotypic variability. In addition, an early childhood stressor of death or divorce was a significant predictor of occasion-specific variables. A Gene × Environment interaction was not a significant predictor of the latent trait or occasion variables. These findings support the importance of genetics on the stable latent trait portion of internalizing symptoms across adolescence.

Previous studies have documented the serotonin transporter linked polymorphic region (5-HTTLPR) as a genetic susceptibility variant that contributes to variability in outcomes related to affective psychopathology, with the short allele associated with negative affectivity and the long allele associated with positive affectivity. In a separate but related line of research, extensive evidence suggests that frontal electroencephalography (EEG) hemispheric asymmetry in the alpha band is also associated with risk for affective psychopathologies, with leftward asymmetry associated with approach-related behavior patterns and rightward frontal EEG asymmetry associated with withdrawn behavioral tendencies. We examined frontal EEG hemispheric asymmetries in relation to 5-HTTLPR genotyping in 70 children between 4 and 6 years of age. Analyses revealed that frontal EEG lateralization interacted with genotype such that children homozygous for the short allele exhibited rightward frontal EEG asymmetries, children who were homozygous for the long allele consistently exhibited a positive pattern of leftward asymmetry, and heterozygotes exhibited equivalent left and right frontal activity. These findings suggest that the 5-HTTLPR short allele may provide a degree of susceptibility for later affective psychopathology in adolescence and adulthood, through mediation of frontal brain activity that is associated with cognitive–behavioral withdrawal tendencies and negative affectivity.

A total of 149 children, who spent an average of 13.8 months in Russian institutions, were transferred to Russian families of relatives and nonrelatives at an average age of 24.7 months. After residing in these families for at least 1 year (average = 43.2 months), parents reported on their attachment, indiscriminately friendly behavior, social–emotional competencies, problem behaviors, and effortful control when they were 1.5–10.7 years of age. They were compared to a sample of 83 Russian parents of noninstitutionalized children, whom they had reared from birth. Generally, institutionalized children were rated similarly to parent-reared children on most measures, consistent with substantial catch-up growth typically displayed by children after transitioning to families. However, institutionalized children were rated more poorly than parent-reared children on certain competencies in early childhood and some attentional skills. There were relatively few systematic differences associated with age at family placement or whether the families were relatives or nonrelatives. Russian parent-reared children were rated as having more problem behaviors than the US standardization sample, which raises cautions about using standards cross-culturally.

Temperament and parental practices (PP) are important predictors of adolescent alcohol use (AU); however, less is known about how they combine to increase or decrease risk of AU. This study examined whether age 6 temperament (i.e., impulsivity and inhibitory control) interacted with age 6 coercive PP and/or age 14 parental monitoring to predict AU at 15 years among 209 adolescents. Results showed that low parental monitoring was associated with more frequent AU and that coercive PP interacted with impulsivity to predict AU. This interaction was examined as a function of two models that were not studied before in the prediction of AU: the diathesis–stress model (i.e., impulsive children are more “vulnerable” to adverse PP than those with an easy temperament); and the differential susceptibility model (i.e., impulsive children are also more likely to benefit from good PP). Results supported the differential susceptibility model by showing that impulsive children were not only at higher risk for AU when combined with high coercive PP but also benefit from the absence of coercive PP. This supports the suggestion that the conception of certain temperament characteristics, or in this case impulsivity, as a “vulnerability” for adolescent AU, may need revision because it misrepresents the malleability it may imply.