Previous research has documented socioeconomic-related disparities in children's working memory; however, the putative proximal caregiving mechanisms that underlie these effects are less known. The present study sought to examine whether the effects of early family socioeconomic status on children's working memory were mediated through experiences of caregiving, specifically maternal harsh discipline and responsiveness. Utilizing a psychobiological framework of parenting, the present study also tested whether maternal working memory moderated the initial paths between the family socioeconomic context and maternal harsh discipline and responsiveness in the mediation model. The sample included 185 socioeconomically diverse mother–child dyads assessed when children were 3.5 and 5 years old. Results demonstrated that maternal harsh discipline was a unique mediator of the relation between early experiences of family socioeconomic adversity and lower working memory outcomes in children. Individual differences in maternal working memory emerged as a potent individual difference factor that specifically moderated the mediating influence of harsh discipline within low socioeconomic contexts. The findings have implications for early risk processes underlying deficits in child working memory outcomes and potential targets for parent–child interventions.

Individuals with psychopathic traits show an attenuated emotional response to aversive stimuli. However, recent evidence suggests heterogeneity in emotional reactivity among individuals with psychopathic or callous–unemotional (CU) traits in the identification of primary and secondary subtypes, or variants. We hypothesized that primary CU variants will respond with blunted affect to negatively valenced stimuli, whereas individuals with a history of childhood maltreatment, fitting with theoretical conceptualizations of secondary psychopathy, will display heightened emotional reactivity. To test this hypothesis, we examined fear-potentiated startle between CU variants while viewing aversive, pleasant, and neutral scenes. Two hundred thirty-eight incarcerated adolescent (M age = 16.8 years, SD = 1.11 years) boys completed a picture-startle paradigm and self-report questionnaires assessing CU traits, aggressive behavior, and maltreatment. Latent profile analysis of CU trait, aggression, and maltreatment scores identified four classes: primary psychopathy variants (high CU traits, high aggression, low maltreatment; n = 46), secondary psychopathy variants (high CU traits, high aggression, high maltreatment; n = 42), and two nonpsychopathic groups differentiated on maltreatment experience (n = 148). Primary CU variants displayed reduced startle potentiation to aversive images relative to control, maltreated, and also secondary variants that exhibited greater startle modulation. Findings add to a rapidly growing body of literature supporting the possibility of multiple developmental pathways to psychopathic traits (i.e., equifinality), and extend it by finding support for divergent potential biomarkers between primary and secondary CU variants.

Poor physiological self-regulation has been proposed as a potential biological vulnerability for adolescent suicidality. This study tested this hypothesis by examining the effect of parasympathetic stress responses on future suicide ideation. In addition, drawing from multilevel developmental psychopathology theories, the interplay between parasympathetic regulation and friendship support, conceptualized as an external source of regulation, was examined. At baseline, 132 adolescent females (M age = 14.59, SD = 1.39) with a history of mental health concerns participated in an in vivo interpersonal stressor (a laboratory speech task) and completed self-report measures of depressive symptoms and perceived support within a close same-age female friendship. Respiratory sinus arrhythmia (RSA) was measured before and during the speech task. Suicide ideation was assessed at baseline and at 3, 6, and 9 months follow-up. The results revealed that females with greater relative RSA decreases to the laboratory stressor were at higher risk for reporting suicide ideation over the subsequent 9 months. Moreover, parasympathetic responses moderated the effect of friendship support on suicide ideation; among females with mild changes or higher relative increases in RSA, but not more pronounced RSA decreases, friendship support reduced risk for future suicide ideation. Findings highlight the crucial role of physiological and external regulation sources as protective factors for youth suicidality.

Previous research has established that parental marital discord is associated with higher levels of offspring externalizing behaviors, but it is unclear how parental relationship functioning is associated with the genetic and environmental variance on a factor of externalizing problems. Thus, the current study assessed how parental marital discord moderates genetic and environmental variance on offspring externalizing problems at two different ages: childhood and late adolescence. That is, the magnitude of genetic and environmental influences on offspring externalizing at ages 11 and 17 was examined as a function of parental marital discord. Consistent with a diathesis–stress model of psychopathology, it was hypothesized that with increasing marital discord, genetic influences on externalizing would be more pronounced. Rather, results indicated that for the 11-year-old sample, nonshared environmental influences were greater when parental marital discord was low, and comparatively, shared environmental influences contributed more to the variance in externalizing problems when parental marital discord was high. No moderation was found for the 17-year-old cohort. In contrast to studies that do not find an effect of the shared environment, these results provide evidence that the common rearing environment has an impact on externalizing problems in preadolescent children.

Individuals with Williams syndrome and those with Down syndrome are both characterized by heightened social interest, although the manifestation is not always similar. Using a dot-probe task, we examined one possible source of difference: allocation of attention to facial expressions of emotion. Thirteen individuals with Williams syndrome (mean age = 19.2 years, range = 10–28.6), 20 with Down syndrome (mean age = 18.8 years, range = 12.1–26.3), and 19 typically developing children participated. The groups were matched for mental age (mean = 5.8 years). None of the groups displayed a bias to angry faces. The participants with Williams syndrome showed a selective bias toward happy faces, whereas the participants with Down syndrome behaved similarly to the typically developing participants with no such bias. Homogeneity in the direction of bias was markedly highest in the Williams syndrome group whose bias appeared to result from enhanced attention capture. They appeared to rapidly and selectively allocate attention toward positive facial expressions. The complexity of social approach behavior and the need to explore other aspects of cognition that may be implicated in this behavior in both syndromes is discussed.

Longitudinal bidirectional effects between parents and children are usually studied in samples of typically developing children, but remain understudied in families with a child with autism spectrum disorder. This three-wave longitudinal study examined how parents and children with autism spectrum disorder influence one another, relying on parent reports of parenting behaviors and children's problem behaviors across 9 years, in a sample of 139 youngsters (M age Time 1 = 10.2 years, 83% boys). Cross-lagged analyses indicated that children's externalizing problems at Time 1 predicted negative controlling parenting 6 years later (Time 2) that in turn predicted externalizing problems 3 years later (Time 3). Negative parental control at Time 1 also increased the risk for internalizing problems at Time 2. It was surprising that externalizing problems at Time 2 also predicted positive parental involvement at Time 3. Thus, although results indicate that externalizing problems generally elicit maladaptive reactions in parents, this study also suggests that parents adjust their way of reacting to externalizing child problems as their child reaches adolescence/emerging adulthood. Implications for future research on parenting dynamics in families with a child with autism spectrum disorder are discussed.

Multiple studies have shown that reading abilities and attention-deficit/hyperactivity disorder symptoms, mainly inattention symptoms, are phenotypically and genetically associated during childhood. However, few studies have looked at these associations during adolescence to investigate possible developmental changes. The aim of the study is to examine the genetic and environmental etiology of the associations between inattention and hyperactivity reported by parents, and reading accuracy, reading speed, and word reading in a population-based twin sample (Quebec Newborn Twin Study). Participants were between 14 and 15 years of age at the time of testing (N = 668–837). Phenotypic results showed that when nonverbal and verbal abilities were controlled, inattention, but not hyperactivity/impulsivity, was a modest and significant predictor of reading accuracy, reading speed, and word reading. The associations between inattention and all reading abilities were partly explained by genetic and unique environmental factors. However, the genetic correlations were no longer significant after controlling for verbal abilities. In midadolescence, inattention is the attention-deficit/hyperactivity disorder dimension associated with reading abilities, but they could also share genetic factors with general verbal skills.

Callous–unemotional (CU) behaviors demonstrate meaningful individual differences in early childhood, even in nonclinical samples with low mean levels of CU, but the factors underlying this variation have not been examined. This study investigated genetic and environmental contributions to individual differences and to sources of continuity and change in CU in toddler twins (145 monozygotic, 169 dizygotic) assessed at ages 2 and 3 years. CU, as assessed by the Child Behavior Checklist 1.5–5 (Achenbach & Rescorla, 2000), was moderately stable across age (r = .45, p < .0001). Longitudinal biometric analyses revealed genetic and nonshared environmental influences on CU at both ages, with no significant contribution from shared environmental factors. Stability from age 2 to 3 was due to genetic factors, whereas change was due to both genetic and nonshared environmental influences. This genetic and nonshared environmental change was substantial, suggesting malleability of CU in early childhood. Over 50% of the genetic influences and 100% of the nonshared environmental influences on CU at age 3 were independent of those that operated at age 2. Implications of novel sources of variance across age are discussed.

Previous studies demonstrate that boys' monoamine oxidase A (MAOA) genotype interacts with adverse rearing environments in early childhood, including punitive discipline, to predict later antisocial behavior. Yet the mechanisms by which MAOA and punitive parenting interact during childhood to amplify risk for antisocial behavior are not well understood. In the present study, hostile attributional bias and aggressive response generation during middle childhood, salient aspects of maladaptive social information processing, were tested as possible mediators of this relation in a sample of 187 low-income men followed prospectively from infancy into early adulthood. Given racial–ethnic variation in MAOA allele frequencies, analyses were conducted separately by race. In both African American and Caucasian men, those with the low-activity MAOA allele who experienced more punitive discipline at age 1.5 generated more aggressive responses to perceived threat at age 10 relative to men with the high-activity variant. In the African American subsample only, formal mediation analyses indicated a marginally significant indirect effect of maternal punitiveness on adult arrest records via aggressive response generation in middle childhood. The findings suggest that maladaptive social information processing may be an important mechanism underlying the association between MAOA × Parenting interactions and antisocial behavior in early adulthood. The present study extends previous work in the field by demonstrating that MAOA and harsh parenting assessed in early childhood interact to not only predict antisocial behavior in early adulthood, but also predict social information processing, a well-established social–cognitive correlate of antisocial behavior.

The main objective of this prospective longitudinal study was to investigate bidirectional associations between adolescent cannabis use (CU) and neurocognitive performance in a community sample of 294 young men from ages 13 to 20 years. The results showed that in early adolescence, and prior to initiation to CU, poor short-term and working memory, but high verbal IQ, were associated with earlier age of onset of CU. In turn, age of CU onset and CU frequency across adolescence were associated with (a) specific neurocognitive decline in verbal IQ and executive function tasks tapping trial and error learning and reward processing by early adulthood and (b) lower rates of high-school graduation. The association between CU onset and change in neurocognitive function, however, was found to be accounted for by CU frequency. Whereas the link between CU frequency across adolescence and change in verbal IQ was explained (mediated) by high school graduation, the link between CU frequency and tasks tapping trial and error learning were independent from high school graduation, concurrent cannabis and other substance use, adolescent alcohol use, and externalizing behaviors. Findings support prevention efforts aimed at delaying onset and reducing frequency of CU.

Statistical tests of differential susceptibility have become standard in the empirical literature, and are routinely used to adjudicate between alternative developmental hypotheses. However, their performance and limitations have never been systematically investigated. In this paper I employ Monte Carlo simulations to explore the functioning of three commonly used tests proposed by Roisman et al. (2012). Simulations showed that critical tests of differential susceptibility require considerably larger samples than standard power calculations would suggest. The results also showed that existing criteria for differential susceptibility based on the proportion of interaction index (i.e., values between .40 and .60) are especially likely to produce false negatives and highly sensitive to assumptions about interaction symmetry. As an initial response to these problems, I propose a revised test based on a broader window of proportion of interaction index values (between .20 and .80). Additional simulations showed that the revised test outperforms existing tests of differential susceptibility, considerably improving detection with little effect on the rate of false positives. I conclude by noting the limitations of a purely statistical approach to differential susceptibility, and discussing the implications of the present results for the interpretation of published findings and the design of future studies in this area.

Harsh, abusive, and rejecting behavior by parents toward their children is associated with increased risk for many developmental problems for youth. Children raised by harsh parents are also more likely to treat their own children harshly. The present study addresses conditions that would break this intergenerational cycle of harsh parenting. Data come from a three-generation study of a cohort of 290 adolescents (Generation 2 [G2], 52% female) grown to adulthood and their parents (Generation 1 [G1]). During adolescence, observers rated G1 harsh parenting to G2. Several years later observers rated G2 harsh parenting toward their oldest child (Generation 3 [G3]). Several adaptive systems fundamental to human resilience attenuate intergenerational continuity in harshness. G2 parents were relatively less harsh to G3 children (notwithstanding a history of harshness from G1) when G2's romantic partner (a) communicated positively with G2 and (b) had a good relationship with G3, and (c) when G2 was high on self-control. Interventions that target all of these protective factors may not only break but also reverse the intergenerational cycle of child maltreatment.

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

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

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

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

The aims were to identify the correspondence between simultaneous, longitudinal changes in cortisol reactivity and diurnal testosterone and to test the hypothesis that cortisol reactivity and diurnal testosterone interact so as to influence antisocial behavior. Participants were 135 children and young adolescents assessed at 6-month intervals over 1 year. Upon enrollment girls were age 8, 10, or 12 years (N = 69, M = 10.06 years) and boys were age 9, 11, or 13 years (N = 66, M = 10.94 years). Assessments included Tanner staging by a nurse, cortisol reactivity (Trier Social Stress Test for Children), diurnal testosterone, and interviews and questionnaires. Growth models showed that cortisol reactivity and diurnal testosterone basal levels (intercept) and rate of change (slopes) were not related, suggesting different mechanisms of growth. Longitudinal regression analyses assessed cortisol reactivity and diurnal testosterone longitudinally. The interactions of cortisol reactivity and diurnal testosterone showed that when diurnal testosterone was low, boys with low cortisol reactivity were reported to have more behavior problems (i.e., oppositional defiant disorder symptoms and attention problems) than when testosterone was high. In addition, when diurnal testosterone was high, boys with high or moderate cortisol reactivity were significantly higher on total antisocial behavior, attention behavior problems, and oppositional defiant disorder symptoms than when testosterone was low or moderate. The results were similar but less frequent for girls. These findings advance the science of young adolescence by showing the interaction between preexisting sensitivity to stressors and the normative testosterone changes of puberty and antisocial behavior.

This study used four waves of data from a longitudinal study of 749 Mexican origin youths to test a developmental cascades model linking contextual adversity in the family and peer domains in late childhood to a sequence of unfolding processes hypothesized to predict problem substance use and risky sexual activity (greater number of sex partners) in late adolescence. Externalizing and internalizing problems were tested as divergent pathways, with youth-reported and mother-reported symptoms examined in separate models. Youth gender, nativity, and cultural orientation were tested as moderators. Family risk, peer social rejection, and their interaction were prospectively related to externalizing symptoms and deviant peer involvement, although family risk showed stronger effects on parent-reported externalizing and peer social rejection showed stronger effects on youth-reported externalizing. Externalizing symptoms and deviant peers were related, in turn, to risk taking in late adolescence, including problem alcohol–substance use and number of sexual partners. Peer social rejection predicted youth-reported internalizing symptoms, and internalizing was related, in turn, to problem alcohol and substance use in late adolescence. Tests of moderation showed some of these developmental cascades were stronger for adolescents who were female, less oriented to mainstream cultural values, and more oriented to Mexican American cultural values.

The current study examines the relation between distress tolerance, perceived stress, and internalizing symptoms across adolescence. Participants included 331 youth, ages 10 to 14 at the first wave of the study, assessed annually over 5 years. A latent growth curve approach was used to test three research questions, including whether perceived stress would increase across adolescence, whether distress tolerance (as measured by a behavioral task) would predict changes in perceived stress, and whether changes in perceived stress would mediate the relation between distress tolerance and internalizing symptoms. Results suggest that, consistent with previous findings, rates of perceived stress do increase across adolescence. Further, findings indicate that distress intolerance at baseline predicted increases in perceived stress, which in turn drove increases in internalizing symptoms. These findings point to the critical role of distress tolerance in bringing about changes in depression and anxiety symptoms and suggest support for utilizing a negative reinforcement framework to understand the emergence of internalizing symptomology.

Research on developmental trajectories of early maladaptive features for understanding later personality disorders (PDs) is increasingly recognized as an important study area. The course of early odd features is highly relevant in this regard, as only a few researchers have addressed childhood oddity in the context of emerging PDs. Using latent growth modeling, the current study explores growth parameters of odd features in a mixed sample of Flemish community and referred children (N = 485) across three measurement waves with 1-year time intervals. Personality pathology was assessed at a fourth assessment point in adolescence. Beyond a general declining trend in oddity characteristics, the results demonstrated that both an early onset and an increasing trend of oddity-related characteristics over time are independent predictors of adolescent PDs. Childhood oddity tends to be the most manifest precursor for PDs with a core oddity feature (i.e., the schizotypal and borderline PD), but also appears to predict most of the other DSM-5 PDs. Results are discussed from an overarching developmental framework on PDs (Cicchetti, 2014), specifically focusing on the principle of multifinality. From a clinical perspective, the significance of increasing or steady-high childhood oddity trajectories for adolescent PDs highlights the relevance of systematic screening processes across time.