Adolescence is a period of substantial maturation in brain regions underlying Executive Functioning (EF). Adolescence is also associated with initiation and escalation of Alcohol Use (AU), and adolescent AU has been proposed to produce physiological and neurobiological events that derail healthy EF development. However, support has been mixed, which may be due to (1) failure to consider co-occurring externalizing symptoms (including other drug use) and poor social adaptation, and (2) heterogeneity and psychometric limitations in EF measures. We aimed to clarify the AU-EF association by: (1) distinguishing general externalizing symptoms from specific symptoms (AU, aggression, drug use) using bifactor modeling, (2) testing prospective associations between general externalizing symptoms and specific symptoms, and task-general EF, as indexed by a well-validated computational modeling framework (diffusion decision model), and (3) examining indirect pathways from externalizing symptoms to deficits in task-general EF through poor social adaptation. A high-risk longitudinal sample (N = 919) from the Michigan Longitudinal Study was assessed at four time-points spanning early adolescence (10–13 years) to young adulthood (22–25). Results suggested a critical role of social adaptation within peer and school contexts in promoting healthy EF. There was no evidence that specific, neurotoxic effects of alcohol or drug use derailed task-general EF development.

The ways that psychopathology manifests in adolescence have shifted dramatically over the past twenty-five years, with rates of many externalizing behaviors declining substantially while rates of anxiety and depressive disorders have skyrocketed. This paper argues that understanding these changes requires rethinking the field’s historically somewhat negative views of intense peer connections, peer influences, and adolescent risk-taking behavior. It is argued that intense peer connections are critical to development, and that peer influence and risk taking have important, often overlooked, adaptive components. The shift in observed manifestations of adolescent psychopathology over this period can be viewed at least partly in terms of a shift away from strong peer connections and toward greater risk aversion. Implications for research and intervention based on a focus on the adaptive aspects of peer influences and risk taking are discussed.

Dimensional psychopathology scores measure symptom severity; cutting across disorder categories. Their clinical utility is high given comorbidity, but their neural basis is unclear. We used scalp electroencephalography (EEG) to concurrently assess neural activity across internalizing and externalizing traits. “Theta rhythm” (4–7 Hz) spectral power at the frontal midline site Fz in specific goal conflict and action error phases within a trial of a Stop-Signal Task was extracted using process-specific contrasts. A final sample of 146 community participants (63 males, 83 females; mean age = 36; SD = 9; range = 18 – 56), oversampled for externalizing disorder (49% diagnosed with a DSM-5 externalizing disorder), also supplied psychopathology and personality data. We used the Minnesota Multiphasic Personality Inventory−3 (MMPI-3) to measure symptoms and traits of psychopathology. An MMPI-3 measure of the higher-order internalizing psychopathology spectrum was positively correlated with action error theta. An MMPI-3 measure of the higher-order spectrum of externalizing psychopathology was negatively correlated with goal-conflict theta. We showed that goal-conflict and error theta activity are higher-order processes that index psychopathology severity. The associations extend into the nominally healthy range, and so reflect theta-related factors that apply to the general population as well as patients with sub-threshold diagnoses.

Development and Psychopathology has been a premier resource for understanding stressful childhood experiences and the intergenerational continuity of psychopathology. Building on that tradition, we examined the unique and joint influences of maternal stress on children’s effortful control (age 7) and externalizing behavior (age 11) as transmitted via genetics, the prenatal environment, and the postnatal environment. The sample included N = 561 adopted children and their biological and adoptive parents. Path models identified a direct effect of biological mother life stress on children’s effortful control (β = −.08) and an indirect effect of her life stress on child externalizing behavior via effortful control (β = .52), but no main or indirect effects of biological parent psychopathology, prenatal stress, or adoptive mother adverse childhood experiences (ACES). Adoptive mother ACES amplified the association between biological mother life stress and child effortful control (β = −.08), externalizing behavior (β = 1.41), and the indirect effect via effortful control, strengthening associations when adoptive mothers reported average or high ACES during their own childhoods. Results suggest that novel study designs are needed to enhance the understanding of how life stress gets “under the skin” to affect psychopathology in the offspring of adults who have experienced stress.

Understanding how youth perceive household economic hardship and how it relates to their behavior is vital given associations between hardship and behavioral development. Yet, most studies ignore youth’s own perceptions of economic hardship, instead relying solely on caregiver reports. Moreover, the literature has tended to treat economic hardship as a stable force over time, rather than a volatile one that varies month-to-month. This study addressed extant limitations by collecting monthly measures of economic hardship, specifically caregiver- and youth-reported material deprivation and youth-reported financial stress, and youth internalizing and externalizing problems from 104 youth–caregiver dyads (youth: 14–16 years, 55% female, 37% Black, 43% White) over nine months. We examined month-to-month variability of these constructs and how youth-reports of material deprivation and financial stress predicted their behavior problems, controlling for caregiver-reports of material deprivation. We found that hardship measures varied month-to-month (ICCs = 0.69–0.73), and youth-reported material deprivation positively predicted internalizing when examining both within- and between-individual variability (β = .19–.47). Youth-reported financial stress positively predicted within-individual variation in externalizing (β = .18), while youth reports of material deprivation predicted externalizing when looking between families (β = .41). Caregiver-reported material deprivation was unrelated to youth behavior when accounting for youth perceptions of economic hardship.

There is limited evidence on heterogenous co-developmental trajectories of internalizing (INT) and externalizing (EXT) problems from childhood to adolescence and predictors of these joint trajectories. We utilized longitudinal data from Raine Study participants (n = 2393) to identify these joint trajectories from 5 to 17 years using parallel-process latent class growth analysis and analyze childhood individual and family risk factors predicting these joint trajectories using multinomial logistic regression. Five trajectory classes were identified: Low-problems (Low-INT/Low-EXT, 29%), Moderate Externalizing (Moderate-EXT/Low-INT, 26.5%), Primary Internalizing (Moderate High-INT/Low-EXT, 17.5%), Co-occurring (High-INT/High-EXT, 17%), High Co-occurring (Very High-EXT/High-INT, 10%). Children classified in Co-occurring and High Co-occurring trajectories (27% of the sample) exhibited clinically meaningful co-occurring problem behaviors and experienced more adverse childhood risk-factors than other three trajectories. Compared with Low-problems: parental marital problems, low family income, and absent father predicted Co-occurring and High Co-occurring trajectories; maternal mental health problems commonly predicted Primary Internalizing, Co-occurring, and High Co-occurring trajectories; male sex and parental tobacco-smoking uniquely predicted High Co-occurring membership; other substance smoking uniquely predicted Co-occurring membership; speech difficulty uniquely predicted Primary Internalizing membership; child’s temper-tantrums predicted all four trajectories, with increased odds ratios for High Co-occurring (OR = 8.95) and Co-occurring (OR = 6.07). Finding two co-occurring trajectories emphasizes the importance of early childhood interventions addressing comorbidity.

Childhood adversity is common and associated with elevated risk for transdiagnostic psychopathology. Reward processing has been implicated in the link between adversity and psychopathology, but whether it serves as a mediator or moderator is unclear. This study examined whether alterations in behavioral and neural reward processing function as a mechanism or moderator of psychopathology outcomes following adversity experiences, including threat (i.e., trauma) and deprivation. A longitudinal community sample of 10–15-year-old youths was assessed across two waves (Wave 1: n = 228; Wave 2: n = 206). Wave 1 assessed adverse experiences, psychopathology symptoms, reward processing on a monetary incentive delay task, and resting-state fMRI. At Wave 2, psychopathology symptoms were reassessed. Greater threat experiences were associated with blunted behavioral reward sensitivity, which, in turn, predicted increases in depression symptoms over time and mediated the prospective association between threat and depression symptoms. In contrast, reward sensitivity moderated the association between deprivation experiences and prospective externalizing symptoms such that the positive association of deprivation with increasing externalizing symptoms was absent for children with high levels of reward sensitivity.

Longitudinal trajectories of psychopathology in previously institutionalized (PI) youth were identified and biobehavioral emotion regulation processes were examined as developmental mechanisms that predict these trajectories. Mental health data were collected from PI (N = 132) and nonadopted (NA; N = 175) youth across four time points (participant age ranged from 7- to 21-year-old). Using semiparametric group-based methods, the probability that each individual belonged to a distinct group that followed a specific pattern of behavior across time was estimated. We then tested whether unique aspects of emotion regulation (global, observed, and biological) were differentially associated with membership in externalizing and internalizing trajectory groups using multinomial logistic regression models. Four externalizing trajectories were identified for the PI and NA groups. For PI youth, global, observed, and biological emotion regulation processes were uniquely predictive of more adaptive externalizing trajectories. For NA youth, only parent-reported global emotion regulation was predictive of externalizing patterns. Three internalizing trajectories were identified for PI and NA youth. Generally, only parent-reported global emotion regulation predicted internalizing group membership for both PI and NA youth. Results suggest that biobehavioral emotion regulation processes may be particularly important predictors and potential points of intervention when targeting trajectories of externalizing behaviors in PI children.

Parenting can protect against the development of, or increase risk for, child psychopathology; however, it is unclear if parenting is related to psychopathology symptoms in a specific domain, or to broad liability for psychopathology. Parenting differs between and within families, and both overall family-level parenting and the child-specific parenting a child receives may be important in estimating transdiagnostic associations with psychopathology. Data come from a cross-sectional epidemiological sample (N = 10,605 children ages 4–17, 6434 households). Parents rated child internalizing and externalizing symptoms and their parenting toward each child. General and specific (internalizing, externalizing) psychopathology factors, derived with bifactor modeling, were regressed on parenting using multilevel modeling. Less warmth and more aversive/inconsistent parenting in the family, and toward an individual child relative to family average, were associated with higher general psychopathology and specific externalizing problems. Unexpectedly, more warmth in the family, and toward an individual child relative to family average, was associated with higher specific internalizing problems in 4–11 (not 12–17) year-olds. Less warmth and more aversive/inconsistent parenting are broad correlates of child psychopathology. Aversive/inconsistent parenting, is also related to specific externalizing problems. Parents may behave more warmly when their younger children have specific internalizing problems, net of overall psychopathology.

The early caregiving environment can have lasting effects on child mental health. Animal models suggest that glucocorticoid receptor gene (NR3C1) DNA methylation plays a mediating role in linking more responsive caregiving to improved behavioral outcomes by its impact on the stress regulatory system. In this longitudinal study, we examined whether children’s NR3C1 methylation levels mediate an effect of maternal sensitivity in infancy on levels of child internalizing and externalizing behavior in a community sample. Maternal sensitivity of 145 mothers was rated at infant age 5 weeks, 12 months, and 30 months by observing mother–infant interactions. Buccal DNA methylation was assessed in the same children at age 6 years and maternal-reported internalizing and externalizing behavior was assessed at age 6 and 10 years. Higher sensitivity at age 5 weeks significantly predicted lower DNA methylation levels at two NR3C1 CpG loci, although methylation levels at these loci did not mediate an effect of maternal sensitivity on levels of child internalizing and externalizing behavior. Overall, the study provides evidence that maternal sensitivity in early infancy is associated with DNA methylation levels at loci involved in stress regulation, but the significance of this finding for child mental health remains unclear.

Internalizing and externalizing problems that emerge during adolescence differentially increase boys’ and girls’ risk for developing psychiatric disorders. It is not clear, however, whether there are sex differences in the intrinsic functional architecture of the brain that underlie changes in the severity of internalizing and externalizing problems in adolescents. Using resting-state fMRI data and self-reports of behavioral problems obtained from 128 adolescents (73 females; 9–14 years old) at two timepoints, we conducted multivoxel pattern analysis to identify resting-state functional connectivity markers at baseline that predict changes in the severity of internalizing and externalizing problems in boys and girls 2 years later. We found sex-differentiated involvement of the default mode network in changes in internalizing and externalizing problems. Whereas changes in internalizing problems were associated with the dorsal medial subsystem in boys and with the medial temporal subsystem in girls, changes in externalizing problems were predicted by hyperconnectivity between core nodes of the DMN and frontoparietal network in boys and hypoconnectivity between the DMN and affective networks in girls. Our results suggest that different neural mechanisms predict changes in internalizing and externalizing problems in adolescent boys and girls and offer insights concerning mechanisms that underlie sex differences in the expression of psychopathology in adolescence.

The present study examined the intergenerational transmission of internalizing and externalizing symptom severity, which indexes comorbidity, and symptom directionality, which indicates differentiation toward externalizing versus internalizing problems. Data are from 854 male and female, same-sex adult twin pairs born between 1926 and 1971 (32–60 years old, M = 44.9 years, SD = 4.9 years) from the Twin and Offspring Study in Sweden and their adolescent offspring (11–22 years old, M = 15.7 years, SD = 2.4 years, 52% female). Children-of-twins models revealed additive (9%) and dominant (45%) genetic and nonshared environmental (47%) influences on twins’ symptom severity, and additive genetic (39%) and nonshared environmental (61%) influences on twins’ symptom directionality. Both comorbid problems and preponderance of symptoms of a particular – internalizing versus externalizing – spectrum were correlated across parent and child generations, although associations were modest especially for directionality (i.e., transmission of specific symptom type). By interpreting findings alongside a recent study of adolescent twins, we demonstrate that the intergenerational transmission of symptom severity and symptom directionality are both unlikely to be attributable to genetic transmission, are both likely to be influenced by direct phenotypic transmission and/or nonpassive rGE, and the intergenerational transmission of symptom severity is also likely to be influenced by passive rGE.

Externalizing behavior in early adolescence is associated with alcohol use in adolescence and early adulthood and these behaviors often emerge as part of a developmental sequence. This pattern can be the result of heterotypic continuity, in which different behaviors emerge over time based on an underlying shared etiology. In particular, there is largely a shared genetic etiology underlying externalizing and substance use behaviors. We examined whether polygenic risk for alcohol use disorder predicted (1) externalizing behavior in early adolescence and alcohol use in adolescence in the Early Steps Multisite sample and (2) externalizing behavior in adolescence and alcohol use in early adulthood in the Project Alliance 1 (PAL1) sample. We examined associations separately for African Americans and European Americans. When examining European Americans in the Early Steps sample, greater polygenic risk was associated with externalizing behavior in early adolescence. In European Americans in PAL1, we found greater polygenic risk was associated with alcohol use in early adulthood. Effects were largely absent in African Americans in both samples. Results imply that genetic predisposition for alcohol use disorder may increase risk for externalizing and alcohol use as these behaviors emerge developmentally.