Dishion and Patterson's work on the unique role of fathers in the coercive family process showed that fathers' coercion explained twice the variance of mothers' in predicting children's antisocial behavior and how treatment and prevention of coercion and promotion of prosocial parenting can mitigate children's problem behaviors. Using these ideas, we employed a sample of 426 divorced or separated fathers randomly assigned to Fathering Through Change (FTC), an interactive online behavioral parent training program or to a waitlist control. Participating fathers had been separated or divorced within the past 24 months with children ages 4 to 12 years. We tested an intent to treat (ITT) mediation hypothesis positing that intervention-induced changes in child problem behaviors would be mediated by changes in fathers' coercive parenting. We also tested complier average causal effects (CACE) models to estimate intervention effects, accounting for compliers and noncompliers in the treatment group and would-be compliers in the controls. Mediation was supported. ITT analyses showed the FTC obtained a small direct effect on father-reported pre–post changes in child adjustment problems (d = .20), a medium effect on pre–post changes in fathers' coercive parenting (d = .61), and a moderate indirect effect to changes in child adjustment (d = .30). Larger effects were observed in CACE analyses.

We investigated whether children born preterm are at risk for language delay using a sibling-control design in the Norwegian Mother and Child Cohort Study (MoBa), conducted by the Norwegian Institute of Public Health. Participants included 26,769 siblings born between gestational weeks 23 and 42. Language delay was assessed when the children were 1.5, 3, and 5 years old. To adjust for familial risk factors, comparisons were conducted between preterm and full-term siblings. Pregnancy-specific risk factors were controlled for by means of observed variables. Findings showed that preterm children born before week 37 had increased risk for language delays at 1.5 years. At 3 and 5 years, only children born before week 34 had increased risk for language delay. Children born weeks 29–33 and before week 29 had increased risk for language delay at 1.5 years (RR = 4.51, 95% CI [3.45, 5.88]; RR = 10.32, 95% CI [6.7, 15.80]), 3 years (RR = 1.50, 95% CI [1.02, 2.21]; RR = 2.78, 95% CI [1.09, 7.07]), and 5 years (RR = 1.63, 95% CI [1.06, 2.51]; RR = 2.98, 95% CI [0.87, 10.26]), respectively. In conclusion, children born preterm are at risk for language delays, with familial confounders only explaining a moderate share of the association. This suggests a cause-effect relationship between early preterm birth and risk for language delay in preschool children.

Anxiety sensitivity (AS), the belief that anxious arousal is harmful, is a malleable risk factor that has been implicated in anxiety and depression symptoms in adolescents. Although there is some evidence that adolescents possess distinct developmental trajectories, few studies have explored this topic. This study examined the developmental trajectory of AS in 248 adolescents (M age = 11.0 years, SD = 0.82; 56% male) across 6 years, beginning when children were age 11. This study also examined the influence of AS trajectories on anxiety and depression at age 16. Finally, this study examined the utility of AS classes in identifying anxiety and depression growth. Three AS classes were found, described by normative-stable, high-stable, and high-unstable trajectories. Adolescents in the high-stable and the high-unstable AS classes had higher levels of anxiety and depression at age 16 than did adolescents in the normative-stable AS class. In addition, the anxiety and depression trajectories fit by AS class mirrored the AS class trajectories. These findings suggest three AS trajectories can be identified in adolescents. These trajectories are discussed in relation to a developmental perspective of AS.

This study examined the childhood history of maltreatment, peer relations, and externalizing problems among individuals who manifested low, moderate, or high symptom levels of paranoid personality disorder (PPD) in adolescence. Participants included 174 children who attended a longitudinal summer camp research program between the ages of 9 to 12. Multiple sources of information (self-, peer, and counselor reports) were utilized. Subsequently, they participated in a personality disorder assessment during adolescence (mean age = 15.30). The results indicated that children who manifested higher levels of PPD symptoms in adolescence had higher odds of having a history of child maltreatment. Children who manifested high levels of PPD symptoms in adolescence showed a faster growth rate for peer bullying and externalizing problems in childhood. In addition, their peers rated them as less cooperative, less likely to be leaders, and more likely to initiate fights. These findings suggested that children who manifested elevated PPD symptoms in adolescence had shown early signs of behavioral disturbances in childhood, some of which gradually worsened as they approach adolescence.

Past research has documented pervasive genetic influences on emotional and behavioral disturbance across the life span and on liability to adult psychiatric disorder. Increasingly, interest is turning to mechanisms of gene–environment interplay in attempting to understand the earliest manifestations of genetic risk. We report findings from a prospective adoption study, which aimed to test the role of evocative gene–environment correlation in early development. Included in the study were 561 infants adopted at birth and studied between 9 and 27 months, along with their adoptive parents and birth mothers. Birth mother psychiatric diagnoses and symptoms scales were used as indicators of genetic influence, and multiple self-report measures were used to index adoptive mother parental negativity. We hypothesized that birth mother psychopathology would be associated with greater adoptive parent negativity and that such evocative effects would be amplified under conditions of high adoptive family adversity. The findings suggested that genetic factors associated with birth mother externalizing psychopathology may evoke negative reactions in adoptive mothers in the first year of life, but only when the adoptive family environment is characterized by marital problems. Maternal negativity mediated the effects of genetic risk on child adjustment at 27 months. The results underscore the importance of genetically influenced evocative processes in early development.

Children born to older fathers are at higher risk to develop severe psychopathology (e.g., schizophrenia and bipolar disorder), possibly because of increased de novo mutations during spermatogenesis with older paternal age. Because severe psychopathology is correlated with antisocial behavior, we examined possible associations between advancing paternal age and offspring violent offending. Interlinked Swedish national registers provided information on fathers' age at childbirth and violent criminal convictions in all offspring born from 1958 to 1979 (N = 2,359,921). We used ever committing a violent crime and number of violent crimes as indices of violent offending. The data included information on multiple levels; we compared differentially exposed siblings in within-family analyses to rigorously test causal influences. In the entire population, advancing paternal age predicted offspring violent crime according to both indices. Congruent with a causal effect, this association remained for rates of violent crime in within-family analyses. However, in within-family analyses, we found no association with ever committing a violent crime, suggesting that factors shared by siblings (genes and environment) confounded this association. Life-course persistent criminality has been proposed to have a partly biological etiology; our results agree with a stronger biological effect (i.e., de novo mutations) on persistent violent offending.

Aberrant face emotion processing has been demonstrated in youth with and at a familial risk for bipolar and major depressive disorders. However, the neurobiological factors related to emotion processing that underlie resilience from youth-onset mood disorders are not well understood. Functional magnetic resonance imaging data during an implicit emotion processing task were collected at baseline from a sample of 50 youth, ages 8–17, who were healthy but also familially at high risk for either bipolar disorder or major depressive disorder, and 24 healthy controls with no family history of psychopathology (HCL). Participants were reevaluated 3 years later and classified into three groups for analysis: high-risk youth who converted to a psychiatric diagnosis (CVT; N = 23), high-risk youth who were resilient from developing any psychopathology (RES; N = 27), and HCL youth (N = 24) who remained healthy at follow-up. For happy > calm faces, the CVT and RES groups had significantly lower activation in the left inferior parietal lobe (IPL), while the RES group had lower activation in the right supramarginal gyrus. For fear > calm faces, the RES group had lower activation in the right precuneus and inferior frontal gyrus (IFG) compared to the CVT group. Connectivity analyses revealed the RES group exhibited higher left IPL connectivity with visual cortical regions for happy > calm faces, and higher IFG connectivity with frontal, temporal, and limbic regions for fear > calm faces. These connectivities were correlated with improvements in prosocial behaviors and global functioning. Our findings suggest that differential activation and connectivity in the IPL, IFG, and precuneus in response to emotional stimuli may represent distinct resilience and risk markers for youth-onset mood disorders.

Samples of poor and normal readers were followed into early adulthood to assess the implications of childhood reading difficulties for the transition to adulthood, and for early adult psychosocial functioning. Some group differences were found in patterns of early adult transitions, and, for women only, on wider measures of early adult functioning. Global self-esteem in adulthood did not differ between the childhood reading groups, and there were few marked variations in vulnerability to later psychiatric disorder. The findings are discussed in regard to differing developmental pathways for problems in adult functioning, ant the possible role of contextual changes in enabling more positive functioning for many childhood poor readers.

Norepinephrine (NE), dopamine (DA), and serotonin (5HT) are three of the more than thirty neurotransmitters (NTs) in the brain. Axons from a relatively small number of cell bodies located in the midbrain and brainstem branch out to connect with virtually all areas of the brain. Via these connections, these three NTs participate in the regulation of several behavioral systems that help modulate the interaction of the individual with his/her environment. Because the NT systems continue to develop after birth, interactions between the individual and his/her environment after birth may affect the development of these systems and have long-term effects on the individual's behavior. Animal studies indicate that early experience affects behavior and biogenic amine systems in the adult. For instance, one study showed that maternal deprivation, which is analogous to human neglect, affects the NE system in monkeys and may have a long-lasting effect on its development and function. In a previous study, similar relationships between early neglect and the NE system in humans were examined. Our results show that emotionally disturbed children with a history of neglect have lower dopamine-β-hydroxylase (DβH) activity, an enzyme involved in the synthesis of NE, than do children with no history of neglect. Additionally, the children with a history of neglect have lower systolic and diastolic blood pressure, both of which are functions mediated by the NE system, than the other children studied. These results support findings in animal studies that neglect affects the development of the NE system in a long-lasting, if not permanent way.

Although borderline personality disorder (BPD) traits decline from adolescence to adulthood, comorbid psychopathology such as symptoms of major depressive disorder (MDD), alcohol use disorder (AUD), and drug use disorders (DUDs) likely disrupt this normative decline. Using a longitudinal sample of female twins (N = 1,763), we examined if levels of BPD traits were correlated with changes in MDD, AUD, and DUD symptoms from ages 14 to 24. A parallel process biometric latent growth model examined the contributions of genetic and environmental factors to the relationships between developmental components of these phenotypes. Higher BPD trait levels predicted a greater rate of increase in AUD and DUD symptoms, and higher AUD and DUD symptoms predicted a slower rate of decline of BPD traits from ages 14 to 24. Common genetic influences accounted for the associations between BPD traits and each disorder, as well as the interrelationships of AUD and DUD symptoms. Both genetic and nonshared environmental influences accounted for the correlated levels between BPD traits and MDD symptoms, but solely environmental influences accounted for the correlated changes between the two over time. Results indicate that higher levels of BPD traits may contribute to an earlier onset and faster escalation of AUD and DUD symptoms, and substance use problems slow the normative decline in BPD traits. Overall, our data suggests that primarily genetic influences contribute to the comorbidity between BPD features and substance use disorder symptoms. We discuss our data in the context of two major theories of developmental psychopathology and comorbidity.

Although substantial human and animal evidence suggests a role for the amygdala in anxiety, literature linking amygdala volume to anxiety symptomatology is inconclusive, with studies finding positive, negative, and null results. Clarifying this brain–behavior relation in middle to late childhood is especially important, as this is a time both of amygdala structural maturation and the emergence of many anxiety disorders. The goal of the current study was to clarify inconsistent findings in previous literature by identifying factors moderating the relation between amygdala volume and anxiety traits in a large sample of typically developing children aged 6–13 years (N = 72). In particular, we investigated the moderating effects of informant (parent vs. child), age, and sex. We found that children's reports (i.e., self-reports) were related to amygdala volume; children who reported higher anxiety levels had smaller amygdalae. This negative relation between amygdala volume and anxiety weakened with age. There was also an independent effect of sex, such that relations were stronger in males than in females. These results indicate the importance of considering sample and informant characteristics when charting the neurobiological mechanisms underlying developmental anxiety.

This study examined contextual factors (caregiver depression, family resources, ethnicity, and initial levels of youth problem behavior) related to the effectiveness of the Family Check-Up (FCU) and evaluated family processes as a mediator of FCU intervention response and adolescent antisocial behavior. We followed a sample of 180 ethnically diverse youths of families who engaged in the FCU intervention. Family data were collected as part of the FCU assessment, and youth data were collected over 4 years, from sixth through ninth grade. Findings indicated that caregiver depression and minority status predicted greater caregiver motivation to change. In turn, caregiver motivation was the only direct predictor of FCU intervention response during a 1-year period. Growth in family conflict from sixth through eighth grade mediated the link between FCU response and ninth-grade antisocial behavior. This study explicitly tested core aspects of the FCU intervention model and demonstrated that caregiver motivation is a central factor that underlies family response to the FCU. The study also provided support for continued examination of family process mechanisms that account for enduring effects of the FCU and other family-centered interventions.

Although adolescence is characterized by hormonal changes and increased disinhibited behaviors, explanations for these developmental changes that include personality and environmental factors have not been fully elucidated. We examined the interactions between psychosocial stress and the traits of negative emotionality and constraint on impulsive and risk-taking behaviors as well as salivary cortisol reactivity in 88 adolescents. In terms of behavioral outcomes, analyses revealed that negative emotionality and constraint were protective of impulsivity and risk taking, respectively, for adolescents in the no-stress condition; personality did not relate to either behavior in the stress condition. Low-constraint adolescents in the stress condition engaged in less risk taking than low-constraint adolescents in the no-stress condition, whereas there was no effect of stress group for high-constraint adolescents. In terms of cortisol reactivity, analyses revealed that low-constraint adolescents in the stress condition exhibited greater cortisol reactivity compared to high-constraint adolescents, which suggests that low-constraint adolescents mobilize greater resources (e.g., increased cognitive control, heightened attention to threat) in stressful situations relative to nonstressful ones. These results demonstrate that two facets of disinhibition and cortisol reactivity are differentially affected by psychosocial stress and personality (and their interactions) in adolescents.

This study focuses on the importance of patterns of adjustment problems in early adolescence and convictions for alcohol abuse in the mid-teens for the development of alcohol abuse manifested in early adulthood. The study was performed on a large and representative cohort of Swedish males, prospectively followed from age 13 to age 25. A person approach was applied in which the individuals and individual patterns of adjustment problems were the objects of interest, not single variables per se. The results showed that patterns of multiple adjustment problems in early adolescence, as well as convictions for alcohol abuse in the mid-teens, significantly increased the risk for later alcohol abuse. Among multiproblem boys also convicted for alcohol abuse in their mid-teens, 72% were registered for alcohol abuse at ages 18–24. However, early single adjustment problems did not significantly increase the risk for later alcohol abuse. The importance of studying the background of alcohol abuse from a developmental and interactionistic perspective was emphasized.

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.

Behavioral Inhibition (BI) is a temperament type that predicts social withdrawal in childhood and anxiety disorders later in life. However, not all BI children develop anxiety. Attention bias (AB) may enhance the vulnerability for anxiety in BI children, and interfere with their development of effective emotion regulation. In order to fully probe attention patterns, we used traditional measures of reaction time (RT), stationary eye-tracking, and recently emerging mobile eye-tracking measures of attention in a sample of 5- to 7-year-olds characterized as BI (N = 23) or non-BI (N = 58) using parent reports. There were no BI-related differences in RT or stationary eye-tracking indices of AB in a dot-probe task. However, findings in a subsample from whom eye-tracking data were collected during a live social interaction indicated that BI children (N = 12) directed fewer gaze shifts to the stranger than non-BI children (N = 25). Moreover, the frequency of gazes toward the stranger was positively associated with stationary AB only in BI, but not in non-BI, children. Hence, BI was characterized by a consistent pattern of attention across stationary and ambulatory measures. We demonstrate the utility of mobile eye-tracking as an effective tool to extend the assessment of attention and regulation to social interactive contexts.

Recent proposals suggest early adversity sets in motion particularly chronic and neurobiologically distinct trajectories of internalizing symptoms. However, few prospective studies in high-risk samples delineate distinct trajectories of internalizing symptoms from preschool age onward. We examined trajectories in a high-risk cohort, oversampled for internalizing symptoms, several preschool risk/maintenance factors, and school-age outcomes. Parents of 325 children completed the Strengths and Difficulties Questionnaire on up to four waves of data collection from preschool (3–5 years) to school age (8–9 years) and Preschool Age Psychiatric Assessment interviews at both ages. Multi-informant data were collected on risk factors and symptoms. Growth mixture modelling identified four trajectory classes of internalizing symptoms with stable low, rising low-to-moderate, stable moderate, and stable high symptoms. Children in the stable high symptom trajectory manifested clinically relevant internalizing symptoms, mainly diagnosed with anxiety disorders/depression at preschool and school age. Trajectories differed regarding loss/separation experience, maltreatment, maternal psychopathology, temperament, and stress-hormone regulation with loss/separation, temperament, maternal psychopathology, and stress-hormone regulation (trend) significantly contributing to explained variance. At school age, trajectories continued to differ on symptoms, disorders, and impairment. Our study is among the first to show that severe early adversity may trigger a chronic and neurobiologically distinct internalizing trajectory from preschool age onward.

Suicidal thoughts and behaviors (STBs) are major public health concerns among adolescents, and research is needed to identify how risk is conferred over the short term (hours and days). Sleep problems may be associated with elevated risk for STBs, but less is known about this link in youth over short time periods. The current study utilized a multimodal real-time monitoring approach to examine the association between sleep problems (via daily sleep diary and actigraphy) and next-day suicidal thinking in 48 adolescents with a history of STBs during the month following discharge from acute psychiatric care. Results indicated that specific indices of sleep problems assessed via sleep diary (i.e., greater sleep onset latency, nightmares, ruminative thoughts before sleep) predicted next-day suicidal thinking. These effects were significant even when daily sadness and baseline depression were included in the models. Moreover, several associations between daily-level sleep problems and next-day suicidal thinking were moderated by person-level measures of the construct. In contrast, sleep indices assessed objectively (via actigraphy) were either not related to suicidal thinking or were related in the opposite direction from hypothesized. Together, these findings provide some support for sleep problems as a short-term risk factor for suicidal thinking in high-risk adolescents.

The aim of the current research was to disentangle four theoretically sound models of externalizing behavior etiology (i.e., attachment, language, inhibition, and parenting) by testing their relation with behavioral trajectories from early childhood to adolescence. The aim was achieved through a 10-year prospective longitudinal study conducted over five waves with 111 referred children aged 3 to 5 years at the onset of the study. Clinical referral was primarily based on externalizing behavior. A multimethod (questionnaires, testing, and observations) approach was used to estimate the four predictors in early childhood. In line with previous studies, the results show a significant decrease of externalizing behavior from early childhood to adolescence. The decline was negatively related to mothers’ coercive parenting and positively related to attachment security in early childhood, but not related to inhibition and language. The study has implications for research into externalizing behavior etiology recommending to gather hypotheses from various theoretically sound models to put them into competition with one another. The study also has implications for clinical practice by providing clear indications for prevention and early intervention.

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.