Experiences of child abuse and neglect are risk factors for youth suicidal thoughts and behaviors. Accordingly, suicide risk may emerge as a developmental process that is heavily influenced by the rearing environment. We argue that a developmental, theoretical framework is needed to guide future research on child maltreatment and youth (i.e., adolescent and emerging adult) suicide, and to subsequently inform suicide prevention efforts. We propose a developmental model that integrates principles of developmental psychopathology and current theories of suicide to explain the association between child maltreatment and youth suicide risk. This model bears significant implications for future research on child maltreatment and youth suicide risk, and for suicide prevention efforts that target youth with child maltreatment experiences.

Parenting behaviors are significantly linked to youths’ behavioral adjustment, an association that is moderated by youths’ and parents’ self-regulation. The biological sensitivity to context theory suggests that respiratory sinus arrhythmia (RSA) indexes youths’ varying susceptibility to rearing contexts. However, self-regulation in the family context is increasingly viewed as a process of “coregulation” that is biologically embedded and involves dynamic Parent×Child interactions. No research thus far has examined physiological synchrony as a dyadic biological context that may moderate associations between parenting behaviors and preadolescent adjustment. Using a two-wave sample of 101 low-socioeconomic status (SES) families (children and caretakers; mean age 10.28 years), we employed multilevel modeling to examine dyadic coregulation during a conflict task, indicated by RSA synchrony, as a moderator of the linkages between observed parenting behaviors and preadolescents’ internalizing and externalizing problems. Results showed that high dyadic RSA synchrony resulted in a multiplicative association between parenting and youth adjustment. High dyadic synchrony intensified the relations between parenting behaviors and youth behavior problems, such that in the context of high dyadic synchrony, positive and negative parenting behaviors were associated with decreased and increased behavioral problems, respectively. Parent–child dyadic RSA synchrony is discussed as a potential biomarker of biological sensitivity in youth.

Child maltreatment is a robust risk factor for suicidal ideation and behaviors during adolescence. Elevations in internalizing and externalizing symptomology have been identified as two distinct developmental pathways linking child maltreatment and adolescent risk for suicide. However, recent research suggests that the co-occurrence of internalizing and externalizing symptomology may form a distinct etiological pathway for adolescent risk behaviors. Using the Longitudinal Studies on Child Abuse and Neglect (LONGSCAN) sample (N = 1,314), the present study employed a person-centered approach to identify patterns of concurrent change in internalizing and externalizing psychopathology over five time points from early childhood to adolescence in relation to previous experiences of child maltreatment and subsequent suicidal ideation and behaviors. Results indicated four distinct bivariate externalizing and internalizing growth trajectories. Group membership in a heightened comorbid internalizing and externalizing symptom trajectory mediated the association between childhood abuse and adolescent suicidal ideation and suicidal behaviors. These findings suggest that the concurrent development of externalizing and internalizing symptoms in childhood and adolescence may constitute a unique developmental trajectory that confers risk for suicide-related outcomes.

Emerging developmental perspectives suggest that adverse rearing environments promote neurocognitive adaptations that heighten impulsivity and increase vulnerability to risky behavior. Although studies document links between harsh rearing environments and impulsive behavior on substance use, the developmental hypothesis that impulsivity acts as mechanism linking adverse rearing environments to downstream substance use remains to be investigated. The present study investigated the role of impulsivity in linking child abuse and neglect with adult substance use using data from (a) a longitudinal sample of youth (Study 1, N = 9,421) and (b) a cross-sectional sample of adults (Study 2, N = 1,011). In Study 1, the links between child abuse and neglect and young adult smoking and marijuana use were mediated by increases in adolescent impulsivity. In Study 2, indirect links between child abuse and neglect and substance use were evidenced via delayed reward discounting and impulsivity traits. Among impulsivity subcomponents, robust indirect effects connecting childhood experiences to cigarette use emerged for negative urgency. Negative urgency, positive urgency, and sensation seeking mediated the effect of child abuse and neglect on cannabis and alcohol use. Results suggest that child abuse and neglect increases risk for substance use in part, due to effects on impulsivity. Individuals with adverse childhood experiences may benefit from substance use preventive intervention programs that target impulsive behaviors.

A randomized clinical trial was conducted to evaluate the efficacy of interpersonal psychotherapy (IPT) for ethnically and racially diverse, economically disadvantaged women with major depressive disorder. Non-treatment-seeking urban women (N = 128; M age = 25.40, SD = 4.98) with infants were recruited from the community. Participants were at or below the poverty level: 59.4% were Black and 21.1% were Hispanic. Women were screened for depressive symptoms using the Center for Epidemiologic Studies Depression Scale; the Diagnostic Interview Schedule was used to confirm major depressive disorder diagnosis. Participants were randomized to individual IPT or enhanced community standard. Depressive symptoms were assessed before, after, and 8 months posttreatment with the Beck Depression Inventory—II and the Revised Hamilton Rating Scale for Depression. The Social Support Behaviors Scale, the Social Adjustment Scale—Self-Report, and the Perceived Stress Scale were administered to examine mediators of outcome at follow-up. Treatment effects were evaluated with a growth mixture model for randomized trials using complier-average causal effect estimation. Depressive symptoms trajectories from baseline through postintervention to follow-up showed significant decreases among the IPT group compared to the enhanced community standard group. Changes on the Perceived Stress Scale and the Social Support Behaviors Scale mediated sustained treatment outcome.

Child maltreatment, peer victimization, and a polymorphism of the serotonin transporter gene (5-HTTLPR) were examined as predictors of depressive symptomatology. Children (M age = 11.26, SD = 1.65), including 156 maltreated and 145 nonmaltreated children from comparable low socioeconomic backgrounds, provided DNA samples and self-reports of relational peer victimization, overt peer victimization, and depressive symptoms. Path analysis showed that relational and overt victimization mediated the association between child maltreatment and depressive symptoms. Bootstrapping procedures were used to test moderated mediation and demonstrated that genotype moderated the indirect effects of relational and overt victimization on child depressive symptoms, such that victimized children with the long/long variation were at an increased risk for depressive symptoms compared to victimized children carrying a short allele. Results highlight the utility of examining process models that incorporate biological and psychological factors contributing to the development of depressive symptomatology and provide direction toward understanding and promoting resilience among high-risk youth from a multiple levels of analysis approach.

Childhood maltreatment is associated with lasting changes in neuroendocrine regulation, alterations in brain structure and function, and symptoms of “limbic irritability.” Limbic irritability symptoms include somatic, sensory, and behavioral phenomena and may stem from increased excitatory neurotransmission following maltreatment. We tested the hypotheses that child maltreatment is indirectly associated with depressive and dissociative symptomatology via indicators of limbic irritability and that variation within the FK506 binding protein 5 gene (FKBP5), a gene involved in glucorticoid receptor functioning, moderates these effects. The sample consisted of high-risk, low-income women (N = 236) living in an inner-city environment. Child maltreatment, limbic irritability, and symptoms of depression and dissociation were measured cross-sectionally using self-report assessments. Haplotype analyses were conducted across four FKBP5 single nucleotide polymorphisms: rs3800373, rs9296158, rs1360870, and rs9470080. Path analysis using bootstrapping procedures was performed to test hypotheses regarding indirect and conditional indirect effects. We found significant indirect effects of maltreatment on depression (β = 0.088, p < .01) and dissociation (β = 0.105, p < .01) via limbic irritability. In addition, variation within FKBP5 moderated these significant indirect effects. For individuals with one to two copies of the CATT haplotype, the indirect effects of maltreatment on depression (β = 0.137, p < .01) and dissociation (β = 0.132, p < .01) via limbic irritability were significant, whereas the indirect paths were not significant for individuals with no copies of this haplotype (depression: β = 0.037, p > .05; dissociation: β = 0.002, p > .05). These results add to the growing evidence that child maltreatment may lead to symptoms of internalizing psychopathology through its impact on the limbic system. In addition, this study revealed a potential role of FKBP5 gene variants in contributing to risk for limbic system dysfunction.

We tested for gender moderation within a multidomain model of antisocial behavior (ASB) among community youth, drawn from the Project on Human Development in Chicago Neighborhoods study. Youths (N = 1,639) were 9 to 12 years old at baseline and were followed for two additional waves, spaced approximately 2.5 years apart. We hypothesized that harsh and physically coercive parenting, a familial level risk factor, would impact individual level risk factors for ASB, such as childhood temperament ratings of emotionality and inhibitory control, and preadolescent externalizing and internalizing symptoms, as well as involvement with antisocial peers. We further hypothesized that this process and its impact on ASB would be moderated by gender. We used both multiple indicator multiple causes and multiple group analyses to test for gender moderation and a structural equation modeling multiple mediation framework to evaluate the strength of indirect effects. We tested the role of family, individual, and peer level influences on ASB, after accounting for the role of known contextual factors, including poverty, race, and neighborhood. Our overall model fit the data well for males and females, indicating harsh parenting, disinhibition, emotionality, and peers exert a strong influence on risk for ASB. Gender moderated the pathway from harsh parenting to externalizing behavior, such that this was a significant pathway for girls, but not boys. We discussed the importance of these findings with regard to intervention planning for youth at risk for ASB and future gender-informed models of ASB.

Within an allostatic load framework, the effect of Gene × Environment (G × E) interactions on diurnal cortisol regulation and internalizing symptomatology were investigated. Variation in the corticotropin releasing hormone receptor 1 (CRHR1) TAT haplotype and serotonin transporter linked polymorphic region (5-HTTLPR) was determined in a sample of maltreated (n = 238, 21.4% with early physical and sexual abuse) and nonmaltreated (n = 255) children (M age = 10.08) participating in a summer research camp. Internalizing and depressive symptoms were assessed by other and self-report. G × E effects for CRHR1 and maltreatment and early abuse on diurnal cortisol regulation were observed; CRHR1 variation was related to cortisol dysregulation only among maltreated children. Early abuse and high internalizing symptoms also interacted to predict atypical diurnal cortisol regulation. The interaction of CRHR1, 5-HTTLPR, and child maltreatment (G × G × E) identified a subgroup of maltreated children with high internalizing symptoms who shared the same combination of the two genes. The findings support an allostatic load perspective on the effects of the chronic stress associated with child maltreatment on cortisol regulation and internalizing symptomatology as moderated by genetic variation.

A developmental cascade model tested associations among child maltreatment, internalizing and externalizing psychopathology, social competence, and cannabis abuse and dependence symptoms in a longitudinal cohort (N = 415). Nested structural equation models evaluated continuity and cross-domain influences among broad multi-informant constructs across four developmental periods: age 7 to 9, 10 to 12, 13 to 15, and 15 to 18. Results indicated significant paths from child maltreatment to early externalizing and internalizing problems and social competence, as well as to cannabis abuse and dependence (CAD) symptoms in adolescence. Youth CAD symptoms were primarily related directly to child maltreatment and externalizing problems. Childhood internalizing symptoms contributed to later childhood decreases in social competence, which predicted increases in late adolescent externalizing problems. Using a developmental psychopathology framework, results are discussed in relation to cascade and transactional effects and the interplay between problem behaviors during childhood and development of CAD symptoms during early and late adolescence.