Waters, Ruiz, and Roisman (2017) recently published evidence based on the Minnesota Longitudinal Study of Risk and Adaptation (MLSRA) that sensitive caregiving during childhood is associated with higher levels of secure base script knowledge during the Adult Attachment Interview (AAIsbs). At present, however, little is known about the role of variation in atypical caregiving, including abuse and/or neglect, in explaining individual differences in AAIsbs. This study revisited data from the MLSRA (N = 157) to examine the association between experiencing abuse and/or neglect in the first 17.5 years of life and secure base script knowledge measured at ages 19 and 26 years. Several aspects of abuse and/or neglect experiences were assessed, including perpetrator identity, timing, and type. Regressions revealed that childhood abuse and/or neglect was robustly associated with lower AAIsbs scores in young adulthood, above and beyond previously documented associations with maternal sensitivity and demographic covariates. Follow-up analyses provided evidence that the predictive significance of abuse for secure base script knowledge was specific to perpetration by parental figures, rather than non-caregivers. Exploratory analyses indicated that abuse and/or neglect: (a) in middle childhood and adolescence (but not infancy and early childhood) and (b) physical abuse (but not sexual abuse or neglect) were uniquely associated with lower AAIsbs scores.

Growing evidence suggests that emotion socialization may be disrupted by maternal depression. However, little is known about emotion-related parenting by mothers with bipolar disorder or whether affective modeling in early childhood is linked to young adults’ recollections of emotion socialization practices. The current study investigates emotion socialization by mothers with histories of major depression, bipolar disorder, or no mood disorder. Affective modeling was coded from parent–child interactions in early childhood and maternal responses to negative emotions were recollected by young adult offspring (n = 131, 59.5% female, M age = 22.16, SD = 2.58). Multilevel models revealed that maternal bipolar disorder was associated with more neglecting, punishing, and magnifying responses to children's emotions, whereas maternal major depression was associated with more magnifying responses; links between maternal diagnosis and magnifying responses were robust to covariates. Young adult recollections of maternal responses to emotion were predicted by affective modeling in early childhood, providing preliminary validity evidence for the Emotions as a Child Scale. Findings provide novel evidence that major depression and bipolar disorder are associated with altered emotion socialization and that maternal affective modeling in early childhood prospectively predicts young adults’ recollections of emotion socialization in families with and without mood disorder.

Callous-unemotional (CU) traits characterize a subset of youth at risk for persistent and serious antisocial behavior. Differences in resting state connectivity in the default mode network (DMN) have been associated with CU traits in forensic and clinical samples of adolescents and with deficient interpersonal/affective traits (often operationalized as Factor 1 psychopathy traits) in adults. It is unclear whether these brain-behavior associations extend to community-based children. Using mixed model analyses, we tested the associations between CU traits and within-network resting-state connectivity of seven task-activated networks and the DMN using data from 9,636 9–11-year-olds in the Adolescent Brain Cognitive Development (ABCD) study. Even after accounting for comorbid externalizing problems, higher levels of CU traits were associated with reduced connectivity within the DMN. This finding is consistent with prior literature surrounding psychopathy and CU traits in clinically and forensically based populations, suggesting the correlation likely exists on a spectrum, can be detected in childhood, and is not restricted to children with significant antisocial behavior.

Teenage childbearing (age 15–19 years) represents a significant public health issue that can generate considerable deleterious, multigenerational consequences for teen-childbearing mothers and their offspring. However, few studies have examined the potential mediating mechanisms that may explain if and how teen childbearing is associated with the development of offspring psychopathology. The current study used a developmental model to test the mediating role of chronic child maltreatment in the relationship between teen childbearing and offspring internalizing symptoms in childhood and emerging adulthood. The study participants were 384 individuals from socioeconomically disadvantaged, ethnically diverse backgrounds, assessed across two longitudinal waves of data (i.e., ages 10–12 and 18–20). The sample included maltreated and nonmaltreated children, all of whom were comparable in terms of family income. Structural equation modeling was conducted to test direct and indirect pathways from teen childbearing to offspring psychopathology. A multigenerational developmental cascade was found such that individuals born to mothers who began their childbearing in adolescence were more likely to experience chronic maltreatment during childhood, which in turn predicted greater internalizing symptoms throughout childhood and emerging adulthood. Using a developmental psychopathology framework, the results are discussed with regard to implications for prevention and early intervention.

Existing research has suggested children of caregivers with histories of exposure to trauma are at heightened risk for victimization, but few studies have explored potential mechanisms that explain this intergenerational transmission of risk. With data from peri-urban households in Lima, Peru (N = 402), this study analyzes parenting behaviors in the relation between caregivers’ trauma history and child victimization for children aged 4–17. Results indicated caregivers’ trauma history and negative parenting behaviors related to child victimization, and negative parenting behaviors mediated this relation. Positive parenting behaviors did not have significant direct effects and were not mediators of risk transmission. Parenting behaviors did not moderate the relation between caregiver and child victimization, suggesting parenting behaviors may not buffer or exacerbate intergenerational transmission. Post-hoc analyses revealed family type (e.g., single, cohabitating/married) exerted significant direct and moderating effects on child risk, interacting with positive parenting. Families with married/cohabitating caregivers reported overall lower levels of child victimization; however, the relation between positive parenting and victimization was slightly stronger for children in single-parent families. Results highlight potential pathways of the intergenerational cycle of victimization and suggest high-risk families in Peru may benefit from parenting supports, especially pertaining to remediation of negative parenting behaviors.

There is a growing body of evidence highlighting the presence of a single general dimension of psychopathology that can account for multiple associations across mental and substance use disorders. However, relatively little evidence has emerged regarding the validity of this model with respect to a range of factors that have been previously implicated across multiple disorders. The current study utilized a cross-sectional population survey of adolescents (n = 2,003) to examine the extent to which broad psychopathology factors account for specific associations between psychopathology and key validators: poor sleep, self-harm, suicidality, risky sexual behavior, and low self-esteem. Confirmatory factor models, latent class models, and factor mixture models were estimated to identify the best structure of psychopathology. Structural equation models were then estimated to examine the broad and specific associations between each psychopathology indicator and the validators. A confirmatory factor model with three lower-order factors, representing internalizing, externalizing, and psychotic-like experiences, and a single higher-order factor evidenced the best fit. The associations between manifest indicators of psychopathology and validators were largely nonspecific. However, significant and large direct effects were found between several pairwise associations. These findings have implications for the identification of potential targets for intervention and/or tailoring of prevention programs.

Research suggests an increased prevalence of callous-unemotional (CU) traits in children with autism spectrum disorder (ASD), and a similar impairment in fear recognition to that reported in non-ASD populations. However, past work has used measures not specifically designed to measure CU traits and has not examined whether decreased attention to the eyes reported in non-ASD populations is also present in individuals with ASD. The current paper uses a measure specifically designed to measure CU traits to estimate prevalence in a large community-based ASD sample. Parents of 189 adolescents with ASD completed questionnaires assessing CU traits, and emotional and behavioral problems. A subset of participants completed a novel emotion recognition task (n = 46). Accuracy, reaction time, total looking time, and number of fixations to the eyes and mouth were measured. Twenty-two percent of youth with ASD scored above a cut-off expected to identify the top 6% of CU scores. CU traits were associated with longer reaction times to identify fear and fewer fixations to the eyes relative to the mouth during the viewing of fearful faces. No associations were found with accuracy or total looking time. Results suggest the mechanisms that underpin CU traits may be similar between ASD and non-ASD populations.

Differential susceptibility theory (DST) posits that individuals differ in their developmental plasticity: some children are highly responsive to both environmental adversity and support, while others are less affected. According to this theory, “plasticity” genes that confer risk for psychopathology in adverse environments may promote superior functioning in supportive environments. We tested DST using a broad measure of child genetic liability (based on birth parent psychopathology), adoptive home environmental variables (e.g., marital warmth, parenting stress, and internalizing symptoms), and measures of child externalizing problems (n = 337) and social competence (n = 330) in 54-month-old adopted children from the Early Growth and Development Study. This adoption design is useful for examining DST because children are placed at birth or shortly thereafter with nongenetically related adoptive parents, naturally disentangling heritable and postnatal environmental effects. We conducted a series of multivariable regression analyses that included Gene × Environment interaction terms and found little evidence of DST; rather, interactions varied depending on the environmental factor of interest, in both significance and shape. Our mixed findings suggest further investigation of DST is warranted before tailoring screening and intervention recommendations to children based on their genetic liability or “sensitivity.”

Early threat exposure is a transdiagnostic risk factor for psychopathology, and evidence suggests that genetic variation in the oxytocin receptor (OXTR) moderates this association. However, it is unclear if this gene-by-environment (G×E) interaction is tied to unique risk for disorder-specific outcomes or instead increases shared risk for general psychopathology. Moreover, little is known about how this G×E interaction increases risk. The current study utilized a prospective, longitudinal sample of females (n = 2,020) to examine: (a) whether the interaction between early threat exposure and OXTR variation (rs53576, rs2254298) confers risk for disorder-specific outcomes (depression, anxiety, borderline and antisocial personality disorders) and/or general psychopathology in early adulthood; and (b) whether social–emotional deficits (emotion dysregulation, callousness, attachment quality) during adolescence constitute mediating mechanisms. Consistent with hypotheses, the interactive effects of early threat exposure and OXTR variation (rs53576) predicted general psychopathology, with threat-exposed women carrying at least one copy of the rs53576 A-allele at greatest risk. This interaction was mediated via emotional dysregulation in adolescence, with threat-exposed A-allele carriers demonstrating greater emotion dysregulation, and greater emotion dysregulation predicting general psychopathology in early adulthood. Findings suggest that this G×E places women at risk for a broad range of psychopathology via effects on emotion dysregulation.

Childhood adversity appears to sensitize youth to stress, increasing depression risk following stressful life events occurring throughout the lifespan. Some evidence suggests hypothalamic–pituitary–adrenal (HPA) axis-related and serotonergic genetic variation moderates this effect, in a “gene-by-environment-by-environment” interaction (G × E × E). However, prior research has tested single genetic variants, limiting power. The current study uses a multilocus genetic profile score (MGPS) approach to capture polygenic risk relevant to HPA axis and serotonergic functioning. Adolescents (N = 241, Mage = 15.90) completed contextual-threat-based interviews assessing childhood adversity and acute life events, and diagnostic interviews assessing depression. Established MGPSs indexed genetic variation linked to HPA axis (10 single nucleotide polymorphisms [SNPs]) and serotonergic (five SNPs) functioning. Results showed significant MGPS × Childhood Adversity × Recent Life Stress interactions predicting depression for both HPA axis and serotonergic MGPSs, with both risk scores predicting stronger Childhood Adversity × Recent Stress interactions. Serotonergic genetic risk specifically predicted sensitization to major interpersonal stressors. The serotonergic MGPS G × E × E was re-tested in an independent replication sample of early adolescent girls, with comparable results. Findings support the notion that genetic variation linked to these two neurobiological symptoms alters stress sensitization, and that gene-by-environment (G × E) interactions may be qualified by environmental exposures occurring at different points in development.

Maternal depression is associated with instability within the family environment and increases in offspring substance use across adolescence. Rates of delay discounting, or the tendency to select smaller rewards that are immediately available relative to larger, but delayed rewards, are also associated with steeper increases in substance use among youth. Moreover, recent research suggests that early unstable environments may reinforce youths’ propensity towards opportunistic decision making and delay discounting specifically. The current prospective, longitudinal study examined links between maternal depressive symptoms, adolescent delay discounting, and subsequent substance use. Participants included 247 adolescents and their mothers who were assessed annually over a 6-year period (from ages 13 to 19 years). Results supported a small but significant mediation effect. Specifically, maternal depressive symptoms predicted increases in adolescent delay discounting, which, in turn, predicted steeper increases in adolescent substance use over time. Thus, youth decision making may represent a mechanism linking maternal depression and adolescent risk behaviors. Findings indicate the potential for interventions targeting parental psychopathology to prevent subsequent adolescent substance use.

Based on attachment theory and a social-cognitive model of posttraumatic stress disorder (PTSD), this study examined the roles of parent–child communication, perceived parental depression, and intrusive rumination in the association between insecure attachment to parents and PTSD among adolescents following the Jiuzhaigou earthquake. In this study, 620 adolescents were recruited to complete self-report questionnaires. The results showed that the direct association between anxious attachment and PTSD was significant, but that between avoidant attachment and PTSD was non-significant. In addition, both anxious and avoidant attachment had indirect associations with PTSD via the mediating effects of parent–child communication openness and problems, perceived parental depression, and intrusive rumination. However, the specific paths between anxious and avoidant attachment and PTSD were different. The findings indicated that insecure attachment among adolescents following the earthquake was predictive for their PTSD, and the mechanisms underlying the association between anxious attachment and PTSD and the association between avoidant attachment and PTSD were distinct. To alleviate PTSD, more attention should be paid to improving the quality of parent–child communication for adolescents with avoidant attachment to parents, and to reducing negative cognition in adolescents with anxious attachment.

Maltreatment by parents can be conceptualized as pathogenic escalations of a disturbed parent–child relationship that have devastating consequences for children's development and mental health. Although parental psychopathology has been shown to be a risk factor both for maltreatment and insecure attachment representations, these factors` joint contribution to child psychopathology has not been investigated. In a sample of Burundian refugee families living in refugee camps in Western Tanzania, the associations between attachment representations, maltreatment, and psychopathology were examined by conducting structured interviews with 226 children aged 7 to 15 and both their parents. Structural equation modeling revealed that children's insecure attachment representations and maltreatment by mothers fully mediated the relation between maternal and child psychopathology [model fit: comparative fit index (CFI) = 0.96; root mean square error of approximation (RMSEA) = 0.05]. A direct association between paternal and child psychopathology was observed (model fit: CFI = 0.96; RMSEA = 0.05). The findings suggest a vicious cycle, wherein an insecure attachment to a mother suffering from psychopathology may be linked to children's risk to be maltreated, which may reinforce insecure representations and perpetuate the pathogenic relational experience. Interventions targeting the attachment relationship and parental mental health may prevent negative child outcomes.

Affect reactivity to stress may play a role in the development of internalizing symptoms during the college transition, a critical developmental juncture for Latinx adolescents, the largest ethnic minority group on college campuses. This study examined whether affect reactivity during high school is associated with internalizing symptoms in college and explored two potential protective factors, perceived family and peer support. Participants were 209 Latinx adolescents (Mage = 18.10; 64.4% female) who completed standard surveys and four diary assessments per day over 7 days (N > 4,500 momentary observations). First, to measure affect reactivity, we assessed whether perceived stress was associated with negative affect at the momentary level during high school (senior year). Second, we tested whether affect reactivity predicted internalizing symptoms during the first year of college. Third, we tested whether perceived family or peer support buffered the negative consequences of affect reactivity. Results indicated statistically significant within- and between-person associations between stress and negative affect. Moreover, affect reactivity significantly predicted depressive, but not anxiety, symptoms. Buffering was found for family, but not peer, support. Findings extend previous research by detecting associations between momentary affect reactivity and internalizing symptoms during a sociocultural shift in Latinx adolescents’ lives and have implications for culturally appropriate programs to prevent depressive symptoms.

Prior research has shown that sipping of alcohol begins to emerge during childhood and is potentially etiologically significant for later substance use problems. Using a large, community sample of 9- and 10-year-olds (N = 11,872; 53% female), we examined individual differences in precocious alcohol use in the form of alcohol sipping. We focused explicitly on features that are robust and well-demonstrated correlates of, and antecedents to, alcohol excess and related problems later in the lifespan, including youth- and parent-reported externalizing traits (i.e., impulsivity, behavioral inhibition and activation) and psychopathology. Seventeen percent of the sample reported sipping alcohol outside of a religiously sanctioned activity by age 9 or 10. Several aspects of psychopathology and personality emerged as small but reliable correlates of sipping. Nonreligious sipping was related to youth-reported impulsigenic traits, aspects of behavioral activation, prodromal psychotic-like symptoms, and mood disorder diagnoses, as well as parent-reported externalizing disorder diagnoses. Religious sipping was unexpectedly associated with certain aspects of impulsivity. Together, our findings point to the potential importance of impulsivity and other transdiagnostic indicators of psychopathology (e.g., emotion dysregulation, novelty seeking) in the earliest forms of drinking behavior.

Attention-deficit/hyperactivity disorder (ADHD) is associated with self-harm during adolescence and young adulthood, especially among females. Yet little is known about the developmental trajectories or childhood predictors/moderators of self-harm in women with and without childhood histories of ADHD. We characterized lifetime risk for nonsuicidal self-injury (NSSI), suicidal ideation (SI), and suicide attempts (SA), comparing female participants with (n = 140) and without (n = 88) childhood ADHD. We examined theory-informed childhood predictors and moderators of lifetime risk via baseline measures from childhood. First, regarding developmental patterns, most females with positive histories of lifetime self-harm engaged in such behaviors in adolescence yet desisted by adulthood. Females with positive histories of self-harm by late adolescence emanated largely from the ADHD-C group. Second, we found that predictors of NSSI were early externalizing symptoms, overall executive functioning, and father's negative parenting; predictors of SI were adverse childhood experiences and low self-esteem; and predictors of SA were early externalizing symptoms, adverse childhood experiences, and low self-esteem. Third, receiver operating characteristics analyses helped to ascertain interactive sets of predictors. Findings indicate that pathways to self-harm are multifaceted for females with ADHD. Understanding early childhood predictors and moderators of self-harm can inform both risk assessment and intervention strategies.

The links between sexual harassment victimization and aspects of psychopathology are well-established in adolescent research, but whether sexual harassment victimization undermines positive aspects of psychological health and the moderating role of relational support in the link between sexual harassment victimization and psychological ill-health remains unknown. Using a cross-lagged model, we examined (a) the bidirectional and longitudinal links between sexual harassment victimization and adolescent psychological health (emotional problems and well-being) and (b) the moderating role of relational support from parents, teachers, and peers (best friends and classmates) in the link between sexual harassment victimization and adolescent psychological health. We used two waves of self-reported data (separated by 1 year) from 676 Swedish adolescents (50% female; mean age = 13.85 years at the point of first data collection). Controlling for the effects of gender and subjective socioeconomic status, the cross-lagged model revealed that sexual harassment predicted emotional problems positively and well-being negatively. Moreover, well-being predicted sexual harassment negatively. Relational support from classmates moderated the link in the direction from sexual harassment victimization to emotional problems. Relational support did not moderate the link to well-being. The findings provide new and important insights into the role of sexual harassment victimization in adolescent psychological adjustment and potential approaches to intervention.

Endophenotypes are measurable markers of genetic vulnerability to current or future disorder. Autism spectrum disorder (ASD) is well-suited to be examined within an endophenotype framework given past and current emphases on the broader autism phenotype and early detection. We conducted a scoping review to identify potential socially-related endophenotypes of ASD. We focused on paradigms related to sociality (e.g., theory of mind (TOM), social attention), which comprise most of this literature. We integrated findings from traditional behavioral paradigms with brain-based measures (e.g., electroencephalography, functional magnetic resonance imaging). Broadly, infant research regarding social attention and responsivity (Research Domain Criteria (RDoC) domain of affiliation) and attention to faces and voices (social communication) finds consistent abnormality in vulnerable infant siblings. Several additional paradigms that have shown differences in vulnerable infants and young children include animacy perception tasks (perception and understanding of others), measures of recognition and response to familiar faces (attachment), and joint attention and false-belief tasks (understanding mental states). Research areas such as alexithymia (the perception and understanding of self), empathic responding, and vocal prosody may hold interest; however, challenges in measurement across populations and age ranges is a limiting factor. Future work should address sex differences and age dependencies, specificity to ASD, and heterogeneous genetic pathways to disorder within samples individuals with ASD and relatives.

Alcohol and other substance use problems are common, and the efficacy of current prevention and intervention programs is limited. Genetics may contribute to differential effectiveness of psychosocial prevention and intervention programs. This paper reviews gene-by-intervention (G×I) studies of alcohol and other substance use, and implications for integrating genetics into prevention science. Systematic review yielded 17 studies for inclusion. Most studies focused on youth substance prevention, alcohol was the most common outcome, and measures of genotype were heterogeneous. All studies reported at least one significant G×I interaction. We discuss these findings in the context of the history and current state of genetics, and provide recommendations for future G×I research. These include the integration of genome-wide polygenic scores into prevention studies, broad outcome measurement, recruitment of underrepresented populations, testing mediators of G×I effects, and addressing ethical implications. Integrating genetic research into prevention science, and training researchers to work fluidly across these fields, will enhance our ability to determine the best intervention for each individual across development. With growing public interest in obtaining personalized genetic information, we anticipate that the integration of genetics and prevention science will become increasingly important as we move into the era of precision medicine.