Children reared in impoverished environments are at risk for enduring psychological and physical health problems. Mechanisms by which poverty affects development, however, remain unclear. To explore one potential mechanism of poverty's impact on social–emotional and cognitive development, an experimental examination of a rodent model of scarcity-adversity was conducted and compared to results from a longitudinal study of human infants and families followed from birth (N = 1,292) who faced high levels of poverty-related scarcity-adversity. Cross-species results supported the hypothesis that altered caregiving is one pathway by which poverty adversely impacts development. Rodent mothers assigned to the scarcity-adversity condition exhibited decreased sensitive parenting and increased negative parenting relative to mothers assigned to the control condition. Furthermore, scarcity-adversity reared pups exhibited decreased developmental competence as indicated by disrupted nipple attachment, distress vocalization when in physical contact with an anesthetized mother, and reduced preference for maternal odor with corresponding changes in brain activation. Human results indicated that scarcity-adversity was inversely correlated with sensitive parenting and positively correlated with negative parenting, and that parenting fully mediated the association of poverty-related risk with infant indicators of developmental competence. Findings are discussed from the perspective of the usefulness of bidirectional–translational research to inform interventions for at-risk families.

Self-inflicted injury (SII) in adolescence is a serious public health concern that portends prospective vulnerability to internalizing and externalizing psychopathology, borderline personality development, suicide attempts, and suicide. To date, however, our understanding of neurobiological vulnerabilities to SII is limited. Behaviorally, affect dysregulation is common among those who self-injure. This suggests ineffective cortical modulation of emotion, as observed among adults with borderline personality disorder. In borderline samples, structural and functional abnormalities are observed in several frontal regions that subserve emotion regulation (e.g., anterior cingulate, insula, dorsolateral prefrontal cortex). However, no volumetric analyses of cortical brain regions have been conducted among self-injuring adolescents. We used voxel-based morphometry to compare cortical gray matter volumes between self-injuring adolescent girls, ages 13–19 years (n = 20), and controls (n = 20). Whole-brain analyses revealed reduced gray matter volumes among self-injurers in the insular cortex bilaterally, and in the right inferior frontal gyrus, an adjacent neural structure also implicated in emotion and self-regulation. Insular and inferior frontal gyrus gray matter volumes correlated inversely with self-reported emotion dysregulation, over-and-above effects of psychopathology. Findings are consistent with an emotion dysregulation construal of SII, and indicate structural abnormalities in some but not all cortical brain regions implicated in borderline personality disorder among adults.

Drawing on five waves of longitudinal data from 392 families (52% female; mean age of wave 1 [Mage_W1] = 12.89, standard deviation [SD] = .48; Mage_W5 = 21.95, SD = .77; 199 European American and 193 Mexican American families; 217 intact and 175 stepfather families), this study documented transactional relations of mothers’ and fathers’ depressive symptoms with youth's symptomatology from early adolescence to young adulthood. Trait and time-varying cross-lagged models revealed that both mothers’ and fathers’ between- and within-person differences in depressive symptoms were associated with youth's internalizing and externalizing symptoms. Whereas each parent's depressive symptoms uniquely contributed to youth's internalizing symptoms, however, only mothers’ depressive symptoms influenced youth's externalizing symptoms. Although reciprocal effects of youth's internalizing symptoms on parents’ depressive symptoms were not significant, youth's externalizing symptoms predicted changes in mothers’ depressive symptoms over time. Moderation analyses revealed distinct transactional patterns by family ethnicity and child gender, but not by family structure. This study revealed dynamic transactions among family members’ symptomatology that point to opportune times and targets for intervention efforts aimed at mitigating the negative impact of parents’ depressive symptoms on youth's adjustment.

Emotion dysregulation is defined as patterns of emotional experience or expression that interfere with goal-directed activity. This paper considers this functionalist definition from a developmental perspective with the goal of elaborating this approach with respect to its central questions. What are the goals that are impeded by emotionally dysregulated responding, and what alternative goals might motivate emotion dysregulation? What are the developmental processes by which these goals take shape, and what are the influences of the family context, and especially of central relationships in the family, in their emergence? How does this functionalist account address the complex interaction of experience and developing biological processes that also influence emotion regulation and dysregulation? Drawing on research literature concerning children at risk for affective psychopathology and considering relevant examples of the interaction of biology and context, this discussion offers a portrayal of emotion dysregulation as a biologically dynamic, experience-based aspect of adaptation to environments and relationships that, in conditions of risk for the emergence of developmental psychopathology, motivates patterns of emotional responding that serve immediate coping often at the cost of long-term maladaptation. Implications for emotions theory and the study of developmental psychopathology are also considered.

Exposure to maltreatment during childhood (CM) can have deleterious effects throughout the life span of an individual. A parent's history of child maltreatment can also impact his or her own parenting behavior. Theoretically, parents who experienced maltreatment as children may have fewer resources to cope with the challenges of childrearing and may adopt more problematic parenting behaviors. However, empirical studies examining the association between CM and later parenting behavior have yielded mixed results. The aim of this study is to conduct a meta-analysis of studies that have examined the association between exposure to CM and the subsequent parenting outcomes of mothers of 0- to 6-year-old children. A secondary aim is to examine the potential impact of both conceptual and methodological moderators. A total of 32 studies (27 samples, 41 effect sizes, 17,932 participants) were retained for analysis. Results revealed that there is a small but statistically significant association between maternal exposure to CM and parenting behavior (r = –.13, p < .05). Moderator analyses revealed that effect sizes were larger when parenting measures involved relationship-based or negative, potentially abusive behaviors, when samples had a greater number of boys compared to girls, and when studies were older versus more recent. Results are discussed as they relate to the intergenerational transmission of maltreatment and abuse.

Adolescent association with deviant and delinquent friends was examined for its roots in coercive parent–teen interactions and its links to functional difficulties extending beyond delinquent behavior and into adulthood. A community sample of 184 adolescents was followed from age 13 to age 27, with collateral data obtained from close friends, classmates, and parents. Even after accounting for adolescent levels of delinquent and deviant behavior, association with deviant friends was predicted by coercive parent–teen interactions and then linked to declining functioning with peers during adolescence and greater internalizing and externalizing symptoms and poorer overall adjustment in adulthood. Results are interpreted as suggesting that association with deviant friends may disrupt a core developmental task—establishing positive relationships with peers—with implications that extend well beyond deviancy-training effects.

Epigenetic DNA modifications in genes related to the hypothalamic–pituitary–adrenal (HPA) axis are discussed as a mechanism underlying the association between prenatal depression and altered child HPA activity. In a longitudinal study, DNA methylation changes related to prenatal depressive symptoms were investigated in 167 children aged 6 to 9 years. At six candidate genes, 126 cytosine–guanine dinucleotides were considered without correcting for multiple testing due to the exploratory nature of the study. Further associations with the basal child HPA activity were examined. Children exposed to prenatal depressive symptoms exhibited lower bedtime cortisol (p = .003, ηp2 = 0.07) and a steeper diurnal slope (p = .023, ηp2 = 0.06). For total cortisol release, prenatal exposure was related to lower cortisol release in boys, and higher release in girls. Furthermore, prenatal depressive symptoms were associated with altered methylation in the glucocorticoid receptor gene (NR3C1), the mineralocorticoid receptor gene (NR3C2), and the serotonin receptor gene (SLC6A4), with some sex-specific effects (p = .012–.040, ηp2 = 0.03–0.04). In boys, prenatal depressive symptoms predicted bedtime cortisol mediated by NR3C2 methylation, indirect effect = –0.07, 95% confidence interval [–0.16, –0.02]. Results indicate relations of prenatal depressive symptoms to both child basal HPA activity and DNA methylation, partially fitting a mediation model, with exposed boys and girls being affected differently.

The proopiomelanocortin (POMC) molecule has been implicated in models of self-injurious behavior (SIB) in neurodevelopmental disorders, but it has never been specifically sequenced in search of base specific polymorphisms. The empirical focus of this preliminary study was to sequence the POMC gene in 11 children (mean age = 41.8 months, range = 12–60 months; 73% male) with clinical concerns regarding global developmental delay, 5 with reported self-injury. Genomic DNA was extracted from blood samples, and the POMC gene was amplified by specific oligonucleotide primers via polymerase chain reaction. The amplified gene products were sequenced by the University of Minnesota Genomic Center, and the results were analyzed using Sequencher software. A single nucleotide polymorphism (SNP), 1130 C>T, was found in the 3’ untranslated region (UTR) of two samples (one of whom had SIB). The program TargetScanHuman was used to predict the function of this mutation. Variant c.1130 C<T was predicted to be located in the target site of two microRNAs (miRNAs; hsa-mir-3715 and hsa-mir-1909), and the variant allele T may result in an increased minimum free energy for the two miRNAs. Further work with much larger samples is needed to continue the investigation of POMC’s possible function as a risk factor for the development of SIB in children with developmental delay/disability. The findings presented in this study show that the SNP found in the 3’ UTR could alter the binding of miRNAs to POMC 3'UTR, thus, increasing POMC expression and affecting several biological systems with high relevance to the biology of self-injury. There was a significant difference in β-endorphin levels between SIB (M = 169.25 pg/mL) and no SIB (M = 273.5 pg/mL, SD = 15.2) cases (p < .01). Intervention implications are tied to prior observations of individual differences among SIB responders and nonresponders to treatment with the opioid antagonist naltrexone. Stratifying individuals with SIB by POMC mutation status may provide a potential tailoring-like variable to guide the selection of who is more (or less) likely to respond to opiate antagonist treatment. Currently, opioid antagonistic treatment for SIB is empiric (trial and error).

It has long been claimed that “maltreatment begets maltreatment,” that is, a parent's history of maltreatment increases the risk that his or her child will also suffer maltreatment. However, significant methodological concerns have been raised regarding evidence supporting this assertion, with some arguing that the association weakens in samples with higher methodological rigor. In the current study, the intergenerational transmission of maltreatment hypothesis is examined in 142 studies (149 samples; 227,918 dyads) that underwent a methodological quality review, as well as data extraction on a number of potential moderator variables. Results reveal a modest association of intergenerational maltreatment (k = 80; d = 0.45, 95% confidence interval; CI [0.37, 0.54]). Support for the intergenerational transmission of specific maltreatment types was also observed (neglect: k = 13, d = 0.24, 95% CI [0.11, 0.37]; physical abuse: k = 61, d = 0.41, 95% CI [0.33, 0.49]; emotional abuse: k = 18, d = 0.57, 95% CI [0.43, 0.71]; sexual abuse: k = 18, d = 0.39, 95% CI [0.24, 0.55]). Methodological quality only emerged as a significant moderator of the intergenerational transmission of physical abuse, with a weakening of effect sizes as methodological rigor increased. Evidence from this meta-analysis confirms the cycle of maltreatment hypothesis, although effect sizes were modest. Future research should focus on deepening understanding of mechanisms of transmission, as well as identifying protective factors that can effectively break the cycle of maltreatment.

The World Health Organization recently reported that maternal mental health is a major public health concern. As many as one in four women suffer from psychiatric disorders at some point during pregnancy or the first postpartum year. Furthermore, self-injurious thoughts and behaviors (SITBs) represent one of the leading causes of death among women during this time. Thus, efforts to identify women at risk for serious forms of psychopathology and especially for SITBs are of utmost importance. Despite this urgency, current single-diagnostic approaches fail to recognize a significant subset of women who are vulnerable to perinatal stress and distress. The current study was among the first to investigate emotion dysregulation—a multilevel, transdiagnostic risk factor for psychopathology—and its associations with stress, distress, and SITBs in a sample of pregnant women (26–40 weeks gestation) recruited to reflect a range of emotion dysregulation. Both self-reported emotion dysregulation and respiratory sinus arrhythmia, a biomarker of emotion dysregulation, demonstrated expected associations with measures of mental health, including depression, anxiety, borderline personality pathology, and SITBs. In addition, self-reported emotion dysregulation was associated with blunted respiratory sinus arrhythmia responsivity to an ecologically valid infant cry task. Findings add to the literature considering transdiagnostic risk during pregnancy using a multiple-levels-of-analysis approach.

Adolescents’ peer networks provide an important context that can contribute to increases in antisocial behavior. By a process called deviancy training, peers can both model and reinforce these behaviors, thereby conveying group norms about the acceptability of such behaviors. This research examined the relationship between the proportion of adolescents’ peers who exchanged antisocial text messages and externalizing behaviors during high school. In Study 1, parent-, teacher-, and self-reports of rule-breaking and aggression were collected for a sample of adolescents (n = 167, 80 girls; 22.2% Black, 51.5% Caucasian, 18.7% Hispanic) during the summers before and after 9th grade. Total text frequency, frequency of antisocial texts, and the proportion of the peer network who exchanged antisocial messages were examined as predictors of antisocial behavior. The proportion of peers who exchanged antisocial texts significantly predicted rule-breaking, but not aggression. Study 2 examined the direction of the relationship documented in Study 1 more thoroughly. Externalizing behaviors at 9th, 10th, and 11th grade were evaluated as predictors of the proportion of the peer network that exchanged texts about antisocial topics (n = 205, 98 girls; 22.4% Black, 53.7% Caucasian, 16.9% Hispanic). Externalizing behaviors predicted the proportion of adolescents’ peer network that exchanged antisocial texts in each of the subsequent years, but this proportion of the peer network exchanging antisocial communication did not predict subsequent externalizing behaviors. The findings suggest that the extent to which antisocial communication permeates the peer group is a selection effect.

The impact of maltreatment spreads across many developmental domains and extends across the entire life span. Identifying unidirectional or bidirectional drivers of developmental cascades of the effects of maltreatment experiences is critical to efficiently employing interventions to promote resilient development in maltreated children. This 1-year longitudinal study utilized a multiple-levels approach, investigating “bottom-up” and “top-down” cascades using structural equation modeling between cortisol regulation, externalizing behavior, and peer aggression. Neither a bottom-up model driven by cortisol regulation nor a top-down model driven by peer aggression fit the data well. Instead, lower rates of externalizing behavior at Year 1 most strongly predicted improvements at all levels of analysis (reduced cortisol, externalizing behavior, and peer aggression) at Year 2. These results provide initial indication of a mechanism through which interventions for maltreated children may be most effective and result in the most substantial positive changes across developmental domains.

We investigated whether neurobehavioral markers of risk for emotion dysregulation were evident among newborns, as well as whether the identified markers were associated with prenatal exposure to maternal emotion dysregulation. Pregnant women (N = 162) reported on their emotion dysregulation prior to a laboratory assessment. The women were then invited to the laboratory to assess baseline respiratory sinus arrhythmia (RSA) and RSA in response to an infant cry. Newborns were assessed after birth via the NICU Network Neurobehavioral Scale. We identified two newborn neurobehavioral factors—arousal and attention—via exploratory factor analysis. Low arousal was characterized by less irritability, excitability, and motor agitation, while low attention was related to a lower threshold for auditory and visual stimulation, less sustained attention, and poorer visual tracking abilities. Pregnant women who reported higher levels of emotion dysregulation had newborns with low arousal levels and less attention. Larger decreases in maternal RSA in response to cry were also related to lower newborn arousal. We provide the first evidence that a woman's emotion dysregulation while pregnant is associated with risks for dysregulation in her newborn. Implications for intergenerational transmission of emotion dysregulation are discussed.

A recent article in this journal reported a number of gene × environment interactions involving a serotonin transporter–gene network polygenic score and a composite index of prenatal adversity predicting several problem behavior outcomes at 48 months (e.g., anxious/depressed, pervasive developmental problems) and at 60 months (e.g., withdrawal, internalizing problems), yet did not illuminate the nature or form these genetic × environment interactions took. Here we report results of six additional analyses to evaluate whether these interactions reflected diathesis–stress or differential–susceptibility related processes. Analyses of the regions of significance and proportion of interaction index are consistent with the diathesis–stress model, seemingly because of the truncated nature of the adversity score (which did not extend to supportive/positive prenatal experiences/exposures); in contrast, the proportion (of cases) affected index favors the differential–susceptibility model. These results suggest the need for future studies to extend measurement of the prenatal environment to highly supportive experiences and exposures.

Growing evidence suggests that maltreatment is reproduced across generations as victims of maltreatment are at an increased risk for maltreatment perpetration. Unfortunately, little information about mediating pathways exists to provide an explanation for why maltreatment begets maltreatment. We use the number of types of maltreatment experienced to predict later maltreatment perpetration and then examine two developmental pathways that may serve as bridges between maltreatment victimization and perpetration: adolescent problem behaviors and precocious transitions to adulthood. With prospective, longitudinal data from the Rochester Youth Development Study, we assess the relevance of these pathways for the number of maltreatment experiences as well as the number of maltreatment victimization experiences by developmental period (i.e., childhood and adolescence). Our results demonstrate a significant relationship between maltreatment victimization and maltreatment perpetration. Adolescent delinquency and two precocious transitions, dropping out of school and independent living, as well as the accumulation of precocious transitions and problem behaviors, serve as mediators of this intergenerational relationship. Furthermore, the relationship between the number of types of maltreatment and subsequent perpetration is primarily driven by experiences of maltreatment during adolescence. We discuss the implications of these results and set an agenda for the development of programs and policies to interrupt the cycle of maltreatment.

To advance research from Dishion and others on associations between parenting and peer problems across childhood, we used a sample of 177 sibling pairs reared apart since birth (because of adoption of one of the siblings) to examine associations between parental hostility and children's peer problems when children were ages 7 and 9.5 years (n = 329 children). We extended conventional cross-lagged parent–peer models by incorporating child inhibitory control as an additional predictor and examining genetic contributions via birth mother psychopathology. Path models indicated a cross-lagged association from parental hostility to later peer problems. When child inhibitory control was included, birth mother internalizing symptoms were associated with poorer child inhibitory control, which was associated with more parental hostility and peer problems. The cross-lagged paths from parental hostility to peer problems were no longer significant in the full model. Multigroup analyses revealed that the path from birth mother internalizing symptoms to child inhibitory control was significantly higher for birth parent–reared children, indicating the possible contribution of passive gene–environment correlation to this association. Exploratory analyses suggested that each child's unique rearing context contributed to his or her inhibitory control and peer behavior. Implications for the development of evidence-based interventions are discussed.

Childhood maltreatment robustly predicts adolescent externalizing behaviors (EB; e.g., violence, delinquency, substance use) and may crystalize patterns of EB by influencing sensitivity to the social environment (e.g., parenting, friendships). In a nationally representative sample of 9,421 adolescents, we modeled latent growth curves of EB from age 13 to 32 years. Next, we explored whether maltreated youth differed from nonmaltreated youth in their sensitivity to parental closeness, friendship involvement, and polymorphisms from dopamine genes linked to EB (dopamine receptors D2 and D4, dopamine transporter). Overall, maltreated youth had significantly higher levels of EB across adolescence and adulthood; however, maltreated and nonmaltreated youth showed similar patterns of EB change over time: violent behavior decreased in adolescence before stabilizing in adulthood, whereas nonviolent delinquency and substance use increased in adolescence before decreasing in the transition to adulthood. Maltreatment reduced sensitivity to parental closeness and friendship involvement, although patterns varied based on type of EB outcome. Finally, none of the environmental effects on EB were significantly moderated by the dopamine polygenic risk score after accounting for multiple testing. These findings underline the enduring effects of early maltreatment and implicate that maltreatment may contribute to long-term risk for EB by influencing children's sensitivity to social relationship factors in adolescence.