Recent research suggests that psychosocial resources and life stressors are mediating pathways explaining socioeconomic variation in young adults' health risks. However, less research has examined both these pathways simultaneously and their genetic moderation. A nationally representative sample of 11,030 respondents with prospective data collected over 13 years from the National Study of Adolescent to Adult Health was examined. First, the association between early cumulative socioeconomic adversity and young adults' (ages 25–34) cardiometabolic disease risk, as measured by 10 biomarkers, through psychosocial resources (educational attainment) and life stressors (accelerated transition to adulthood) was examined. Second, moderation of these pathways by the serotonin transporter linked polymorphic region gene (5-HTTLPR) was examined. There was evidence for the association between early socioeconomic adversity and young adults' cardiometabolic disease risk directly and indirectly through educational attainment and accelerated transitions. These direct and mediating pathways were amplified by the 5-HTTLPR polymorphism. These findings elucidate how early adversity can have an enduring influence on young adults' cardiometabolic disease risk directly and indirectly through psychosocial resources and life stressors and their genetic moderation. This information suggests that effective intervention and prevention programs should focus on early adversity, youth educational attainment, and their transition to young adulthood.

Social anhedonia is well established as a transdiagnostic factor, but little is known about its development. This study examined whether temperament and parenting in early childhood predict social anhedonia in early adolescence. We also explored whether the relationships between early predictors and social anhedonia are moderated by a child's sex. A community sample of children participated in laboratory observations of temperament and parenting practices at age 3 (n = 275). The participants returned at age 12 and completed the Anticipatory and Consummatory Interpersonal Pleasure Scale–Child Version (ACIPS-C). Our results indicated that, at age 3, lower observed sociability predicted higher levels of social anhedonia at age 12. These associations were moderated by child sex, such that males with diminished sociability reported greater social anhedonia. These findings indicate that predictors of early adolescent social anhedonia are evident as early as 3 years of age. However, these effects were evident only for males, suggesting that the pathways to social anhedonia in early adolescence differ as a function of sex.

Most research has studied self-regulation by presenting experimenter-controlled test stimuli and measuring change between baseline and stimulus. In the real world, however, stressors do not flash on and off in a predetermined sequence, and there is no experimenter controlling things. Rather, the real world is continuous and stressful events can occur through self-sustaining interactive chain reactions. Self-regulation is an active process through which we adaptively select which aspects of the social environment we attend to from one moment to the next. Here, we describe this dynamic interactive process by contrasting two mechanisms that underpin it: the “yin” and “yang” of self-regulation. The first mechanism is allostasis, the dynamical principle underlying self-regulation, through which we compensate for change to maintain homeostasis. This involves upregulating in some situations and downregulating in others. The second mechanism is metastasis, the dynamical principle underling dysregulation. Through metastasis, small initial perturbations can become progressively amplified over time. We contrast these processes at the individual level (i.e., examining moment-to-moment change in one child, considered independently) and also at the inter-personal level (i.e., examining change across a dyad, such as a parent–child dyad). Finally, we discuss practical implications of this approach in improving the self-regulation of emotion and cognition, in typical development and psychopathology.

Maladaptive offspring emotion regulation has been identified as one pathway linking maternal and child psychological well-being in school-aged children. Whether such a pathway is present earlier in life still remains unclear. The present study investigated the role of preschoolers’ emotion reactivity and regulation in the association between maternal psychological distress and child internalizing and externalizing problems. Children’s emotion reactivity and regulation were assessed through both observed behavior and physiology. At 42 months of age, children (n = 251; 128 girls) completed a fear induction task during which their heart-rate variability was assessed and their behavior was monitored, and maternal self-reports on depressive mood and anxiety were collected. At 48 months mothers and fathers reported on their children’s internalizing and externalizing problems. Higher maternal depressive mood was associated with lower child fear-related reactivity and regulation, as indexed by heart-rate variability. The latter mediated the association between higher maternal depressive mood and higher preschoolers’ externalizing problems. Overall, our findings support the role of preschoolers’ emotion reactivity and regulation in the relationship between maternal psychological distress and children’s socio-emotional difficulties. This role may also depend on the discrete emotion to which children react or seek to regulate as, here, we only assessed fear-related reactivity and regulation.

The present study examined the developmental value of parsing different forms of children's risky involvement in interparental conflict as predictors of children's subsequent psychological adjustment. Participants included a diverse sample of 243 preschool children (Mage = 4.6 years) and their mothers across two measurement occasions spaced 2 years apart. Three forms of risky involvement (i.e., cautious, caregiving, and coercive) were identified using maternal narratives describing children's emotional and behavioral reactivity during and immediately following interparental conflict. Utilizing a multimethod, multi-informant design, findings revealed that each form of involvement prospectively predicted unique configurations of children's developmental outcomes. Greater coercive involvement was associated with higher levels of externalizing problems, callous and unemotional traits, and extraversion. Higher levels of caregiving involvement were linked with greater separation anxiety. Finally, cautious involvement predicted more separation anxiety and social withdrawal.

As a founder of the field of applied developmental psychology, Dr Edward Zigler promoted public policy that translated scientific knowledge into real-world programs to improve the outcomes of high-risk children and families. Many researchers, practitioners, and public policy proponents have sought to carry on his legacy through integration of empirical research, evidence-based prevention and intervention, and advocacy to address a range of challenges facing families with young children. To advance the field of child maltreatment, a multidisciplinary team of investigators from the Universities of Rochester and Minnesota partnered with the Eunice Kennedy Shriver National Institute of Child Health and Human Development to create the Translational Research that Adapts New Science FOR Maltreatment Prevention Center (Transform). Building on state-of-the-art research methodologies and clinical practices, Transform leverages theoretically grounded research and evidence-based interventions to optimize outcomes for individuals across the life span who have experienced, or may be at risk for, maltreatment. Inspired by the work of Dr Zigler, Transform is committed to bridging science and real-world practice. Therefore, in addition to creating new science, Transform's Community Engagement Core provides translational science to a broad audience of investigators, child-serving professionals, and parental and governmental stakeholders. This article describes Transform's purpose, theoretical framework, current activities, and future directions.

Broken bones, cigarette burns, and profound malnourishment are unambiguous signs of child maltreatment, but defining the causes and consequences of psychological maltreatment is a more challenging task. For child advocates who are concerned with optimizing the developmental potential of each youngster, defining psychological maltreatment is an essential first step, and McGee and Wolfe (1991) should be commended for undertaking such a challenging but necessary task.

The purpose of this report is to provide evidence of an association between within-person variability in diurnal testosterone over 1 year, lifetime exposure to violence, and the manifestation of antisocial behavior in 135 pubertal-aged adolescents across 1 year. Adolescents' sex and lifetime history of violence exposure moderated the association between within-person variability in diurnal testosterone and antisocial behavior. Furthermore, sex-stratified analyses revealed that lifetime history of exposure to violence moderated the association between within-person variability in diurnal testosterone and antisocial behavior in females only. This report is unique in that it illuminates sex differences in within-person associations among exposure to violence, individual variability in diurnal testosterone, and antisocial behavior.

Many studies demonstrate that marriage protects against risky alcohol use and moderates genetic influences on alcohol outcomes; however, previous work has not considered these effects from a developmental perspective or in high-risk individuals. These represent important gaps, as it cannot be assumed that marriage has uniform effects across development or in high-risk samples. We took a longitudinal developmental approach to examine whether marital status was associated with heavy episodic drinking (HED), and whether marital status moderated polygenic influences on HED. Our sample included 937 individuals (53.25% female) from the Collaborative Study on the Genetics of Alcoholism who reported their HED and marital status biennially between the ages of 21 and 25. Polygenic risk scores (PRS) were derived from a genome-wide association study of alcohol consumption. Marital status was not associated with HED; however, we observed pathogenic gene-by-environment effects that changed across young adulthood. Among those who married young (age 21), individuals with higher PRS reported more HED; however, these effects decayed over time. The same pattern was found in supplementary analyses using parental history of alcohol use disorder as the index of genetic liability. Our findings indicate that early marriage may exacerbate risk for those with higher polygenic load.

A variety of childhood experiences can lead to anxious/depressed (A/D) symptoms. The aim of the present study was to explore the brain morphological (cortical thickness and surface area) correlates of A/D symptoms and the extent to which these phenotypes vary depending on the quality of the parenting context in which children develop. Structural magnetic resonance imaging (MRI) scans were acquired on 45 children with Child Protective Services (CPS) involvement due to risk of not receiving adequate care (high-risk group) and 25 children without CPS involvement (low-risk group) (rangeage = 8.08–12.14; Mage = 10.05) to assess cortical thickness (CT) and cortical surface area (SA). A/D symptoms were measured using the Child Behavioral Checklist. The association between A/D symptoms and CT, but not SA, differed by risk status such that high-risk children showed decreasing CT as A/D scores increased, whereas low-risk children showed increasing CT as A/D scores increased. This interaction was specific to CT in prefrontal, frontal, temporal, and parietal cortical regions. The groups had marginally different A/D scores, in the direction of higher risk being associated with lower A/D scores. Results suggest that CT correlates of A/D symptoms are differentially shaped by the quality of early caregiving experiences and should be distinguished between high- and low-risk children.

To date, a deficit-oriented approach dominates autism spectrum disorder (ASD) research, including studies of infant siblings of children with ASD at high risk (HR) for the disabilities associated with this disorder. Despite scientific advances regarding early ASD-related risk, there remains little systematic investigation of positive development, limiting the scope of research and quite possibly a deeper understanding of pathways toward and away from ASD-related impairments. In this paper, we argue that integrating a resilience framework into early ASD research has the potential to enhance knowledge on prodromal course, phenotypic heterogeneity, and developmental processes of risk and adaptation. We delineate a developmental systems resilience framework with particular reference to HR infants. To illustrate the utility of a resilience perspective, we consider the “female protective effect” and other evidence of adaptation in the face of ASD-related risk. We suggest that a resilience framework invites focal questions about the nature, timing, levels, interactions, and mechanisms by which positive adaptation occurs in relation to risk and developmental pathways toward and away from ASD-related difficulties. We conclude with recommendations for future research, including more focus on adaptive development and multisystem processes, pathways away from disorder, and reconsideration of extant evidence within an integrated risk-and-resilience framework.

Social disability in youth is an important precursor of long-term social and mental health problems. Social inclusion is a key policy driver and fits well within a new paradigm of health and well-being rather than illness-oriented services, yet little is known about social inclusion and its facilitators for “healthy” young people. We present a novel exploratory structural analysis of social inclusion using measures from 387 14- to 36-year-olds. Our model represents social inclusion as comprising social activity and community belonging, with both domains predicted by hopeful and dysfunctional self-beliefs but hopefulness more uniquely predicting social inclusion in adolescence. We conclude that social inclusion can be modeled for meaningful comparison across spectra of development, mental health, and functioning.

Parenting practices and relationships with peers are crucial aspects of youth socialization. Although theoretically expected reciprocal associations between changes in maladaptive parenting and adolescent peer victimization exist, there is a lack of studies that examine this link and address the mediating mechanisms at the within-person level. This longitudinal study examined reciprocal relations between peer victimization and two types of maladaptive parenting including harsh punishment and psychological control, and the potential mediating roles of internalizing and externalizing problems within these relations, by disentangling between- and within-person effects. A total of 4,731 Chinese early adolescents (44.9% girls; Mage = 10.91 years, SD = 0.72) participated in a four-wave longitudinal study with 6-month intervals. The results of random intercept cross-lagged panel modeling showed: (a) harsh punishment did not directly predict peer victimization, and vice versa; (b) psychological control directly predicted peer victimization, and vice versa; (c) psychological control indirectly predicted peer victimization via internalizing problems, and peer victimization also indirectly predicted psychological control via internalizing problems. These findings provide evidence of a bidirectional spillover effect between psychological control and peer victimization at the within-person level, suggesting Chinese early adolescents may become caught in a vicious cycle directly or indirectly via their internalizing problems.

The aim of this project was to evaluate the relationship of matrix metalloproteinase-9 (MMP-9) genetic variation and its serum concentration with autism spectrum disorder (ASD). One hundred ASD and 120 controls were enrolled in this study. Genomic DNA was extracted from blood and MMP-9 polymorphism was determined by polymerase chain reaction restriction fragment length polymorphism and serum levels were measured by enzyme-linked immunosorbent assay. The frequencies of CC, CT, and TT genotypes were 72%, 26%, and 2% in controls and 31%, 57%, and 12% in ASD, respectively. The frequencies of C and T alleles in ASD were 59.5% and 40.5%, and controls were 86% and 14%, respectively. There is a significant increase in serum MMP-9 levels in ASD as compared to controls. We have also shown that TT genotype is significantly associated with increase serum MMP-9 levels in patients (TT, CT, and CC serum levels were 91.77 ± 10.53, 70.66 ± 7.21, and 38.66 ± 5.52 and in controls were 55.55 ± 11.39, 42.66 ± 7.85, and 30.55 ± 6.34 ng/ml, respectively). It is concluded that there is a significant association between rs3918242 MMP-9 polymorphism and its serum concentration with autism. We also suggest that TT genotype is associated with increased MMP9 expression and may be a risk factor for ASD.

Children with autism spectrum disorders (ASDs), attention deficit hyperactivity disorder (ADHD) and disinhibited and reactive attachment disorders (RAD/DAD) often experience socioemotional problems. Elucidating a clear picture of these profiles is essential. Strengths and Difficulties Questionnaires (SDQs) were analysed from cohort of children with ASD (n = 1430), ADHD (n = 1193), and RAD/DAD (n = 39). Kruskal–Wallis Tests and network analytic techniques were used to investigate symptom profiles. Children with ASD experienced more emotional problems, peer problems and fewer prosocial behaviours. Children with ADHD and RAD/DAD had higher levels of hyperactivity and conduct problems. Overall, ASD and ADHD networks were highly correlated (rs = 0.82), and we did not observe a statistically significant difference in terms of global Strength.

A quarter of the global population meets diagnostic criteria for metabolic syndrome (MetS). MetS prevalence stratifies by socioeconomic status (SES), such that low SES is associated with higher MetS risk starting in childhood. Despite this trend, some low-SES children maintain good metabolic health across the life span, but the factors responsible for their resilience are not well understood. This study examined the role of threat vigilance as either a moderator or a mediator of the effects of low early life SES on adult metabolic risk. Three hundred twenty-five Canadians aged 15–55 participated (M = 36.4 years, SD = 10.7; 55.4% female). We coded parental occupational status between the ages of 0 and 5 to index early life SES. We used the International Diabetes Federation case definition for MetS based on waist circumference, blood pressure, triglyceride levels, HDL cholesterol, and glycosylated hemoglobin measures. Threat vigilance was assessed using the Weapons Identification Procedure, a visual discrimination paradigm that captures implicit perceptions of threat. Analyses supported the moderator hypothesis: low early life SES was associated with MetS diagnosis exclusively among those with high levels of threat vigilance. This suggests that low early life SES environments that heighten vigilance to threat might be particularly detrimental for metabolic health. Conversely, low threat vigilance may buffer against the metabolic risks associated with socioeconomic disadvantage.

Although there is increasing attention for the interrelationship between obsessive–compulsive personality disorder (OCPD) and obsessive–compulsive disorder (OCD), their shared characteristics in terms of childhood trait antecedents remain understudied. Perfectionism may be a viable candidate trait antecedent, given its role in the clinical manifestation of both OCPD and OCD in adulthood, and the evidence that perfectionism reflects a dispositional tendency observable from childhood onwards. However, little is known about childhood trajectories of perfectionism with prospective links to later OCPD versus OCD. Using latent growth curve modeling, this study explored the baseline and growth of childhood perfectionism in 485 community and referred children (55.5% girls, 7.17–14.78 years old, Mage = 10.74, SD = 1.50) across three waves. Adolescent OCPD traits and OCD symptoms were measured in Wave 4. An overall decreasing trend of perfectionism from childhood through adolescence appeared, without inter-individual differences in growth. Individual differences in baseline levels of childhood perfectionism were significant, and equally predicting adolescent OCPD and OCD outcomes. At a more specific level, childhood perfectionism predicted most strongly the rigid perfectionism component of OCPD, and the orderliness/cleanliness/perfectionism and obsession domain of OCD. This demonstrates the value of childhood perfectionism for understanding differential outcomes of adolescent OCPD traits and OCD symptoms.

Maternal substance use has often been associated with insecure and disorganized child attachment. We evaluated this association with a meta-analysis of young children and, further, systematically reviewed mediating and moderating factors between maternal substance use and child attachment. We performed a systematic database search of quantitative English language studies on child attachment that included substance-using mothers and their children below 6 years of age. Eleven studies (N = 1,841) met the inclusion criteria and were included in the meta-analysis of attachment security and seven (N = 1,589) studies were included in the meta-analysis of attachment disorganization. We found that maternal substance use was negatively associated with secure attachment in children, but the effect size was small (r = −.10). The association with disorganized attachment was not significant (r = .15). Related to moderating and mediating factors (k = 6), we found evidence on the role of teratogenic and sociological factors on child attachment. Most importantly, the impact of cumulative risks was vital. However, literature was scarce, and studies varied in risk of bias, leaving many unanswered questions on other potential factors underlying the development of attachment in these high-risk children. We discuss the results considering clinical implications and future directions.

This study considers the developmental origins of alcohol use in young adulthood. Despite substantial evidence linking committed romantic relationships to less problematic alcohol use in adulthood, the uniformity of these protective benefits across different romantic relationships is unclear. Further, the extent to which the establishment and maintenance of these romantic relationships is preceded by earlier adolescence alcohol use remains unknown. To address these gaps in the literature, the current study utilized multitiple-dimensional, multiple-informant data spanning 20 years on 585 individuals in the Child Development Project. Findings from both variable- and person-centered analyses support a progression of associations predicting adolescent alcohol use (ages 15–16), drinking, and romantic relationships in early adulthood (ages 18–25), and then problematic young adult alcohol use (age 27). Although adolescent alcohol use predicted greater romantic involvement and turnover in early adulthood, romantic involvement, but not turnover, appeared to reduce the likelihood of later problematic drinking. These findings remained robust even after accounting for a wide array of selection and socialization factors. Moreover, characteristics of the individuals (e.g., gender) and of their romantic relationships (e.g., partner substance use problems and romantic relationship satisfaction) did not moderate these findings. Findings underscore the importance of using a developmental–relational perspective to consider the antecedents and consequences of alcohol use early in the life span.