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Kagan theorized biologically based temperament types that are present in infancy, stable across development, and essential for understanding individual differences. Despite evidence, temperament research remains focused on a few prominent dimensions of temperament, without adequately addressing covariance among dimensions and temperament types. Using longitudinal twin data, we took a person-centered statistical approach to identify temperament types and examined continuity and change across five developmental periods (Ninfancy = 602; Ntoddlerhood = 522; Nearly childhood = 390; Nlate childhood = 718; Nearly adolescence = 700). We then examined the genetic and environmental etiology of temperament types. Twins were boys and girls (51-53% female), primarily Hispanic/Latinx (23-30%) and non-Hispanic/Latinx White (56-63%), and from socioeconomically diverse families (28-38% near-or-below the poverty line). Using latent profile analysis, we identified three temperament types at each age characterized by negative reactivity and dysregulation, positive reactivity and strong self-regulation, and moderate reactivity and regulation. Latent transition analyses revealed considerable continuity in membership type for "negative dysregulated" beginning in infancy, log odds = 1.58 (SE = .65) to 3.16 (SE = .77), p < .01, of remaining relative to transitioning to "typical expressive", and "positive well-regulated" beginning in early childhood, log odds = 1.41 (SE = .56) to 2.25 (SE = .47), p < .05. Twin analyses revealed moderate heritability and a consistent role of the shared environment on positive well-regulated, with negative dysregulated and typical expressive also moderately heritable with the shared environment being important at some ages. Findings support the presence of theorized biologically based temperament types that develop rapidly in infancy and toddlerhood and provide a foundation for the study of individual differences and risk and resilience processes across the lifespan. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

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Premature infants may be at risk for lower effortful control, and subsequent lower academic achievement, peer competence, and emotional and physical wellness throughout the lifespan. However, because prematurity is related to obstetrical and neonatal complications, it is unclear what may drive the effect. Effortful control also has a strong heritable component; therefore, environmental factors during pregnancy and the neonatal period may interact with genetic factors to predict effortful control development. In this study, we aimed to dissect the influences of genetics, prematurity, and neonatal and obstetrical complications on the development of effortful control from 12 months to 10 years using a twin cohort. This study used data from the Arizona Twin Project, an ongoing longitudinal study of approximately 350 pairs of twins. Twins were primarily Hispanic/Latinx (23.8%-27.1%) and non-Hispanic/Latinx White (53.2%-57.8%), and families ranged in socioeconomic status with around one third falling below or near the poverty line. Of the twins, 62.6% were born prematurely. Effortful control was assessed via parent report at six waves. There was not a significant relationship between gestational age and effortful control regardless of whether obstetrical and neonatal complications were controlled for. Biometric twin modeling revealed that the attentional focusing subdomain of effortful control was highly heritable. Gestational age did not moderate genetic and environmental estimates. Our findings help inform the risk assessment of prematurity and provide evidence for the differing etiology of each subdomain of effortful control and the strong role of genetics in effortful control development. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

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STUDY OBJECTIVES: Growing evidence suggests concordance between parent and youth sleep. However, no known study has simultaneously examined concordance among siblings' sleep patterns. This study investigated daily and average concordance in (1) parent-youth and (2) sibling actigraphy-measured sleep, as well as the degree to which sibling concordance varied by sleeping arrangements. METHODS: 516 twin siblings (Mage = 10.74, 51% female; 30% monozygotic (MZ) twin pairs, 37% same-sex dizygotic pairs (DZ-ss), 33% opposite-sex DZ pairs (DZ-os)) and their primary caregivers (Mage = 40.59, 95% female) wore wrist-based accelerometers for 7 consecutive nights to measure sleep duration, efficiency, midpoint time, and latency. Primary caregivers also reported on demographics, youth pubertal status, and room-sharing. Two-level multilevel models were estimated to examine daily and average concordance in parent-youth and sibling sleep. RESULTS: Daily concordance was observed between parent and youth sleep duration and midpoint; average concordance was found for sleep duration, midpoint, and latency. Within sibling dyads, daily and average concordance was evident across all sleep parameters (duration, efficiency, midpoint, latency), with generally stronger concordance patterns for MZ than DZ twin pairs, and for twins who shared a room with their co-twin. CONCLUSIONS: This is the first known study to document concordance among parent-youth and siblings' actigraphy-measured sleep within the same study (i.e., triad). Our findings can help inform the development of family-level interventions targeting daily and overall sleep hygiene.

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There is a need to understand the components of self-regulation, given its link to nearly every domain of functioning across the life span. This study examined the etiological underpinnings of covariance between measures of executive functioning (EF) and effortful control (EC) in middle childhood. The extent that genetic and environmental factors explain the association between EF and EC is unknown. Families were drawn from a longitudinal twin study (N = 894 twins; Mage = 8.87 years, SD = 1.10; 51.4% female; 46.8% non-Hispanic White, 28% Latino/a/x) and twins completed EF tasks during a home visit (Flanker Task, Continuous Performance Task, and Digit Span Backward) and primary caregivers (93.8% mothers) reported on their twins' EC (Attentional Focusing and Inhibitory Control). Univariate twin models showed additive genetic and nonshared environmental influences on the Flanker Task, Continuous Performance Task, Digit Span Backward, and parent-reported Inhibitory Control, and dominant genetic influences were implicated in parent-reported Attentional Focusing. Bivariate twin models revealed that additive genetic influences explained the small covariance between EF and EC. Executive attention could explain the genetic covariance between measures of EF and EC. This study suggests that EF and EC tap into the same underlying self-regulation construct, with weak correlations between constructs being attributed to measurement, rather than conceptual, differences. Elucidating the overlap between EF and EC can bring researchers closer to understanding how best to foster adaptive self-regulation. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

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OBJECTIVE: This study (1) examined pubertal development in relation to actigraphy-assessed sleep in twin children, and tested whether associations differed by child race and gender, (2) modeled genetic and environmental influences on pubertal development and sleep indicators, and (3) examined genetic and environmental influences on the covariation of puberty and sleep. DESIGN: The classic twin design was used to examine genetic and environmental contributions to puberty and sleep and their associations. SETTING: Data were collected from community-dwelling urban and rural families of twins in the southwestern U.S. PARTICIPANTS: The racially and socioeconomically diverse sample included 596 twin children (Mage = 8.41, SD = 0.69; 51.7% female; 66.3% white; 33.7% Hispanic; 170 monozygotic, 236 same-sex dizygotic, 188 opposite-sex dizygotic). MEASUREMENTS: Pubertal development was assessed via parent report. Children wore actigraph watches for 7 nights (M = 6.81, SD = 0.67) to capture sleep duration, efficiency, midpoint, onset latency, and duration variability. RESULTS: In contrast to extant literature with older youth, more advanced pubertal development was associated with longer sleep durations in Hispanic and white girls and higher sleep efficiency in white girls, though Hispanic girls demonstrated later sleep midpoints. Pubertal development was moderately heritable and there was a genetic influence on the covariance between puberty and sleep indicators. CONCLUSIONS: This was the first study to examine the genetic and environmental influences on the covariation between puberty and sleep, and found genetic underpinnings between pubertal development and actigraphy-assessed sleep duration and efficiency, though sleep and puberty were almost entirely independent in twins at this age.

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Relative to other motivations of social withdrawal (i.e., shyness, unsociability), social avoidance is understudied. Furthermore, the relation between social avoidance and externalizing problems seldom has been investigated despite reasons to expect an association. We examined the association between social avoidance and externalizing problems using a sample of early adolescents in the United States using parents' reports (N = 294; 54.1% boys; M age = 12.43 years). Supporting our hypotheses, structural equation models indicated that social avoidance positively predicted concurrent externalizing problems, controlling for shyness, unsociability, and internalizing problems (including depression and anxiety). Findings highlight that socially avoidant adolescents' behaviors may include avoiding others as well as acting out. Longitudinal work is needed to examine the potential bidirectional relations between social avoidance and externalizing problems.

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Aggressive behavior in middle childhood can contribute to peer rejection, subsequently increasing risk for substance use in adolescence. However, the quality of peer relationships a child experiences can be associated with his or her genetic predisposition, a genotype-environment correlation (rGE). In addition, recent evidence indicates that psychosocial preventive interventions can buffer genetic predispositions for negative behavior. The current study examined associations between polygenic risk for aggression, aggressive behavior, and peer rejection from 8.5 to 10.5 years, and the subsequent influence of peer rejection on marijuana use in adolescence (n = 515; 256 control, 259 intervention). Associations were examined separately in control and intervention groups for children of families who participated in a randomized controlled trial of the family-based preventive intervention, the Family Check-Up . Using time-varying effect modeling (TVEM), polygenic risk for aggression was associated with peer rejection from approximately age 8.50 to 9.50 in the control group but no associations were present in the intervention group. Subsequent analyses showed peer rejection mediated the association between polygenic risk for aggression and adolescent marijuana use in the control group. The role of rGEs in middle childhood peer processes and implications for preventive intervention programs for adolescent substance use are discussed.

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Inhibitory control skills are important for academic outcomes across childhood, but it is unknown whether inhibitory control is implicated in the association between genetic variation and academic performance. This study examined the relationship between a GWAS-based (EduYears) polygenic score indexing educational attainment (EA PGS) and inhibitory control in early (Mage  = 3.80 years) and middle childhood (Mage  = 9.18 years), and whether inhibitory control in early childhood mediated the relation between EA PGS and academic skills. The sample comprised 731 low-income and racially/ethnically diverse children and their families from the longitudinal early steps multisite study. EA PGS predicted middle childhood inhibitory control (estimate = 0.09, SE = 0.05, p < 0.05) and academic skills (estimate = 0.18, SE = 0.05, p < 0.01) but did not predict early childhood inhibitory control (estimate = 0.08, SE = 0.05, p = 0.11); thus, mediation was not tested. Sensitivity analyses showed that effect sizes were similar across European and African American groups. This study suggests that inhibitory control could serve as a potential mechanism linking genetic differences to educational outcomes.

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The goals of this study were to examine the longitudinal relations between school readiness and reading and math achievement and to test if these relations were moderated by temperament. The sample included socio-economically and ethnically diverse twins (N=551). Parents reported on school readiness when children were five years old. Teachers reported on temperament (effortful control, anger, and shyness) three years later. Standardized measures of reading and math were obtained when children were eight years old. Effortful control and shyness moderated the effect of school readiness on reading. Prediction of reading from school readiness was strongest when students were high in effortful control and low in shyness. Effortful control and shyness predicted math beyond school readiness. There were no relations involving anger. Findings demonstrate that temperament can potentiate the relations between school readiness and reading and highlight the importance of promoting school readiness and effortful control, while decreasing shyness.

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The present study tested models of polygenic by environment interaction between early childhood family instability and polygenic risk for aggression predicting developmental trajectories of aggression from middle childhood to adolescence. With a longitudinal sample of 515 racially and ethnically diverse children from low-income families, primary caregivers reported on multiple components of family instability annually from child ages 2-5 years. A conservative polygenic risk score (p = 0.05) was generated based on a prior meta-genome wide association study. Trajectories of aggression were identified using a curve of factors model based on a composite of primary caregiver, alternate caregiver, and teacher reports at five ages from 7.5 to 14 years. The family instability by polygenic interaction predicted growth in children's aggression such that children with lower levels of family instability and lower polygenic risk exhibited a steeper decline in aggression from 7.5 to 14. Findings support the need to model gene-environment interplay to elucidate the role of genetics in the development of aggressive behaviors.

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BACKGROUND: Prior research has established links between poor sleep and problems in emotion regulation. Impulsivity and anger/frustration are core features of child psychopathology. Further, sleep problems are commonly associated with psychopathology. This study examined shared and unique genetic and environmental influences on sleep, impulsivity, and anger/frustration in the middle childhood period with potential ramifications for psychopathology. METHODS: Families (29.9% monozygotic, 38.6% same-sex dizygotic, 31.5% opposite-sex dizygotic) from a longitudinal twin study participated (N = 613 twins). Twins (Mage  = 8.37, SD = 0.66; 49% female; 58% non-Latinx European American, 30% Latinx) wore actigraph watches for seven days to assess sleep. Primary caregivers (95.3% mothers) completed standardized questionnaires to assess twins' temperament (impulsivity, anger/frustration). RESULTS: Univariate ACE twin structural equation models indicated strong genetic influences (76%) on impulsivity, whereas the largest proportion of variance in anger/frustration was attributed to the shared environment (56%). Bivariate model fitting indicated that sleep-impulsivity and sleep-anger/frustration associations in children are genetic; thus, a mutual underlying genetic factor likely contributes to the commonality in these associations. CONCLUSIONS: Given evidence that sleep problems, impulsivity, and anger/frustration are mechanisms associated with psychopathology, our findings suggest a genetic commonality and the need to focus on shared and unique risk factors when understanding etiology. Early intervention and prevention efforts should target both sleep problems and high levels of impulsivity and anger/frustration in children, which may have implications for later psychopathology.

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Electronic-media use is associated with sleep disruptions in childhood and adolescence, although research relies primarily on subjective sleep. Effortful control, a dimension of self-regulation, may mitigate this association by helping children disengage from and regulate responses to media. We examined associations between media use and multiple actigraph-measured sleep parameters at mean and day levels and tested children's effortful control as a moderator of mean-level relations. We collected actigraph data and parents' diary reports of children's prebedtime television, video-game, laptop, desktop, cell-phone, and tablet use in 547 twin children (7-9 years old; 51.74% female). Mean-level media use was associated with bedtime and sleep duration. For the proportion of nights on which twins used media, but not the average number of media types, effortful control attenuated associations between media use and reduced sleep duration and efficiency. Day-level media use was related only to bedtime. Findings replicate and extend existing research and highlight self-regulation as a potential protective factor.

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The Arizona Twin Project is an ongoing longitudinal study designed to elucidate gene-environment interplay underlying the development of risk and resilience to common mental and physical health problems during infancy, childhood and adolescence. Specificity of risk is carefully examined across mental and physical health and how these influences vary across socioeconomic and sociocultural environments. Participants are a sample of approximately 700 twins (31% Latinx) recruited from birth records in the state of Arizona, USA. Twins are 32% monozygotic twins, 36% same-sex dizygotic (DZ), 32% opposite-sex DZ, currently 10-11 years of age. Primary caregivers were interviewed on twins' development and early physical and social environments when twins were 1, 2 and 5 years of age. In-depth objective measurement commenced in middle childhood, with in-person assessments at 8-11 years of age, with plans to continue to follow the sample across adolescence. Middle childhood measures focus on children's physical and mental health, including diurnal cortisol, actigraphy-based measures of sleep and activity, cold pressor task assessing acute pain, and reaction time tasks assessing executive functioning. Preliminary findings illustrate that objective assessments of children's health are highly heritable, but they do not always share genetic etiology with more commonly used subjective assessments. Exposure to early adversity moderates genetic influences on both executive functioning and health, with higher heritability typically seen under adverse conditions. Future directions include an examination of how pubertal stage affects genetic and environmental influences on diurnal cortisol, sleep, chronic pain, and mental health.

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Previous approaches for creating polygenic risk scores (PRSs) do not explicitly consider the biological or developmental relevance of the genetic variants selected for inclusion. We applied gene set enrichment analysis to meta-GWAS data to create developmentally targeted, functionally informed PRSs. Using two developmentally matched meta-GWAS discovery samples, separate PRSs were formed, then examined in time-varying effect models of aggression in a second, longitudinal sample of children (n = 515, 49% female) in early childhood (2-5 years old), and middle childhood (7.5-10.5 years old). Functional PRSs were associated with aggression in both the early and middle childhood models.

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The goal of this study was to disentangle the common and unique genetic and environmental influences on social-emotional competence, problem behavior, physiological dysregulation, and negative emotionality (NE) in toddlers. The sample consisted of 243 twin pairs (mean age = 31.94 months) rated by primary caregivers (>95% mothers) on the Children's Behavior Questionnaire and the Infant-Toddler Social and Emotional Assessment. A multivariate Cholesky Decomposition revealed three shared environmental factors, with one set of environmental influences common to competence, problem behavior, and physiological dysregulation, a second common to problem behavior and physiological dysregulation, and a third common to physiological dysregulation and NE. Also, there were two additive genetic factors, with one explaining variance in competence, NE, and a small amount of variance in problem behavior, and a second explaining variance in problem behavior and NE. Given the common shared environmental factors across outcomes, these results suggest that toddlerhood could be a particularly important time to intervene, as interventions could simultaneously improve competencies and reduce problem behaviors. This study also highlights the need for genetically informed research to examine the etiology of multiple outcomes and address overlap.

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Despite identified concurrent socioeconomic disparities in children's sleep, little research has examined pathways explaining such associations. This study examined the quality of the home environment as a direct predictor of sleep and potential mediator of associations between early life socioeconomic status and objective and subjective indicators of sleep in middle childhood. A socioeconomically and ethnically diverse sample of 381 twin children (50% female; 46.6% lower middle class or living at or below the poverty line; 26% Hispanic/Latino) were assessed at 12 months for SES and eight years using gold-standard home environment interviews and actigraphy-measured sleep. Multilevel mediation path models indicated that lower early SES and lower quality concurrent home environments were associated with shorter sleep durations, longer sleep latencies, and greater sleep timing variability. The home environment significantly mediated associations with sleep duration and sleep timing variability. The findings illustrate an important target in the prevention of poor childhood and adolescent sleep.

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Development involves synergistic interplay among genotypes and the physical and cultural environments, and integrating genetics into experimental designs that manipulate the environment can improve understanding of developmental psychopathology and intervention efficacy. Consistent with differential susceptibility theory, individuals can vary in their sensitivity to environmental conditions including intervention for reasons including their genotype. As a consequence, understanding genetic influences on intervention response is critical. Empirically, we tested an interaction between a genetic index representing sensitivity to the environment and the Family Check-Up intervention. Participants were drawn from the Early Steps Multisite randomized prevention trial that included a low-income and racially/ethnically diverse sample of children and their families followed longitudinally (n = 515). As hypothesized, polygenic sensitivity to the environment moderated the effects of the intervention on 10-year-old children's symptoms of internalizing psychopathology, such that children who were genetically sensitive and were randomly assigned to the intervention had fewer symptoms of child psychopathology than genetically sensitive children assigned to the control condition. A significant difference in internalizing symptoms assessed with a clinical interview emerged between the intervention and control groups for those 0.493 SD above the mean on polygenic sensitivity, or 25% of the sample. Similar to personalized medicine, it is time to understand individual and sociocultural differences in treatment response and individualize psychosocial interventions to reduce the burden of child psychopathology and maximize well-being for children growing up in a wide range of physical environments and cultures.

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Children's sleep has both environmental and genetic influences, with stressful family environmental factors like household chaos and marital conflict associated with sleep duration and quality (El-Sheikh, Buckhalt, Mize, & Acebo, 2006; Fiese, Winter, Sliwinski, & Anbar, 2007). However, it is less clear whether sibling conflict is related to sleep duration and children's sleep problems (e.g., nighttime wakings, parasomnias). In addition, few studies have tested whether associations between sleep and stressful family environmental factors are accounted for by an underlying set of genes or shared and unique environmental factors. Participants were 582 twins with sleep assessed longitudinally at 12, 30 months, and 5 years of age. Sibling conflict was assessed at 5 years. Greater sibling conflict was associated with shorter sleep duration and greater number of total sleep problems, over and above the influence of general household stress and other covariates. The heritability of sleep duration increased with age. Shared environmental factors accounted for the covariance between sibling conflict and sleep duration and total sleep problems. Findings hold promise for interventions, including educating parents about fostering positive sibling relationships and healthy sleep habits.

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Two recent papers associated candidate genes with brooding rumination, a possible cognitive endophenotype for depression, in children ages 8-14 years. Stone et al. reported that BDNF val66met polymorphism predicted brooding in adolescence. Woody et al. reported that children carrying at least one copy of a CRHR1 TAT haplotype reported less brooding than their peers in the presence of maternal depression. We attempted to replicate and extend these findings in a sample of twins aged 12-16 years. We analyzed the BDNF val66met (rs6265) polymorphism and two (rs242924 and rs7209436) out of three single nucleotide polymorphisms (SNPs) that Woody et al. used to create a CRHR1 haplotype. We controlled for maternal history of depression and clustering within families. Unlike Stone et al., we found higher brooding among BDNF Met carriers. This main effect was qualified by an interaction with pubertal status, with the effect driven by more physically mature participants. Similar to Woody et al., we found an interaction between CRHR1 SNPs and maternal depression, with the homozygous minor genotype acting as a protective factor against brooding in the presence of maternal depression. Findings provide partial support for the influence of candidate genes in two environmentally sensitive systems on brooding.

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Twin factor mixture modeling was used to identify temperament profiles while simultaneously estimating a latent factor model for each profile with a sample of 787 twin pairs (Mage  = 7.4 years, SD = .84; 49% female; 88.3% Caucasian), using mother- and father-reported temperament. A four-profile, one-factor model fit the data well. Profiles included "regulated, typical reactive," "well-regulated, positive reactive," "regulated, surgent," and "dysregulated, negative reactive." All profiles were heritable, with lower heritability and shared environment also contributing to membership in the "regulated, typical reactive" and "dysregulated, negative reactive" profiles.

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