Study Preregistration: Understanding the Etiology of Externalizing Problems in Young Children: The Roles of Callous-Unemotional Traits and Irritability.

Externalizing behavioral problems in young children are associated with later delinquency and crime,1 which can cause burdens at both personal and socialeconomic levels. The heterogeneity of externalizing problems emphasizes the importance of examining the etiological mechanisms that underlie externalizing problems and related behaviors. The present study focuses on 2 risk factors for externalizing behavioral problems in early childhood: callous-unemotional traits (CU), characterized as a lack of guilt and empathy,2 and irritability, a tendency to show anger and frustration.3 Behavioral genetic studies find that externalizing problems, CU, and irritability are heritable,4,5 raising the possibility of common genetic effects linking the 3 behaviors, but this has not been previously explored. Neurological evidence suggests distinct pathways from CU and irritability to externalizing problems,6 implying that the genetic and environmental factors linking externalizing problems and CU may differ from those linking externalizing problems and irritability. We predict that there will be common genetic influences operating across externalizing problems, CU, and irritability; but we also predict unique genetic and environmental influences representing distinctive risks shared between externalizing problems and CU, and between externalizing problems and irritability, respectively.

Genetic and environmental influences on temperament development across the preschool period.

BACKGROUND: Preschoolers' temperament characteristics are associated with children's long-term development. Such links underscore the importance of understanding factors that shape temperament during preschool. This is the first study to examine genetic and environmental sources of developmental growth in three temperament dimensions: surgency, negative affectivity, and effortful control, during the preschool period. METHODS: Biometric latent growth curve modeling was used to examine genetic, shared, and nonshared environmental contributions to the invariant level of and developmental growth in temperament, using a sample of 310 same-sex twin pairs (MZ = 123, DZ = 187) assessed at 3, 4, and 5 years of age. Temperament was assessed using primary caregiver's report on the Child Behavior Questionnaire-Short Form. RESULTS: All three temperament dimensions demonstrated linear increases from ages 3 to 5 years. The invariant levels of all three temperament dimensions were explained by genetic and nonshared environmental factors. Growth in surgency was fully explained by nonshared environmental factors, while growth in negative affectivity was mainly explained by genetic factors. Growth in effortful control was explained by genetic and nonshared environmental factors, although neither were significant due to large bootstrap standard errors. For negative affectivity and effortful control, the genetic factors that contributed to developmental growth were independent from those associated with their invariant levels. CONCLUSIONS: Collectively, these findings indicate that both genetic and nonshared environmental factors play important roles in the invariant levels of temperament. Findings also accord a critical role of children's nonshared environment in the development of surgency and to a lesser extent negative affectivity and effortful control. It is also notable that novel genetic effects contribute to developmental growth in negative affectivity and effortful control as children age, emphasizing the importance of integrating developmental models in genetic research.

Using the Flanker Task to Examine Genetic and Environmental Contributions in Inhibitory Control Across the Preschool Period.

The limited research exploring genetic and environmental influences on inhibitory control (IC) in preschoolers has relied on parent ratings or simple delay tasks and has produced mixed results. The present study uses a cognitively-challenging Flanker task to examine genetic and environmental contributions to the development of early IC in a longitudinal sample of 310 same-sex twin pairs (123 MZ; 187 DZ; 51% female) assessed at ages 3, 4 and 5 years. IC was significantly heritable at each age (a2: age 3 = .36; age 4 = .36; age 5 = .35). Stability was entirely accounted for by genetic influences, and change was explained by genetic and nonshared environmental factors. No significant shared environmental influences were observed.

Changing genetic architecture of body mass index from infancy to early adulthood: an individual based pooled analysis of 25 twin cohorts.

BACKGROUND: Body mass index (BMI) shows strong continuity over childhood and adolescence and high childhood BMI is the strongest predictor of adult obesity. Genetic factors strongly contribute to this continuity, but it is still poorly known how their contribution changes over childhood and adolescence. Thus, we used the genetic twin design to estimate the genetic correlations of BMI from infancy to adulthood and compared them to the genetic correlations of height. METHODS: We pooled individual level data from 25 longitudinal twin cohorts including 38,530 complete twin pairs and having 283,766 longitudinal height and weight measures. The data were analyzed using Cholesky decomposition offering genetic and environmental correlations of BMI and height between all age combinations from 1 to 19 years of age. RESULTS: The genetic correlations of BMI and height were stronger than the trait correlations. For BMI, we found that genetic correlations decreased as the age between the assessments increased, a trend that was especially visible from early to middle childhood. In contrast, for height, the genetic correlations were strong between all ages. Age-to-age correlations between environmental factors shared by co-twins were found for BMI in early childhood but disappeared altogether by middle childhood. For height, shared environmental correlations persisted from infancy to adulthood. CONCLUSIONS: Our results suggest that the genes affecting BMI change over childhood and adolescence leading to decreasing age-to-age genetic correlations. This change is especially visible from early to middle childhood indicating that new genetic factors start to affect BMI in middle childhood. Identifying mediating pathways of these genetic factors can open possibilities for interventions, especially for those children with high genetic predisposition to adult obesity.

Low social affiliation predicts increases in callous-unemotional behaviors in early childhood.

BACKGROUND: Callous-unemotional (CU) behaviors predict risk for aggression and rule-breaking. Low social affiliation (i.e. reduced motivation for and enjoyment of social closeness) is hypothesized to be a phenotypic marker for CU behaviors in early childhood. However, studies need to establish observational methods to objectively assess social affiliation as well as to establish parenting practices that can buffer pathways from low social affiliation to CU behaviors. METHODS: Using data from a longitudinal twin study of 628 children (age 2, 47% females; age 3, 44.9% females), we examined reciprocal associations between observed social affiliation, CU behaviors, and oppositional-defiant behaviors. We tested whether positive parenting moderated associations over time. RESULTS: We established that an observed measure of social affiliation derived from the Bayley's Behavior Rating Scale and Infant Behavior Record showed high inter-rater reliability and expected convergence with parent-reported temperament measures. Lower social affiliation at age 2 uniquely predicted CU behaviors, but not oppositional-defiant behaviors, at age 3. Finally, low social affiliation at age 2 predicted CU behaviors at age 3 specifically among children who experienced low, but not high, levels of parental positivity. CONCLUSIONS: An objective rating scale that is already widely used in pediatric settings reliably indexes low social affiliation and risk for CU behaviors. The dynamic interplay between parenting and low child social affiliation represents an important future target for novel individual- and dyadic-targeted treatments to reduce risk for CU behaviors.

Fearlessness and low social affiliation as unique developmental precursors of callous-unemotional behaviors in preschoolers.

BACKGROUND: Early callous-unemotional (CU) behaviors identify children at risk for severe and persistent aggression and antisocial behavior. Recent work suggests that fearlessness and low social affiliation are implicated in the etiology of CU behaviors, although more research is needed to clarify these etiological pathways, as well as the role of parenting. METHOD: Using a sample of preschoolers (N = 620), we examined pathways between observed fear in response to social and non-social stimuli and observed social affiliation during social interactions at age 3 and increases child CU behaviors and oppositional-defiant behaviors from ages 3 to 5. To elucidate the role of parenting in exacerbating or buffering the relationships between low fear and social affiliation and CU behaviors, we tested whether parental harshness or low warmth moderated these pathways. RESULTS: Fearlessness and low social affiliation uniquely predicted increases in CU behaviors, but not oppositional-defiant behaviors, from ages 3 to 5. Moreover, there was evidence for differential moderation of the fear pathway by harsh parenting, such that harsh parenting predicted increases in CU behaviors in fearless children but increases in oppositional-defiant behaviors in fearful children. CONCLUSIONS: Fearlessness and low social affiliation contribute to the development of CU behaviors. Harsh parenting can exacerbate the risky fearlessness pathway. Preventative interventions aimed at reducing risk for CU behaviors and persistent aggression and antisocial behavior should target socioaffiliative processes and provide parents with strategies and training to manage and scaffold rule-compliant behavior when children show low fearful arousal.

Genetic and environmental influences on human height from infancy through adulthood at different levels of parental education.

Genetic factors explain a major proportion of human height variation, but differences in mean stature have also been found between socio-economic categories suggesting a possible effect of environment. By utilizing a classical twin design which allows decomposing the variation of height into genetic and environmental components, we tested the hypothesis that environmental variation in height is greater in offspring of lower educated parents. Twin data from 29 cohorts including 65,978 complete twin pairs with information on height at ages 1 to 69 years and on parental education were pooled allowing the analyses at different ages and in three geographic-cultural regions (Europe, North America and Australia, and East Asia). Parental education mostly showed a positive association with offspring height, with significant associations in mid-childhood and from adolescence onwards. In variance decomposition modeling, the genetic and environmental variance components of height did not show a consistent relation to parental education. A random-effects meta-regression analysis of the aggregate-level data showed a trend towards greater shared environmental variation of height in low parental education families. In conclusion, in our very large dataset from twin cohorts around the globe, these results provide only weak evidence for the study hypothesis.

A Twin Study of Inhibitory Control at Age Two and ADHD Behavior Problems at Age Three.

Low levels of childhood inhibitory control (IC) are phenotypically and genetically associated with externalizing behavior problems and attention deficit hyperactivity disorder (ADHD). Unfortunately, there is little research on this topic in early childhood, when IC first emerges. This investigation extends the previous findings of contemporaneous genetic covariance between parent-rated and laboratory-assessed IC and ADHD at age 2 by examining longitudinal links between IC at age two and ADHD behavior problems at age three in a sample of 314 same-sex twin pairs (145 monozygotic or MZ, 169 dizygotic or DZ). There were significant phenotypic associations between both parent and laboratory IC assessments at age two and later ADHD behavioral problems (correlations ranged from - .15 to - .44). In our model-fitting strategy, we included measures of ADHD and IC at age 2 as predictors of ADHD at age 3. Longitudinal genetic analyses showed that phenotypic covariance between age two IC and ADHD behavior problems one year later were explained by overlapping genetic variance (genetic correlations ranged from - .28 to - .60). However, these effects were not unique to IC and reflect variance shared with ADHD at age 2. Parent-rated IC at age two showed higher phenotypic and genetic covariance with ADHD at age three than lab ratings of IC at age two. This is the first investigation examining genetic covariance between parent and lab-based IC at age two and ADHD behavior problems at age three. Findings show that after accounting for co-occurring ADHD, early temperamental IC is not a unique genetic risk factor for later ADHD.

Lexical processing of nouns and verbs at 36 months of age predicts concurrent and later vocabulary and school readiness.

Children's lexical processing speed at 18 to 25 months of age has been linked to concurrent and later language abilities. In the current study, we extend this finding to children aged 36 months. Children (N = 126) participated in a lexical processing task in which they viewed two static images on noun trials (e.g., an ear of corn and a hat), or two dynamic video clips on verb trials (e.g., a woman stretching and the same woman clapping), and heard an auditory prompt labeling one of them (e.g., "Where is she stretching?"). They also participated in standard assessments of language and school readiness. The results indicated that lexical processing speed (i.e., how long they required to look to the labeled image or scene) was associated with measures of concurrent receptive vocabulary, as well as receptive vocabulary and school readiness two years later, although the associations are weaker than for younger children.

Longitudinal Links Between Callous-Unemotional Behaviors and Parenting in Early Childhood: A Genetically Informed Design.

OBJECTIVE: Most research on callous-unemotional behaviors (CU) and parenting does not focus on directions of effect, and work that does so has not been genetically informed. The present study is the first to examine potential reciprocal effects between parenting and CU in a community sample of early childhood. Use of a twin sample also allows us to distinguish child-based genetic effects from environmentally driven effects, which is necessary before translating this research to interventions. METHOD: The present study used biometric cross-lagged models to investigate the relation between CU and parenting in twins at 2 and 3 years of age (monozygotic = 145, dizygotic = 169 twin pairs). CU was assessed using the parent-reported Child Behavior Checklist 1.5-5. Scores were residualized to control for conduct problems assessed on the Revised Rutter Parent Scale for Preschool Children. Parents' reports of negative and positive parenting were obtained using parent ratings of discipline and parent feelings from the Parent Feelings Questionnaire. RESULTS: CU and negative parenting were significantly correlated at both ages. Cross-lagged analyses revealed a unidirectional effect with CU at age 2 years predicting negative parenting at age 3 years. These child-driven effects were primarily genetically mediated, although there were modest nonshared environmental contributions. CU and positive parenting were not consistently correlated, and further biometric analyses were not performed. CONCLUSION: Children's genetically influenced CU behaviors can have an impact on the parenting that they experience. Child-driven CU effects, although less examined in the literature, are important and should receive more attention in future work.

The Boston University Twin Project (BUTP) II.

The Boston University Twin Project (BUTP) uses a multimethod, longitudinal approach to study the role of genetic and environmental factors on the development of child temperament and related behaviors in early childhood. There are two phases in this project. The first, described in the previous Twin Research and Human Genetics special issue on twin registries, focused on activity level and comprised over 300 twin pairs assessed in the home and laboratory at ages 2 and 3. In this article, we describe subject recruitment, sample characteristics, and study procedures and measures of the second phase of the BUTP. This recent study focuses more broadly on the development of multiple temperament dimensions and explores associations between temperament trajectories, parenting and child adjustment in a new cohort of approximately 300 twin pairs assessed at 3, 4 and 5 years of age.

A longitudinal genetically informed analysis of parental negativity and children's negative emotionality in middle childhood.

Children's negative emotionality (NE) is frequently associated with parental negativity, but causal understanding of this relationship is limited. In addition, little is known about how genetic and environmental factors affect this relationship during middle childhood. We addressed these gaps by applying a quantitative genetic analysis to cross-lagged associations between mothers' and fathers' parental negativity and children's NE during middle childhood. The sample comprised of 456 families when the children were 6.5 years old, and 401 families when the children were 8/9 years old. Mothers' and fathers' negativity and children's NE were assessed using questionnaires. Results showed that variation in parental negativity was mainly accounted for by the environment shared by children, with some indication of an evocative effect of the children's genes on mothers, but not fathers. Children's NE was accounted for by both genetic and shared environmental influences. Parental negativity and children's NE had moderate continuity over the course of two years. Mothers' (but not fathers') negativity when the children were 6.5 years old predicted change in children's NE (rated by the same or the other parent) toward age 8/9 years, but not the other way around. Shared environmental influences were the main contributor to the association between earlier mothers' negativity and later children's NE. Thus, although children's NE was partially heritable, and parenting too was partially accounted for by children's genes, the association between parental negativity and children's NE, at this age, reflects environmental effects and is compatible with mothers' influence on children. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Effects of socioeconomic status and executive function on school readiness across levels of household chaos.

Isolating child attributes and familial characteristics that support school readiness in children on the upper half of the socioeconomic spectrum can complement existing research on lower-socioeconomic status (SES) children and facilitate a more complete understanding of how children's performance varies across the full SES spectrum. This study examined if relations between SES, two components of executive function (EF; set-shifting and inhibitory control), and school readiness vary as a function of household chaos in 564 four-year-old children, primarily from middle-to upper-middle class families in the Northeast Region of the United States. Structural equation modeling of direct and indirect effects revealed three major findings: 1) higher levels of EF were related to better school readiness regardless of level of household chaos; 2) SES had an indirect effect on school readiness through set-shifting; and 3) household chaos was negatively associated with school readiness.

Parental Education and Genetics of BMI from Infancy to Old Age: A Pooled Analysis of 29 Twin Cohorts.

OBJECTIVE: The objective of this study was to analyze how parental education modifies the genetic and environmental variances of BMI from infancy to old age in three geographic-cultural regions. METHODS: A pooled sample of 29 cohorts including 143,499 twin individuals with information on parental education and BMI from age 1 to 79 years (299,201 BMI measures) was analyzed by genetic twin modeling. RESULTS: Until 4 years of age, parental education was not consistently associated with BMI. Thereafter, higher parental education level was associated with lower BMI in males and females. Total and additive genetic variances of BMI were smaller in the offspring of highly educated parents than in those whose parents had low education levels. Especially in North American and Australian children, environmental factors shared by co-twins also contributed to the higher BMI variation in the low education level category. In Europe and East Asia, the associations of parental education with mean BMI and BMI variance were weaker than in North America and Australia. CONCLUSIONS: Lower parental education level is associated with higher mean BMI and larger genetic variance of BMI after early childhood, especially in the obesogenic macro-environment. The interplay among genetic predisposition, childhood social environment, and macro-social context is important for socioeconomic differences in BMI.

Parent- and Observer-Rated Positive Affect in Early Childhood: Genetic Overlap and Environmental Specificity.

The sources of individual differences in both observed and parent-rated positive affect (PA) were examined in a sample of 304 3-year-old twin pairs (140 MZ, 164 DZ). Based on model-fitting analyses, individual differences in observed PA were attributed to moderate genetic and high nonshared environmental factors, but not shared environmental factors. In contrast, shared environmental effects accounted for over half of the variance in parent-rated PA and genetic and nonshared environmental effects were more modest. The genetic correlation across the two measures was high, indicating substantial overlap between genetic factors influencing the two. It was these overlapping genetic effects that fully explained the phenotypic correlation between both measures. There was no significant covariance between the environmental influences on parent rated and observed PA. Thus, the two measures of PA in early childhood have common genetic underpinnings, whereas environmental influences are measure-specific. Measurement implications are discussed.

Genetic and environmental factors affecting birth size variation: a pooled individual-based analysis of secular trends and global geographical differences using 26 twin cohorts.

Background: The genetic architecture of birth size may differ geographically and over time. We examined differences in the genetic and environmental contributions to birthweight, length and ponderal index (PI) across geographical-cultural regions (Europe, North America and Australia, and East Asia) and across birth cohorts, and how gestational age modifies these effects. Methods: Data from 26 twin cohorts in 16 countries including 57 613 monozygotic and dizygotic twin pairs were pooled. Genetic and environmental variations of birth size were estimated using genetic structural equation modelling. Results: The variance of birthweight and length was predominantly explained by shared environmental factors, whereas the variance of PI was explained both by shared and unique environmental factors. Genetic variance contributing to birth size was small. Adjusting for gestational age decreased the proportions of shared environmental variance and increased the propositions of unique environmental variance. Genetic variance was similar in the geographical-cultural regions, but shared environmental variance was smaller in East Asia than in Europe and North America and Australia. The total variance and shared environmental variance of birth length and PI were greater from the birth cohort 1990-99 onwards compared with the birth cohorts from 1970-79 to 1980-89. Conclusions: The contribution of genetic factors to birth size is smaller than that of shared environmental factors, which is partly explained by gestational age. Shared environmental variances of birth length and PI were greater in the latest birth cohorts and differed also across geographical-cultural regions. Shared environmental factors are important when explaining differences in the variation of birth size globally and over time.

Associations between birth size and later height from infancy through adulthood: An individual based pooled analysis of 28 twin cohorts participating in the CODATwins project.

BACKGROUND: There is evidence that birth size is positively associated with height in later life, but it remains unclear whether this is explained by genetic factors or the intrauterine environment. AIM: To analyze the associations of birth weight, length and ponderal index with height from infancy through adulthood within mono- and dizygotic twin pairs, which provides insights into the role of genetic and environmental individual-specific factors. METHODS: This study is based on the data from 28 twin cohorts in 17 countries. The pooled data included 41,852 complete twin pairs (55% monozygotic and 45% same-sex dizygotic) with information on birth weight and a total of 112,409 paired height measurements at ages ranging from 1 to 69 years. Birth length was available for 19,881 complete twin pairs, with a total of 72,692 paired height measurements. The association between birth size and later height was analyzed at both the individual and within-pair level by linear regression analyses. RESULTS: Within twin pairs, regression coefficients showed that a 1-kg increase in birth weight and a 1-cm increase in birth length were associated with 1.14-4.25 cm and 0.18-0.90 cm taller height, respectively. The magnitude of the associations was generally greater within dizygotic than within monozygotic twin pairs, and this difference between zygosities was more pronounced for birth length. CONCLUSION: Both genetic and individual-specific environmental factors play a role in the association between birth size and later height from infancy to adulthood, with a larger role for genetics in the association with birth length than with birth weight.

Do Genetic Factors Explain the Links Between Callous-Unemotional, Attention Hyperactivity and Oppositional Defiant Problems in Toddlers?

Research demonstrates that callous-unemotional (CU) behaviors, Attention Deficit Hyperactivity Disorder (ADHD) and Oppositional Defiant Problems (ODD) are related, but little is known about the sources of covariation among the three externalizing behaviors. The present study looked at genetic and environmental links between all three behavioral domains in twins at ages 2 and 3 years (MZ = 145, DZ = 169), a time when CU behaviors are beginning to emerge. CU, ADHD, and ODD behaviors as assessed using the Child Behavior Checklist 1.5-5 (Achenbach and Rescorla 2000) were strongly interrelated at both ages. Genetic factors primarily explained the covariation among the three behavioral domains via a common externalizing factor; however, there were also genetic factors unique to each behavior. Furthermore, the majority of nonshared environmental influences on each externalizing behavior were behavior-specific. The heritable externalizing factor was highly stable across age, largely due to genetic factors shared across ages 2 and 3 years. Despite their extensive phenotypic and genetic overlap, CU, ADHD, and ODD behaviors have unique genetic and nonshared environmental influences as early as toddlerhood. This supports phenotypic research showing that the three are related but distinct constructs in very young children.

Genetic and environmental links between motor activity level and attention problems in early childhood.

Cross-lagged biometric models were used to examine genetic and environmental links between actigraph-assessed motor activity level (AL) and parent-rated attention problems (AP) in 314 same-sex twin pairs (MZ = 145, DZ = 169) at ages 2 and 3 years. At both ages, genetic correlations between AL and AP were moderate (ra2 = .35; ra3 = .39) indicating both overlap and specificity in genetic effects across the two domains. Within- and across-age phenotypic associations between AL and AP were entirely due to overlapping genetic influences. There was a unidirectional effect of AL at age 2 predicting later AP. For AP, genetic and environmental influences from age 2 were transmitted to age 3 via stability effects and from AL. For AL, across-age effects were transmitted only via stability. These results suggest that overactivity in late infancy may impact the later development of problems related to inattention, and that genetic factors explain the association between the two domains.