Weak and uneven associations of home, neighborhood, and school environments with stress hormone output across multiple timescales.

The progression of lifelong trajectories of socioeconomic inequalities in health and mortality begins in childhood. Dysregulation in cortisol, a stress hormone that is the primary output of the hypothalamus-pituitary-adrenal (HPA) axis, has been hypothesized to be a mechanism for how early environmental adversity compromises health. However, despite the popularity of cortisol as a biomarker for stress and adversity, little is known about whether cortisol output differs in children being raised in socioeconomically disadvantaged environments. Here, we show that there are few differences between advantaged and disadvantaged children in their cortisol output. In 8-14-year-old children from the population-based Texas Twin Project, we measured cortisol output at three different timescales: (a) diurnal fluctuation in salivary cortisol (n = 400), (b) salivary cortisol reactivity and recovery after exposure to the Trier Social Stress Test (n = 444), and (c) cortisol concentration in hair (n = 1210). These measures converged on two moderately correlated, yet distinguishable, dimensions of HPA function. We tested differences in cortisol output across nine aspects of social disadvantage at the home (e.g., family socioeconomic status), school (e.g., average levels of academic achievement), and neighborhood (e.g., concentrated poverty). Children living in neighborhoods with higher concentrated poverty had higher diurnal cortisol output, as measured in saliva; otherwise, child cortisol output was unrelated to any other aspect of social disadvantage. Overall, we find limited support for alteration in HPA axis functioning as a general mechanism for the health consequences of socioeconomic inequality in childhood.

The relationship between executive function, processing speed, and attention-deficit hyperactivity disorder in middle childhood.

Attention-Deficit Hyperactivity Disorder (ADHD) is a heterogeneous disorder that is highly impairing. Early, accurate diagnosis maximizes long-term positive outcomes for youth with ADHD. Tests of executive functioning (EF) are potential tools for screening and differential diagnosis of ADHD subtypes. However, previous research has been inconsistent regarding the specificity and magnitude of EF deficits across ADHD subtypes. Here, we advance knowledge of the EF-ADHD relationship by using: (1) dimensional latent factor models of ADHD that captures the heterogeneity of expression, and (2) a comprehensive, reliable battery of EF tasks and modeling relationships with a general factor of EF ability. We tested 1548 children and adolescents (ages 7-15 years) from the Texas Twin Project, a population-based cohort with a diverse socioeconomic and ethnic composition. We show that EF deficits were specific to the inattention domain of ADHD. Moreover, we found that the association between EF task performance and inattention was stable across sociodemographic groups. Our results demonstrate that failures of executive control are selectively manifested as covert inattentive symptoms, such as trouble with organization, forgetfulness, and distractedness, rather than overt symptoms, such as inappropriate talkativeness and interruption. Future research, utilizing a bifactor characterization of ADHD in clinical samples, is needed to further refine understanding of the nature of cognitive deficits in ADHD across the full range of symptom variation.

Error-signaling in the developing brain.

While learning from mistakes is a lifelong process, the rate at which an individual makes errors on any given task decreases through late adolescence. Previous fMRI adult work indicates that several control brain networks are reliably active when participants make errors across multiple tasks. Less is known about the consistency and localization of error processing in the child brain because previous research has used single tasks. The current analysis pooled data across three studies to examine error-related task activation (two tasks per study, three tasks in total) for a group of 232 children aged 8-17 years. We found that, consistent with the adult literature, the majority of applied cingulo-opercular brain regions, including medial superior frontal cortex, dorsal anterior cingulate, and bilateral anterior insula, showed consistent error processing engagement in children across multiple tasks. Error-related activity in many of these cingulo-opercular regions correlated with task performance. However, unlike in the adult literature, we found a lack of error-related activation across tasks in dorsolateral frontal areas, and we also did not find any task-consistent relations with age in these regions. Our findings suggest that the task-general error processing signal in the developing brain is fairly robust and similar to adults, with the exception of lateral frontal cortex.

Developmental transformations in the structure of executive functions.

Comparisons of results from studies of executive function (EF) in early childhood to those of EF in middle and late childhood suggest that individual differences in EFs may differentiate from a unitary factor in early childhood to an increasingly multidimensional structure in middle childhood and adolescence. We tested whether associations among EFs strengthened from middle childhood to adolescence using cross-sectional data from a population-based sample of 1019 children aged 7-15 years (M = 10.79 years). Participants completed a comprehensive EF battery consisting of 15 measures tapping working memory, updating, switching, and inhibition domains. Moderated factor analysis, local structural equation modeling, and network modeling were applied to assess age-related differences in the factor structure of EF. Results from all three approaches indicated that working memory and updating maintained uniformly high patterns of covariation across the age range, whereas inhibition became increasingly differentiated from the other three domains beginning around 10 years of age. However, consistent with past research, inhibition tasks were only weakly intercorrelated. Age-related differences in the organization of switching abilities were mixed.

The neural architecture of executive functions is established by middle childhood.

Executive functions (EFs) are regulatory cognitive processes that support goal-directed thoughts and behaviors and that involve two primary networks of functional brain activity in adulthood: the fronto-parietal and cingulo-opercular networks. The current study assessed whether the same networks identified in adulthood underlie child EFs. Using task-based fMRI data from a diverse sample of N = 117 children and early adolescents (M age = 10.17 years), we assessed the extent to which neural activity was shared across switching, updating, and inhibition domains, and whether these patterns were qualitatively consistent with adult EF-related activity. Brain regions that were consistently engaged across switching, updating, and inhibition tasks closely corresponded to the cingulo-opercular and fronto-parietal networks identified in studies of adults. Isolating brain activity during more demanding task periods highlighted contributions of the dorsal anterior cingulate and anterior insular regions of the cingulo-opercular network. Results were independent of age and time-on-task effects. These results indicate that the two core brain networks that support EFs are in place by middle childhood, in agreement with resting-state findings of adultlike brain network organization. Improvement in EFs from middle childhood to adulthood, therefore, are likely due to quantitative changes in activity within these networks, rather than qualitative changes in the organization of the networks themselves. Improved knowledge of how the brain's functional organization supports EF in childhood has critical implications for understanding the maturation of cognitive abilities.

Accounting for the shared environment in cognitive abilities and academic achievement with measured socioecological contexts.

Behavioral and molecular genetic research has established that child cognitive ability and academic performance are substantially heritable, but genetic variation does not account for all of the stratification of cognitive and academic outcomes across families. Which specific contexts and experiences contribute to these shared environmental influences on cognitive ability and academic achievement? Using an ethnically and socioeconomically diverse sample of N = 1728 twins ages 7-20 from the Texas Twin Project, we identified specific measured family, school, and neighborhood socioecological contexts that statistically accounted for latent shared environmental variance in cognitive abilities and academic skills. Composite measures of parent socioeconomic status (SES), school demographic composition, and neighborhood SES accounted for moderate proportions of variation in IQ and achievement. Total variance explained by the multilevel contexts ranged from 15% to 22%. The influence of family SES on IQ and achievement overlapped substantially with the influence of school and neighborhood predictors. Together with race, the measured socioecological contexts explained 100% of shared environmental influences on IQ and approximately 79% of shared environmental influences on both verbal comprehension and reading ability. In contrast, nontrivial proportions of shared environmental variation in math performance were left unexplained. We highlight the potential utility of constructing "polyenvironmental risk scores" in an effort to better predict developmental outcomes and to quantify children's and adolescents' interrelated networks of experiences. A video abstract of this article can be viewed at: https://youtu.be/77E_DctFsr0.

Home Environment, But Not Socioeconomic Status, is Linked to Differences in Early Phonetic Perception Ability.

Infants perceptually tune to the phonemes of their native languages in the first year of life, thereby losing the ability to discriminate non-native phonemes. Infants who perceptually tune earlier have been shown to develop stronger language skills later in childhood. We hypothesized that socioeconomic disparities, which have been associated with differences in the quality and quantity of language in the home, would contribute to individual differences in phonetic discrimination. Seventy-five infants were assessed on measures of phonetic discrimination at 9 months, on the quality of the home environment at 15 months, and on language abilities at both ages. Phonetic discrimination did not vary according to socioeconomic status (SES), but was significantly associated with the quality of the home environment. This association persisted when controlling for 9-month expressive language abilities, rendering it less likely that infants with better expressive language skills were simply engendering higher quality home interactions. This suggests that infants from linguistically richer home environments may be more tuned to their native language and therefore less able to discriminate non-native contrasts at 9 months relative to infants whose home environments are less responsive. These findings indicate that home language environments may be more critical than SES in contributing to early language perception, with possible implications for language development more broadly.

Coupled changes in brain white matter microstructure and fluid intelligence in later life.

Understanding aging-related cognitive decline is of growing importance in aging societies, but relatively little is known about its neural substrates. Measures of white matter microstructure are known to correlate cross-sectionally with cognitive ability measures, but only a few small studies have tested for longitudinal relations among these variables. We tested whether there were coupled changes in brain white matter microstructure indexed by fractional anisotropy (FA) and three broad cognitive domains (fluid intelligence, processing speed, and memory) in a large cohort of human participants with longitudinal diffusion tensor MRI and detailed cognitive data taken at ages 73 years (n = 731) and 76 years (n = 488). Longitudinal changes in white matter microstructure were coupled with changes in fluid intelligence, but not with processing speed or memory. Individuals with higher baseline white matter FA showed less subsequent decline in processing speed. Our results provide evidence for a longitudinal link between changes in white matter microstructure and aging-related cognitive decline during the eighth decade of life. They are consistent with theoretical perspectives positing that a corticocortical "disconnection" partly explains cognitive aging.

Genes Unite Executive Functions in Childhood.

Individual differences in children's executive functions (EFs) are relevant for a wide range of normal and atypical psychological outcomes across the life span, but the origins of variation in children's EFs are not well understood. We used data from a racially and socioeconomically diverse sample of 505 third- through eighth-grade twins and triplets from the Texas Twin Project to estimate genetic and environmental influences on a Common EF factor and on variance unique to four core EF domains: inhibition, switching, working memory, and updating. As has been previously demonstrated in young adults, the Common EF factor was 100% heritable, which indicates that correlations among the four EF domains are entirely attributable to shared genetic etiology. Nonshared environmental influences were evident for variance unique to individual domains. General EF may thus serve as an early life marker of genetic propensity for a range of functions and pathologies later in life.

Developmental changes in genetic and environmental influences on rule-breaking and aggression: age and pubertal development.

BACKGROUND: Antisocial behavior (ASB) can be meaningfully divided into nonaggressive rule-breaking versus aggressive dimensions, which differ in developmental course and etiology. Previous research has found that genetic influences on rule-breaking, but not aggression, increase from late childhood to mid-adolescence. This study tested the extent to which the developmental increase in genetic influence on rule-breaking was associated with pubertal development compared to chronological age. METHOD: Child and adolescent twins (n = 1,031), ranging in age from 8 to 20 years (M age = 13.5 years), were recruited from public schools as part of the Texas Twin Project. Participants reported on their pubertal development using the Pubertal Development Scale and on their involvement in ASB on items from the Child Behavior Checklist. Measurement invariance of ASB subtypes across age groups (≤12 years vs. >12 years old) was tested using confirmatory factor analyses. Quantitative genetic modeling was used to test whether the genetic and environmental influences on aggression and rule-breaking were moderated by age, pubertal status, or both. RESULTS: Quantitative genetic modeling indicated that genetic influences specific to rule-breaking increased as a function of pubertal development controlling for age (a gene × puberty interaction), but did not vary as a function of age controlling for pubertal status. There were no developmental differences in the genetic etiology of aggression. Family-level environmental influences common to aggression and rule-breaking decreased with age, further contributing to the differentiation between these subtypes of ASB from childhood to adolescence. CONCLUSIONS: Future research should discriminate between alternative possible mechanisms underlying gene × puberty interactions on rule-breaking forms of antisocial behavior, including possible effects of pubertal hormones on gene expression.

Socioeconomic disparities in neurocognitive development in the first two years of life.

Socioeconomic status (SES) is strongly associated with cognition and achievement. Socioeconomic disparities in language and memory skills have been reported from elementary school through adolescence. Less is known about the extent to which such disparities emerge in infancy. Here, 179 infants from socioeconomically diverse families were recruited. Using a cohort-sequential design, 90 infants were followed at 9 and 15 months, and 89 were followed at 15 and 21 months. SES disparities in developmental trajectories of language and memory were present such that, at 21 months of age, children of highly educated parents scored approximately .8 standard deviations higher in both language and memory than children of less educated parents. The home language and literacy environment and parental warmth partially accounted for disparities in language, but not memory development.

An in-laboratory stressor reveals unique genetic variation in child cortisol output.

Dysregulation of biological stress response, as measured by cortisol output, has been a primary candidate mechanism for how social experiences become biologically embedded. Cortisol is the primary output of the hypothalamic pituitary adrenal (HPA) axis. Cortisol levels vary systematically across the day and change in response to both sudden, acute stress experiences as well as prolonged exposure to environmental stress. Using data from 8- to 15-year-old twins in the Texas Twin Project, we investigate the extent to which genetic influences are shared across different measures of cortisol output: chronic cortisol accumulations in hair (n = 1,104), diurnal variation in salivary output (n = 488), and salivary response to a standardized, acute in-laboratory stressor (n = 537). Multivariate twin models indicate that genetic factors regulating cortisol response to the in-laboratory stressor are separable from those regulating baseline cortisol levels, naturally occurring diurnal variation in cortisol, and hair cortisol levels. These findings illustrate that novel environments can reveal unique genetic variation, reordering people in terms of their observed phenotype rather than only magnifying or mitigating preexisting differences. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Pediatric ADHD symptom burden relates to distinct neural activity across executive function domains.

Attention-deficit/hyperactivity disorder (ADHD) is a prevalent childhood disorder marked by inattention and/or hyperactivity symptoms. ADHD may also relate to impaired executive function (EF), but is often studied in a single EF task per sample. The current study addresses the question of unique vs. overlapping relations in brain activity across multiple EF tasks and ADHD symptom burden. Three in-scanner tasks drawn from distinct EF domains (cognitive flexibility, working memory, and inhibition) were collected from children with and without an ADHD diagnosis (N = 63). Whole-brain activity and 11 regions of interest were correlated with parent reports of inattention and hyperactivity symptoms. Across the three EF domains, brain activity related to ADHD symptom burden, but the direction and location of these associations differed across tasks. Overall, activity in sensory and default mode network regions related to ADHD, and these relations did not consistently overlap across EF domains. We observed both distinct and overlapping patterns for inattention and hyperactivity symptoms. By studying multiple EF tasks in the same sample, we identified a heterogenous neural profile related to attention symptom burden in children. Our results inform ADHD characterization and treatment and explain some of the variable brain results related to EF and ADHD reported in the literature.

Functional Connectivity Fingerprints at Rest Are Similar across Youths and Adults and Vary with Genetic Similarity.

Distinguishing individuals from brain connectivity, and studying the genetic influences on that identification across different ages, improves our basic understanding of functional brain network organization. We applied support vector machine classifiers to two datasets of twins (adult, pediatric) and two datasets of repeat-scan individuals (adult, pediatric). Classifiers were trained on resting state functional connectivity magnetic resonance imaging (rs-fcMRI) data and used to predict individuals and co-twin pairs from independent data. The classifiers successfully identified individuals from a previous scan with 100% accuracy, even when scans were separated by months. In twin samples, classifier accuracy decreased as genetic similarity decreased. Our results demonstrate that classification is stable within individuals, similar within families, and contains similar representations of functional connections over a few decades of life. Moreover, the degree to which these patterns of connections predict siblings' data varied by genetic relatedness, suggesting that genetic influences on rs-fcMRI connectivity are established early in life.

Genetic Associations Between Executive Functions and a General Factor of Psychopathology.

OBJECTIVE: Symptoms of psychopathology covary across diagnostic boundaries, and a family history of elevated symptoms for a single psychiatric disorder places an individual at heightened risk for a broad range of other psychiatric disorders. Both twin-based and genome-wide molecular methods indicate a strong genetic basis for the familial aggregation of psychiatric disease. This has led researchers to prioritize the search for highly heritable childhood risk factors for transdiagnostic psychopathology. Cognitive abilities that involve the selective control and regulation of attention, known as executive functions (EFs), are a promising set of risk factors. METHOD: In a population-based sample of child and adolescent twins (n = 1,913, mean age = 13.1 years), we examined genetic overlap between both EFs and general intelligence (g) and a transdiagnostic dimension of vulnerability to psychopathology, comprising symptoms of anxiety, depression, neuroticism, aggression, conduct disorder, oppositional defiant disorder, hyperactivity, and inattention. Psychopathology symptoms in children were rated by children and their parents. RESULTS: Latent factors representing general EF and g were highly heritable (h2 = 86%-92%), and genetic influences on both sets of cognitive abilities were robustly correlated with transdiagnostic genetic influences on psychopathology symptoms (genetic r values ranged from -0.20 to -0.38). CONCLUSION: General EF and g robustly index genetic risk for transdiagnostic symptoms of psychopathology in childhood. Delineating the developmental and neurobiological mechanisms underlying observed associations between cognitive abilities and psychopathology remains a priority for ongoing research.

"Same but different": Associations between multiple aspects of self-regulation, cognition, and academic abilities.

Self-regulation describes the ability to control both behaviors and internal states against a backdrop of conflicting or distracting situations, drives, or impulses. In the cognitive psychology tradition, individual differences in self-regulation are commonly measured with performance-based tests of executive functioning, whereas in the personality psychology tradition, individual differences in self-regulation are typically assessed with report-based measures of impulse control, sustained motivation, and perseverance. The goal of this project was (a) to comprehensively examine the structure of associations between multiple self-regulatory constructs stemming from the cognitive and personality psychology traditions; (b) to estimate how these constructs, individually and collectively, related to mathematics and reading ability beyond psychometric measures of processing speed and fluid intelligence; and (c) to estimate the extent to which genetic and environmental factors mediated the observed associations. Data were available for 1,019 child participants from the Texas Twin Project (M age = 10.79, range = 7.8-15.5). Results highlighted the differentiation among cognitive and personality aspects of self-regulation, both at observed and genetic levels. After accounting for processing speed and fluid intelligence, EF remained a significant predictor of reading and mathematics ability. Educationally relevant measures of personality-particularly an openness factor representing curiosity and intellectual self-concept-incrementally contributed to individual differences in reading ability. Collectively, measures of cognition, self-regulation, and other educationally relevant aspects of personality accounted for the entirety of genetic variance in mathematics and reading ability. The current findings point to the important independent role that each construct plays in academic settings. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Kids becoming less alike: A behavioral genetic analysis of developmental increases in personality variance from childhood to adolescence.

Recent work in personality development has indicated that the magnitude of individual differences in personality increases over child development. Do such patterns reflect the differentiation of individuals by genotype, an increasing influence of environmental factors, or some (interactive) combination of the two? Using a population-based sample of over 2,500 twins and multiples from the Texas Twin Project, we estimated age trends in the variances in self- and parent-reported measures of the Big Five personality traits between Ages 8 and 18 years. We then estimated age trends in the genetic and environmental components of variance in each measure. Individual differences in personality increased in magnitude from childhood through mid-adolescence. This pattern emerged using both children's self-reports and ratings provided by their parents, and was primarily attributable to increases in the magnitude of genetic influences. Most of the increasing genetic variance appeared nonadditive, pointing to the possibility that developmental processes tend to make genetically similar individuals disproportionately more alike in their personality traits over time. These findings could reflect increasing or accumulating effects of trait-by-trait interactions; person-by-environment transactions, whereby genetically similar people are disproportionally likely to experience similar environments; the activation of dominant genes across developmental transitions (e.g., puberty); or some combination of these three processes, among other factors. Theories of personality development will need to accommodate these descriptive findings, and longitudinal, genetically informed designs are needed to test some of the specific hypotheses springing from this study. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Genetic overlap between executive functions and BMI in childhood.

BACKGROUND: Executive functions (EFs) comprise a group of cognitive processes that selectively control and regulate attention. Inverse relations have been reported between EFs and BMI. However, the mechanisms underlying this association are not well understood. OBJECTIVES: We aimed to decompose the inverse relation between EFs and BMI into genetic and environmental components. METHODS: We employed a cross-sectional analysis of data from 869 twins aged 7-15 y from the Texas Twin Project, who completed a neuropsychological test battery measuring 4 EFs (switching, inhibitory control, working memory, and updating); academic achievement (reading and mathematics); and general cognitive abilities (general intelligence/intelligence quotient; crystallized and fluid intelligence; and processing speed). Participants also had their height and weight measured. RESULTS: After controlling for age, sex, and race/ethnicity, BMI was inversely associated with a general EF factor representing the capacity to control and regulate goal-oriented behaviors (r = -0.125; P = 0.01; Q = 0.04). This inverse BMI-EF association was due to a significant overlap in genetic factors contributing to each phenotype (genetic correlation, rA, = -0.15; P < 0.001). Shared genetic influences accounted for 80% of the phenotypic association. CONCLUSIONS: Children with higher general EF have lower BMIs, and this association is primarily attributable to shared genetic influences on both phenotypes. The results emphasize that higher weight associates not only with physical sequelae, but also with important cognitive attributes. This work adds to a growing body of research suggesting there are sets of genetic variants common across physical health and cognitive functioning.

Genetic and Environmental Associations Between Child Personality and Parenting.

Parenting is often conceptualized in terms of its effects on offspring. However, children may also play an active role in influencing the parenting they receive. Simple correlations between parenting and child outcomes may be due to parent-to-child causation, child-to-parent causation, or some combination of the two. We use a multi-rater, genetically informative, large sample (n = 1411 twin sets) to gain traction on this issue as it relates to parental warmth and stress in the context of child Big Five personality. Considerable variance in parental warmth (27%) and stress (45%) was attributable to child genetic influences on parenting. Incorporating child Big Five personality into the model explained roughly half of this variance. This result is consistent with the hypothesis that parents mold their parenting in response to their child's personality. Residual heritability of parenting is likely due to child characteristics beyond the Big Five.

Genetic and environmental influences on pubertal hormones in human hair across development.

Puberty is a complex biopsychosocial process that can affect an array of psychiatric and medical disorders emerging in adolescence. Although the pubertal process is driven by neuroendocrine changes, few quantitative genetic studies have directly measured puberty-relevant hormones. Hair samples can now be assayed for accumulation of hormones over several months. In contrast to more conventional salivary measures, hair measures are not confounded by diurnal variation or hormonal reactivity. In an ethnically and socioeconomically diverse sample of 1286 child and adolescent twins and multiples from 672 unique families, we estimated genetic and environmental influences on hair concentrations of testosterone, DHEA, and progesterone across the period of 8-18 years of age. On average, male DHEA and testosterone were highly heritable, whereas female DHEA, progesterone, and puberty were largely influenced by environmental components. We identified sex-specific developmental windows of maximal heritability in each hormone. Peak heritability for DHEA occurred at approximately 10 years of age for males and females. Peak heritability for testosterone occurred at age 12.5 and 15.2 years for males and females, respectively. Peak heritability for male progesterone occurred at 11.2 years, while the heritability of female progesterone remained uniformly low. The identification of specific developmental windows when genetic signals for hormones are maximized has critical implications for well-informed models of hormone-behavior associations in childhood and adolescence.