No abstract

Executive functions (EFs) and intelligence (IQ) are phenotypically correlated. In twin studies, latent variables for EFs and IQ display moderate to high heritability estimates; however, they show variable genetic correlations in twin studies spanning childhood to middle age. We analyzed data from over 11,000 children (9-to 10-year-olds, including 749 twin pairs) in the Adolescent Brain Cognitive Development (ABCD) Study to examine the phenotypic and genetic relations between EFs and IQ in childhood. We identified two EF factors-Common EF and Updating-Specific-which were both related to IQ (rs = 0.64-0.81). Common EF and IQ were heritable (53%-67%), and their genetic correlation (rG = 0.86) was not significantly different than 1. These results suggest that EFs and IQ are phenotypically but not genetically separable in middle childhood, meaning that this phenotypic separability may be influenced by environmental factors.

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-pituitaryadrenal (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-to 14-year-old children from the population-based Texas Twin Project, we measured cortisol output at three different time-scales: (1) diurnal fluctuation in salivary cortisol (n = 400), (2) salivary cortisol reactivity and recovery after exposure to the Trier Social Stress Test (n = 444), and (3) and cortisol concentration in hair (n = 1,210). These measures converged on two moderately correlated, yet distinguishable, dimensions of HPA function. We then 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..

Executive functions (EFs) and impulsivity are dimensions of self-regulation that are both related to psychopathology. However, self-report measures of impulsivity and laboratory EF tasks typically display small correlations, and existing research indicates that impulsivity and EFs may tap separate aspects of self-regulation that independently statistically predict psychopathology in adulthood. However, relationships between EFs, impulsivity, and psychopathology may be different in childhood compared to adulthood. Here, we examine whether these patterns hold in the baseline assessment of the Adolescent Brain and Cognitive Development (ABCD) sample, a national sample of over 11,000 children (including 749 twin pairs) ages 9–10 years. We examine the phenotypic and genetic relationships among latent variables for different components of EFs and multiple facets of impulsivity. Additionally, we assess how EFs and impulsivity relate to composite measures and latent variables of psychopathology derived from parent report. EFs were weakly correlated with impulsivity, and the strength varied by impulsivity facet, emphasizing their separability. We did not identify significant genetic and environmental correlations between EFs and impulsivity. Moreover, controlling for their small relationships with each other, both EFs and some facets of impulsivity statistically predicted an Externalizing factor, attention problems, and social problems, and twin analyses suggested these relationships were genetic in origin. These findings indicate that EFs and impulsivity represent phenotypically and genetically separable aspects of self-regulation that are both transdiagnostic correlates of psychopathology in childhood.

20The progression of lifelong trajectories of socioeconomic inequalities in health and mortality begins in 21 childhood. Dysregulation in cortisol, a stress hormone that is the primary output of the hypothalamus-pituitary-22 adrenal (HPA) axis, has been hypothesized to be a mechanism for how early environmental adversity 23 compromises health. However, despite the popularity of cortisol as a biomarker for stress and adversity, little is 24 known about whether cortisol output differs in children being raised in socioeconomically disadvantaged 25 environments. Here, we show that there are few differences between advantaged and disadvantaged children in 26 their cortisol output. In 8-to 14-year-old children from the population-based Texas Twin Project, we measured 27 cortisol output at three different time-scales: (1) diurnal fluctuation in salivary cortisol (n = 400), (2) salivary 28 cortisol reactivity and recovery after exposure to the Trier Social Stress Test (n = 444), and (3) and cortisol 29 concentration in hair (n = 1,210). These measures converged on two moderately correlated, yet distinguishable, 30 dimensions of HPA function. We then tested differences in cortisol output across nine aspects of social 31 disadvantage at the home (e.g., family socioeconomic status), school (e.g., average levels of academic 32 achievement), and neighborhood (e.g., concentrated poverty). Children living in neighborhoods with higher 33 concentrated poverty had higher diurnal cortisol output, as measured in saliva; otherwise, child cortisol output 34 was unrelated to any other aspect of social disadvantage. Overall, we find limited support for alteration in HPA 35 axis functioning as a general mechanism for the health consequences of socioeconomic inequality in childhood. 36 37 As income inequality in the United States widens, disparities in health and survival between people in 38 the bottom versus the top of the socioeconomic distribution continue growing. [1][2][3][4] Motivated by the goal of 39 understanding, and ultimately mitigating, socioeconomic disparities in health outcomes, the biosocial research 40 agenda has attempted to identify specific biological mechanisms for how exposure to disadvantage gets 'under 41 the skin' 5 to produce sub-optimal life outcomes. In this effort, perhaps no other biomarker has been more 42 widely studied than cortisol. 6 Cortisol is the human glucocorticoid that is the major output of the hypothalamus-43 pituitary-adrenal (HPA) axis of the neuroendocrine system, which regulates a suite of physiological processes, 44 including immune function, metabolism, cardiovascular function, and central nervous system function, and is 45 highly responsive to both psychological and physical stress. 7 Given the extensive investment of scientific 46 resources into cortisol research, and the gaping health inequalities between poor and rich Americans, 3 it is 47 essential for researchers to be able to make informed choices about which measures of cortisol output are most 48 robustly associated with s...