Delineating genetic and environmentally-mediated influences on socioeconomic inequality in children’s cortisol secretion and executive functions

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Cognitive regulatory processes, called executive functions (EF), are closely linked to decision-making, personality, and health across the lifespan. Children’s EF are positively related to their socioeconomic status (SES), which is indicated by parents’ income, education and occupation. SES can be used as an indicator of circumstances of those ‘better off’ and those ‘worse off’ in society, because it correlates with a myriad of environmental conditions that can elicit stress for example. One theory proposes that higher stress in lower SES dysregulates children’s stress hormone secretion, mainly cortisol, thereby impacting their cognitive development. Emerging research, including my own, has found SES-related disparities in cortisol secretion that is associated with their lower cognitive performance. However, these studies have largely neglected genetic effects, even though these relationships are known to be genetically influenced in part. Behavior genetic methods are able to statistically separate environmental and genetic effects by comparing monozygotic and dizygotic twin pairs. Landmark work by Tucker-Drob and Harden provides evidence that in low SES, cognitive ability is almost entirely predicted by environmental factors, whereas high SES environments facilitate children’s ability to select learning experiences that match their genetically influenced interests. Additionally, animal research suggests stress hormones change gene expression involved in cognitive development. It is therefore conceivable that cortisol secretion is part of an underlying mechanism that suppresses gene expression involved in EF development of low SES children.Therefore, the proposed research will examine the following questions: Is cortisol dysregulation in children driven by SES-related stress or genetic effects, or both? To what degree is the association of cortisol secretion with EF attributable to environmental and genetic effects? Is cortisol part of a mechanism of gene-environment interaction on EF development? The hosts, Elliot Tucker-Drob and Paige Harden, are the principal investigators of the Texas Twin Project, with multivariate cortisol secretion and EF data from a projected number of 1000 twin pairs aged 7–15 years available for analysis by the time of arrival. First, we will use behavior genetic models to disentangle the genetic and environmental dimensions of cortisol secretion. Second, we will delineate whether associations of cortisol with EFs derives from a common genetic pathway or shared environmental effects, or some combination of the two. Third, we will explore whether genetic effects interact with SES effects on EFs as a test of gene suppression in low SES. If this is the case, we will investigate whether cortisol secretion may be mechanistically involved in this gene suppression.