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

认知调节过程，称为执行功能(EF)，与一生中的决策、个性和健康密切相关。儿童的EF与其社会经济地位(SES)呈正相关，这主要表现在父母的收入、受教育程度和职业。社会安全感可以用来衡量社会中“较富裕”和“较差”人群的情况，因为它与各种可能引发压力的环境条件有关。一种理论认为，较低SES的较高压力会扰乱儿童应激激素的分泌，主要是皮质醇，从而影响他们的认知发展。包括我自己在内的新兴研究发现，与SES相关的皮质醇分泌差异与他们的认知表现较差有关。然而，这些研究在很大程度上忽略了遗传效应，尽管这些关系已知在一定程度上受到了基因的影响。行为遗传学方法能够通过比较同卵双胞胎和异卵双胞胎，在统计上区分环境和遗传影响。Tucker-Drob和Harden的里程碑式的工作提供了证据，表明在低SES的情况下，认知能力几乎完全由环境因素预测，而高SES的环境有助于儿童选择与其受遗传影响的兴趣相匹配的学习经验。此外，动物研究表明，应激激素会改变与认知发展有关的基因表达。因此，可想而知，皮质醇分泌是抑制低SES儿童EF发育相关基因表达的潜在机制的一部分。因此，拟议的研究将检验以下问题：儿童皮质醇失调是由SES相关的压力还是遗传效应驱动的，还是两者兼而有之？皮质醇分泌与EF的相关性在多大程度上可归因于环境和遗传效应？皮质醇是EF发育中基因-环境相互作用机制的一部分吗？主持人Elliot Tucker-Drob和Paige Harden是德克萨斯双胞胎项目的主要研究人员，他们拥有多变量皮质醇分泌和EF数据，这些数据来自预计1000对7-15岁的双胞胎，可以在到达时进行分析。首先，我们将使用行为遗传学模型来解开皮质醇分泌的遗传和环境维度。其次，我们将描述皮质醇与EFS的关联是来自共同的遗传途径，还是共同的环境影响，或者两者的某种组合。第三，我们将探索遗传效应是否与SES对EFS的影响相互作用，作为对低SES的基因抑制的测试。如果是这样的话，我们将调查皮质醇分泌是否可能机械地参与了这种基因抑制。

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.