Cortisol, Socioeconomic Status, and Genetic Influences on Cognitive Development

Project: Research project

Project Details

Description

Cortisol (CORT), a steroid hormone that is regulated by the hypothalamic-pituitary-adrenal (HPA) axis, is a
well-established biomarker for chronic stress and stress reactivity. HPA axis function is a cross-cutting
physiological mechanism linked to individual differences in an array of psychiatric, health, and social outcomes,
including childhood cognition. Childhood cognition, in turn, is itself a cross-cutting mechanism underlying
individual differences in psychiatric disorders, physical health, and human capital across the lifespan. Previous
research has conceptualized CORT as a response to environmental stress and disadvantage, as chronically
elevated CORT is associated with low socioeconomic status (SES) and partially mediates the SES-cognition
association. However, the genetic underpinnings of individual differences in CORT are poorly understood.
Moreover, animal research has found that glucocorticoid responses to early stressful rearing experiences
change the expression of genes involved in neural development. This suggests that CORT may also interact
with genetic influences on child cognition, and may be a mechanism that underlies gene × SES interactions
observed in previous research. This project will examine the relations between genes, SES, CORT, and
childhood cognition using both biometric and molecular genetic approaches. We will recruit a diverse
sample of 700 same-sex twin pairs (50% monozygotic, total N = 1400 children) in grades 3-5 identified from
public school rosters in two major metropolitan areas. Multi-method data will be collected from numerous
sources, including (a) parent and child survey responses; (b) in-laboratory cognition and achievement testing;
(c) cumulative individual-level educational records with school grades and performance on state-mandated
achievement tests; (d) administrative data from state and federal agencies on neighborhood context and
school quality; (e) in-laboratory cortisol reactivity and recovery in response to an acute psychosocial stressor;
(f) repeated in-home assessments of cortisol diurnal rhythm; (g) accumulated cortisol levels in hair, and (h)
salivary DNA samples, which we will genotype for polymorphisms in the biological CORT pathway. This
combination of behavioral genetic, genotypic, educational, endocrine, and demographic data will allow us to (1)
examine the genetic etiology of HPA axis function, as indexed by multiple measures of CORT output, using
both twin and measured-gene methodologies; (2) test the genetic and environmental mechanisms by which
CORT output is associated with child cognition; (3) test whether CORT, as well as genetic polymorphisms in
the CORT pathway, interact with latent genetic influences on cognition, as estimated in a twin model (gene ×
hormone and gene × gene interactions). This innovative and interdisciplinary project will break new ground in
understanding the etiology of individual differences in HPA axis function and its relations to socioeconomic
disadvantage and cognitive development in children.
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StatusFinished
Effective start/end date1/1/1612/31/20

Funding

  • University of Texas at Austin (UTA16-000087 // 1R01HD083613-01A1)
  • National Institute of Child Health and Human Development (UTA16-000087 // 1R01HD083613-01A1)

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