Diurnal Cortisol, Cortisol Reactivity, and Telomere Length in Diverse, Low-Income Toddlers

• In Event: Poster Session 14
  In Poster Session: PS 14 Topic - Biological Processes: Psychophysiology

Abstract

Background: Developmental programming of the HPA axis is one potential mechanism through which early life stress relates to later health outcomes (Taylor et al., 2011). Early adversity is well-established as contributing to dysregulated cortisol functioning, including stress reactivity and diurnal cortisol rhythms. As a biological marker of cellular aging, telomerase activity may be another mechanism through which early life experiences such as prenatal stress lead to poorer health outcomes (Entringer et al., 2015). Shorter telomeres and cortisol dysregulation are evident in young children who have experienced stressful events (e.g., Badanes et al., 2011; Drury et al., 2014), but the relationship between these mechanisms is unclear. Indeed, a recent meta-analysis examining telomere length, basal cortisol and cortisol reactivity identified only four studies focusing on infants and children (Jiang et al., 2019). Telomere length was associated with cortisol reactivity but not single-sample basal cortisol, though diurnal cortisol patterning was not examined. In the current study, we will test cortisol reactivity and diurnal cortisol patterns as predictors of telomere length in a sample of diverse, low-income toddlers. We hypothesize that shorter telomere length will be associated with a) flatter diurnal cortisol patterns across the day and b) blunted cortisol reactivity/recovery. Methods: Participants were 66 children ages 6 to 45 months (M=23.95 months) recruited through Early Head Start centers. Among these families, 73.4% were living at or below the poverty line. For diurnal cortisol, caregivers collected five salivary cortisol samples from their child on two consecutive days: wake, 15 minutes after wake, 60 minutes after wake, noon, and bedtime. Cortisol reactivity was measured via five cortisol samples taken before, during, and after a novel stress paradigm over a period of 75 minutes. These samples were collected during home visits by research members who also collected children’s salivary DNA using cheek swabs. The quantitative polymerase chain reaction method (qPCR; Cawthon, 2002) was used to establish relative telomere length values. Analysis Plan: All samples have been collected, assayed, and converted to cleaned data. For diurnal cortisol, we will use morning (highest wake sample to noon) and afternoon (noon to evening sample) slopes given that singular basal cortisol samples were not related to telomere length (Jiang et al, 2019). Cortisol reactivity and recovery slopes will be calculated using the baseline sample, peak sample, and final sample. Hierarchical linear regressions using SPSS will test diurnal cortisol and reactivity/recovery slopes as predictors of telomere length. Potential covariates include child age, child sex, and batch of analysis. Completion of these analyses is highly feasible given completed data collection and previous experience with modeling cortisol patterns. Implications: The authors previously established a link between early life stress and child telomere length in the current sample; therefore, the current study will extend this research and add to the nascent understanding of relationships across multiple biological stress systems. Ultimately, we aim to demonstrate how early life stress affects physiological and cellular functioning in young children with the subsequent goal of identifying resiliency factors that protect children from these effects.

Authors

• Amy Dominguez, University of Denver
  Presenting Author

• Elly Miles, Urban Institute
  Non-Presenting Author

• Neda Senehi, United States Office of Planning, Research & Evaluation (OPRE)
  Non-Presenting Author

• Lisa Schlueter, Colorado Department of Human Services, Office of Early Childhood
  Non-Presenting Author

• Sarah E Watamura, University of Denver
  Non-Presenting Author