Dimensions of Socioeconomic Status in Early Adolescence and DNA Methylation on Promoter of NR3C1 in Young Adulthood

• In Event: Poster Session 03
  In Poster Session: PS 03 Topic - Biological Processes: Neuroscience and Genetics

Abstract

Children from low socioeconomic status (SES) families are at a greater risk of negative health outcomes in adulthood, in part from chronic stress (Kim et al., 2018). The chronic stress of these experiences may become biologically embedded through methylation in stress-related genes (Neppl et al., 2016; Ursache et al., 2015). However, the effects of specific SES dimensions during childhood or adolescence on later epigenetic profiles in adulthood are not well understood (Janusek et al., 2019; Swartz et al., 2017). The present study examined the roles of two objective SES dimensions and two subjective SES dimensions experienced in early adolescence on DNA methylation in young adulthood, focusing on four cytosine-phosphate-guanine (CpG) sites in promoter 1F of the NR3C1 (cg17860381, cg04111177, cg15910486, and cg15645634), because methylation at these regions has been implicated in regulating the stress response (Cicchetti & Handley, 2017; Efstathopoulos et al., 2018; Weder et al., 2014).

Participants included 155 individuals from the Birmingham Youth Violence Study who provided data in early adolescence (M age = 13.1) and young adults (M age = 26.5). They included 62% females, 86% African Americans, and 13% European Americans. Family SES was measured in early adolescence with parent reports of household income level, parental education, perceived social status in their community, and financial hardship. DNA methylation beta values were measured in young adulthood from saliva. Correlations tested bivariate associations between each SES variable in early adolescence and methylation beta values in young adulthood at the four CpG sites. The unique relationships between objective and subjective SES indicators and DNA methylation were tested with hierarchical linear regressions, adjusting for age in young adulthood, sex, ethnicity, and smoking during late adolescence and young adulthood. Bonferroni correction for multiple testing was applied.

The results revealed that methylation at cg17860381 correlated with both lower income-to-need ratio (r = -.25, p = .002) and lower parental education (r = -.18, p = .03), whereas methylation at cg15910486 correlated with lower subjective social stats (r = -.19, p = .02) and greater financial hardship (r = .18, p = .02). However, none of the SES dimensions predicted DNA methylation at either CpG site.

The present study found hypermethylation at specific loci of the glucocorticoid receptor gene in young adults who experienced lower objective and subjective SES during early adolescence, but these associations did not withstand more rigorous testing with adjustment for covariates. These results contrast with other studies that linked early life stressors with higher methylation at the NR3C1 1F promoter region (Beach et al., 2014; Tyrka et al., 2015). It is possible that parent-reported subjective and objective SES during early adolescents are not strong indicators of chronic stress, or that other factors between early adolescence and young adulthood played a greater role in methylation. Future research should include longitudinal examination of DNA methylation to determine the temporal relationships of family SES and chronic stress exposure with the epigenome.

Authors

• Malcolm C Barker-Kamps, University of Alabama, Birmingham
  Presenting Author

• Sylvie Mrug, University of Alabama at Birmingham
  Non-Presenting Author

• Amit Patki, University of Alabama at Birmingham
  Non-Presenting Author

• Hemant Tiwari, University of Alabama at Birmingham
  Non-Presenting Author