Community Disadvantage Moderates Age-related Associations with Telomere Length and Frontoamygdala Connectivity in Adolescents

• In Event: Multidimensional Effects of Neighborhood Socioeconomic Status and Toxin Exposure Across Development

Abstract

Over the course of development, including adolescence, telomere length shortens (Miller et al., 2020) and intrinsic connectivity between the amygdala and ventromedial prefrontal cortex (vmPFC) becomes stronger (Gabard-Durnam et al., 2014). Thus, telomere length and frontoamygdala connectivity may index biological aging at the cellular and neural levels, respectively. Although socioeconomic disadvantage has been broadly associated with accelerated cellular aging (Needham et al., 2013) and neural development (Ramphal et al., 2020), several studies have reported inconsistent findings (Colich et al, 2020; Robertson et al., 2013). Further, although community- and family-level disadvantage have dissociable effects on behavioral development (Brooks-Gunn et al., 1993), few studies have considered whether there are also dissociable effects on biological aging. In a community sample of adolescents, we examined whether community- and family-level disadvantage moderate the associations between chronological age and both telomere length and intrinsic amygdala–vmPFC connectivity.
Participants were adolescents from the San Francisco Bay Area. Community disadvantage was assessed using the Area Deprivation Index (ADI), which maps socioeconomic disadvantage at the census tract level using data from the 2015 American Community Survey. We used the California state deciles of disadvantage, ranging from 1 to 10 (least to most disadvantaged). On average, adolescents in our sample tended to live in more advantaged communities relative to other communities in California (mean=2.62, SD=2.00, range=1-10). We measured telomere length from saliva (n=122, 71 females; mean age=13.32 years, SD=1.03, range=11.15-15.85) and used resting-state fMRI to measure functional connectivity between the bilateral vmPFC and the basolateral (BLA) and centromedial (CMA) amygdala subdivisions (n=135, 75 females; mean age=13.35 years, SD=1.07, range=11.08-15.82). To assess family-level socioeconomic status (SES), we used parental education and computed income-to-needs ratios for each family. We used linear regression with maximum likelihood estimation to test two-way interaction effects of age and our indices of disadvantage (community-level and family-level) on telomere length and frontoamygdala connectivity.
Community disadvantage significantly moderated associations of age with telomere length (B=-.25, p=.025) and right BLA–vmPFC connectivity (B=.22, p=.029). Probing these interaction effects, we found that age was negatively associated with telomere length (B=-.56, p=.021) and positively associated with BLA–vmPFC connectivity (B=.42, p=.041) in more disadvantaged communities, but was unrelated to telomere length (B=.11, p=.373) and right BLA–vmPFC connectivity (B=-.13, p=.282) in the most advantaged communities (see Figure 1). Community disadvantage did not moderate age-related associations with CMA–vmPFC connectivity (all ps>.219). Although adolescents from lower-SES families tended to live in more disadvantaged communities (r=-.46 and -.35, ps<.001 for income-to-needs and parental education, respectively), income-to-needs and parental education did not moderate age-related associations with telomere length or frontoamygdala connectivity (all ps>.104).
Our findings provide support for a social gradient of accelerated biological aging in adolescence. With increasing chronological age, adolescents living in less advantaged communities are biologically older at the cellular and neural levels than are their peers from more highly resourced communities. Our findings were not explained by family-level SES, suggesting that community disadvantage more effectively reflects the nuances of social inequality that are relevant to accelerated biological aging and maturation.

Authors

• Jonas G. Miller, Stanford University
  Presenting Author

• Tiffany C Ho, University of California - San Francisco
  Non-Presenting Author

• Jaclyn Schwartz Kirshenbaum, Columbia University
  Non-Presenting Author

• Ian Gotlib, Stanford University
  Non-Presenting Author