Social disadvantage, genetic sensitivity, and children's telomere length

Abstract

Disadvantaged social environments are associated with adverse health outcomes. This has been attributed, in part, to chronic stress. Telomere length (TL) has been used as a biomarker of chronic stress: TL is shorter in adults in a variety of contexts, including disadvantaged social standing and depression. We use data from 40, 9-y-old boys participating in the Fragile Families and Child Wellbeing Study to extend this observation to African American children. We report that exposure to disadvantaged environments is associated with reduced TL by age 9 y. We document significant associations between low income, low maternal education, unstable family structure, and harsh parenting and TL. These effects were moderated by genetic variants in serotonergic and dopaminergic pathways. Consistent with the differential susceptibility hypothesis, subjects with the highest genetic sensitivity scores had the shortest TL when exposed to disadvantaged social environments and the longest TL when exposed to advantaged environments.

Keywords: adversity; gene–environment; senescence.

Fig. 1.

ln(telomere length) by environment type and serotonin pathway (Upper) and dopamine pathway (Lower) homozygous genotype counts. Although the possible range of homozygous genotypes was 0–4, due to the small number of minor allele frequencies the range is top-coded at 2+. For the serotonin pathway genotypes, the environment effect is borderline for 0 genotypes (P = 0.09), not significant for 1 genotype (P = 0.32), and significant for 2+ genotypes (P = 0.02). For the dopamine pathway genotypes, the environment difference is not significant for 0 genotypes (P = 0.63), significant for 1 genotype (P = 0.05), and borderline for 2+ genotypes (P = 0.08).