BACKGROUND AND OBJECTIVES: Children who grow up in socioeconomic disadvantage face increased burden of disease and disability throughout their lives. One hypothesized mechanism for this increased burden is that early-life disadvantage accelerates biological processes of aging, increasing vulnerability to subsequent disease. To evaluate this hypothesis and the potential impact of preventive interventions, measures are needed that can quantify early acceleration of biological aging in childhood. METHODS: Saliva DNA methylation and socioeconomic circumstances were measured in N = 600 children and adolescents aged 8 to 18 years (48% female) participating in the Texas Twin Project. We measured pace of biological aging using the DunedinPoAm DNA methylation algorithm, developed to quantify the pace-of-aging–related decline in system integrity. We tested if children in more disadvantaged families and neighborhoods exhibited a faster pace of aging as compared with children in more affluent contexts. RESULTS: Children living in more disadvantaged families and neighborhoods exhibited a faster DunedinPoAm-measured pace of aging (r = 0.18; P = .001 for both). Latinx-identifying children exhibited a faster DunedinPoAm-measured pace of aging compared with both White- and Latinx White–identifying children, consistent with higher levels of disadvantage in this group. Children with more advanced pubertal development, higher BMI, and more tobacco exposure exhibited faster a faster DunedinPoAm-measured pace of aging. However, DunedinPoAm-measured pace of aging associations with socioeconomic disadvantage were robust to control for these factors. CONCLUSIONS: Children growing up under conditions of socioeconomic disadvantage exhibit a faster pace of biological aging. DNA methylation pace of aging might be useful as a surrogate end point in evaluation of programs and policies to address the childhood social determinants of lifelong health disparities.

Lower socioeconomic status (SES) environments are marked by higher stress that is hypothesized to alter cortisol secretion in children, thereby damaging hippocampal volume and memory performance. However, empirical evidence demonstrating these putative links is lacking. We assessed the diurnal cortisol awakening response (CAR) on two mornings and cortisol stress reactivity (CSR) with the Trier Social Stress Test for Children in 102 healthy, socio-demographically diverse 6-to-7-year-old children (46% female). Children performed a hippocampal-dependent item-location associative memory task and 60 of these children underwent structural MRI scanning for hippocampal volume. Cortisol values were modeled with latent-change structural equation models to represent overall levels and change. We found lower income is associated with a flatter CAR, blunted reactivity and recovery to acute stress, and smaller hippocampal volume. Furthermore, hyporeactivity in CSR was related to lower memory among lower-income children, whereas there was no reliable association of CSR and memory among higher-income children (an income x cortisol interaction). We found no evidence that smaller hippocampal volume in lower income was associated with poorer memory performance. Notably, hyporeactivity in both CAR and CSR was specific to using income as the SES predictor. The income x cortisol interaction and smaller hippocampal effects, however, were replicated with education and an SES composite score. This suggests that hyporeactivity to acute stress may function as a mediator in SES-cognition associations at the lower end of the SES spectrum, but it does not imply environmental- or genetically-mediated causation.

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