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Parental Job Loss and Adolescent Epigenetic Aging

Wed, April 7, 4:20 to 5:50pm EDT (4:20 to 5:50pm EDT), Virtual

Abstract

Socioeconomic disadvantage is associated with health disparities across the lifespan including markers of biological weathering. Higher than expected epigenetic age, relative to one’s chronological age, is posited as a measure of biological weathering that is associated with greater risk for disease and mortality later in life. However, this biological weathering may begin much earlier. To date, the majority of research examining epigenetic age and socioeconomic disadvantage focuses on measures that tend to be stable (e.g., low SES). We know less about how acute economic changes in the family may impact changes in youth’s rate of epigenetic aging. During the Great Recession, unemployment rates increased and peaked at 10% resulting in millions of lost jobs in the U.S. Parental job loss places additional economic strain and material hardship on the family and is associated with increased parenting stress. Moreover, parental job loss is related to poorer mental and physical health in children. The present study examined the impact of parental job loss during and following the Great Recession on longitudinal changes in youth’s epigenetic age, as an indicator of biological weathering.

Data are from the Fragile Families and Child Wellbeing Study, a nationally representative longitudinal study of approximately 4900 youth born in large urban cities. The study includes a large sample of children from low-income, single-parent, and racially diverse families. Data collection for the age 9 assessment (2007-2010) corresponds with the occurrence of the Great Recession. Saliva samples obtained at ages 9 and 15 were assayed for DNA methylation (Infinium 450K Chip). Epigenetic age was calculated using Horvath’s clock (2013) and chronological age was removed for a measure of biological weathering. Samples were adjusted for cell type distribution (Houseman et al., 2016). At the age 15 assessment, primary caregivers reported whether they were laid off by their employer at any point between the age 9 and 15 surveys. Preliminary analyses are reported for a subset of youth (N=471; 47% Male; 56% Black, 21% White, 19% Hispanic; T1 M age=9.25, SD=.41; T2 M age=15.43, SD=.51) with parental job loss and epigenetic data.

During the six-year period, 26.3% (n=126) of primary caregivers reported being laid off. Latent change score models were fit in Mplus to capture change in epigenetic aging (χ2(5)=2.94, p=.71; RMSEA=0.00; CFI=1.00). Analyses controlled for child sex, race/ethnicity minority status, prenatal maternal smoking, and household income at age 9 (prior to reported job loss; log transformed). Parental job loss was associated with more rapid epigenetic aging (β=.13, p<.04; R2=.05; see Figure 1 for change in epigenetic aging). As a follow-up analysis, job loss was examined as a predictor of epigenetic age at both timepoints. Parental job loss was associated with higher epigenetic ages at age 15 (β=.11, p<.04) but not age 9 (β=.02, p=.77; as expected as the measurement occurred prior to the reported job loss; see Figure 2). These data suggest parental job loss is associated with more rapid biological weathering over and above chronological age changes during this six-year period that may have implications for later health and wellbeing.

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