To test whether cumulative parental impulsivity exposure across childhood is associated with greater accelerated epigenetic age across adolescence.

Data were drawn from the Future of Families and Child Wellbeing Study, a population-based birth cohort (1998-2000) study of 4898 families across 20 major US cities. We analyzed data from families who provided self-reported survey data on maternal and paternal impulsivity when children were in early childhood (between the ages of 1 and 5 years); scores of parental impulsivity were created for each parent. Youth provided saliva samples to assess adolescent accelerated epigenetic age at ages 9 and 15 years old using 3 epigenetic clocks: PhenoAge, GrimAge, and DunedinPACE (n = 1971). Analyses jointly modeled the associations between maternal and paternal impulsivity during childhood and longitudinal change in accelerated epigenetic age using a latent variable constructed from these clocks in the structural equation modeling framework. We also conducted analyses using the individual clocks as the dependent variables. The autoregressive effect of age 9 accelerated epigenetic age was included to model residualized change from age 9 to 15.

Maternal impulsivity during early childhood, but not paternal impulsivity, was significantly associated with greater residualized change in the latent factor of accelerated epigenetic age ( β = 0.06, P = .03) at age 15 years. Maternal impulsivity was also associated with greater residualized change in accelerated aging using the individual clocks (GrimAge: β = 0.06, P < .001, PhenoAge: β = 0.04, P = .06, DunedinPACE: β = 0.05, P = .01).

Maternal impulsivity may constitute an environmental stressor that is correlated with greater accelerated epigenetic aging across adolescence. Variations in maternal impulsivity should be considered within the broader constellation of social and ecological factors as parental behavior may reflect adaptations to the broader contexts in which both parents and children reside.