Early-life adversity is widely linked to accelerated biological ageing, yet it remains unclear whether such associations reflect exposure during sensitive developmental periods, the cumulative burden of exposures, or temporal proximity to later outcomes.
Here, we leverage life-history theory and a life course framework to nuance how the timing of adverse childhood experiences (ACEs) becomes biologically embedded through epigenetic ageing.
We find that adversity exposure during specific developmental periods, rather than cumulative burden or recent exposure, are most strongly associated with epigenetic age acceleration in late childhood (\(R^2_{pooled\ ACEs}\)=0.003).
Epigenetic ageing is in turn associated with later health-related risks (\(\beta _{bmi}\)=0.29, SE=0.06; \(OR_{depression}\)=1.62, SE=0.27) and demographic behaviour (\(\beta _{no.\ births}\)=0.21, SE=0.08; \(\beta _{no.\ pregnancies}\)=0.22, SE=0.11), and further mediates the association between ACEs and outcomes in young adulthood, particularly for BMI (\(\beta _{bmi}\)=0.003, SE=0.002, \(prop.\ mediated\)=11%).
These findings demonstrate that childhood adversity may be linked to biological ageing in developmentally specific and domain-dependent ways, with certain developmental periods appearing more sensitive to adversity exposure than others.
Early-life adversity is widely linked to accelerated biological ageing, yet it remains unclear whether such associations reflect exposure during sensitive developmental periods, the cumulative burden of exposures, or temporal proximity to later outcomes. Here, we leverage life-history theory and a life course framework to nuance how the timing of adverse childhood experiences (ACEs) becomes biologically embedded through epigenetic ageing. Using longitudinal data from the Future of Families and Child Wellbeing Study (N=1,974), we apply statistical learning and structured life course modelling to test sensitive period, cumulative risk, and recency hypotheses across multiple domains of adversity (poverty, instability, deprivation, and maltreatment). We find that adversity exposure during specific developmental periods, rather than cumulative burden or recent exposure, are most strongly associated with epigenetic age acceleration in late childhood (\(R^2_{pooled\ ACEs}\)=0.003). Moreover, the timing and direction of these effects vary by adversity type. Epigenetic ageing is in turn associated with later health-related risks (\(\beta _{bmi}\)=0.29, SE=0.06; \(OR_{depression}\)=1.62, SE=0.27) and demographic behaviour (\(\beta _{no.\ births}\)=0.21, SE=0.08; \(\beta _{no.\ pregnancies}\)=0.22, SE=0.11), and further mediates the association between ACEs and outcomes in young adulthood, particularly for BMI (\(\beta _{bmi}\)=0.003, SE=0.002, \(prop.\ mediated\)=11%). These findings demonstrate that childhood adversity may be linked to biological ageing in developmentally specific and domain-dependent ways, with certain developmental periods appearing more sensitive to adversity exposure than others.
