Adolescent disordered eating and epigenetic age acceleration

Abstract Disordered eating is associated with a range of poor health outcomes that affect various body systems, including immune, metabolic, and stress-related processes. Biological ageing represents a potential mechanism through which disordered eating may impact these processes and can be measured through epigenetic age acceleration. Epigenetic age acceleration has been explored in various psychiatric disorders, but no study has investigated epigenetic age acceleration in those with eating disorders, or disordered eating. The present study examined the association between disordered eating at ages 14 and 17, and epigenetic age acceleration at age 17 in a representative community cohort ( N = 797). Disordered eating was assessed using global scores on the Eating Disorder Examination Questionnaire (EDE-Q), as well as scores on behavioural items relating to restriction, bingeing, and purging. After FDR correction, restriction at age 14 was longitudinally associated with a small (β = 0.09) increase in DunedinPACE, but not PhenoAge, GrimAge, Horvath, or Hannum. The association between age 14 restriction and DunedinPACE was partially mediated through higher BMI at ages 14 and 17, consistent with a role for BMI in the adverse health outcomes associated with disordered eating. No concurrent relationships were found between disordered eating at age 17 and epigenetic age acceleration. Findings suggest that third generation clocks may capture some of the long-term biological correlates of disordered eating, but – because the effect was small – it may not be clinically relevant. Replication using large community samples is required, along with studies that measure disordered eating and epigenetic age at multiple time points, to enhance causal inference.