Adolescent Disordered Eating and Epigenetic Age Acceleration

Why It Matters

The findings suggest that restrictive disordered eating may accelerate biological ageing in teens, highlighting a potential early‑life health risk and a novel biomarker for intervention.

Key Takeaways

• Restrictive eating at 14 predicts higher DunedinPACE at 17
• BMI partially mediates the restriction‑age acceleration link
• Other disordered‑eating behaviors showed no significant epigenetic effects
• First study to examine epigenetic age in adolescent eating pathology
• Third‑generation clocks detect metabolic impacts better than mortality clocks

Pulse Analysis

Disordered eating, affecting up to 15% of adolescents, is traditionally evaluated through psychological and behavioral lenses, yet its physiological sequelae remain under‑explored. Recent advances in epigenetics have introduced DNA‑methylation‑based clocks that estimate biological age, offering a window into how lifestyle factors may hasten or slow the ageing process. First‑generation clocks such as Horvath and Hannum estimate chronological age, while second‑generation mortality clocks (PhenoAge, GrimAge) predict lifespan risk. The third‑generation DunedinPACE clock, however, quantifies the pace of ageing and is particularly sensitive to metabolic disturbances, making it a promising tool for detecting subtle health impacts of adolescent behaviors.

In the Raine Study cohort, researchers leveraged five epigenetic clocks to test whether self‑reported disordered‑eating symptoms at ages 14 and 17 correlated with EAA at age 17. While most clocks showed no significant links, the DunedinPACE metric revealed a modest but statistically robust association between early‑adolescent restriction and accelerated ageing. Importantly, the relationship weakened after accounting for body‑mass‑index (BMI) and smoking, and mediation analysis confirmed that higher BMI partially explained the effect. This pattern suggests that restrictive eating may promote weight gain or metabolic dysregulation, which in turn speeds biological ageing—a pathway not captured by traditional mortality clocks.

The study’s implications extend beyond academic interest. Clinicians could consider epigenetic age as an early indicator of physiological stress in youths exhibiting restrictive eating, prompting timely nutritional and psychological interventions. Moreover, the differential sensitivity of third‑generation clocks underscores the need for refined biomarkers when assessing mental‑health‑related somatic risk. Future research should replicate these findings in larger, more diverse samples, incorporate repeated epigenetic measurements, and explore whether therapeutic remission of disordered eating can reverse accelerated ageing trajectories. Such work could pave the way for personalized prevention strategies that address both mental health and long‑term biological resilience.