Abstract
Background: Epigenetic clocks derived from DNA methylation patterns provide estimates of biological age, which may be modifiable by lifestyle factors. Chrononutrition, the timing of meals relative to circadian rhythms, is increasingly recognized as a potential modulator of health outcomes, but its effect on epigenetic aging remains unexplored.Methods: In a 12-week randomized controlled trial, 128 overweight adults (BMI 25–32 kg/m²) were assigned to either an early time-restricted feeding (eTRF) group (meals between 8:00 and 16:00) or a late TRF group (meals between 12:00 and 20:00). Blood DNA methylation was measured at baseline and week 12 using the Illumina EPIC array. Epigenetic age was calculated using five clocks: Horvath, Hannum, PhenoAge, GrimAge, and DNAmTL. Linear mixed models assessed changes in epigenetic age acceleration (ΔAgeAccel) between groups, adjusting for confounders.Results: The eTRF group showed a significant decrease in ΔAgeAccel for PhenoAge (mean difference: −1.8 years, 95% CI: −2.9 to −0.7, p = 0.002) and GrimAge (−1.5 years, 95% CI: −2.6 to −0.4, p = 0.008) compared to the late TRF group. No significant changes were observed for Horvath, Hannum, or DNAmTL clocks. Exploratory analyses revealed that the effect was more pronounced in participants with higher baseline BMI and later chronotype.Conclusions: Early time-restricted feeding may slow epigenetic aging, particularly for second-generation clocks that capture morbidity and mortality risk. These findings support the integration of chrononutrition into precision nutrition strategies for aging mitigation in overweight populations.
Keywords
Epigenetic clocks, chrononutrition, time-restricted feeding, biological age, DNA methylation, overweight, circadian rhythm, precision nutrition