Epigenetic clocks have been suggested to capture one feature of the complexity between aging and the epigenome. However, little is known about the epigenetic clock in childhood allergy and asthma.
To examine associations of DNA methylation age (DNAmAge) and epigenetic age acceleration with childhood allergy and asthma.
We calculated DNAmAge and age acceleration at birth, early and mid-childhood based on IlluminaHumanMethylation450BeadChip in Project Viva. We evaluated epigenetic clock associations with allergy and asthma using covariate-adjusted linear- and logistic-regressions. We attempted to replicate our findings in the 'Genetics of Asthma in Costa Rica Study'.
At mid-childhood (mean age=7.8 years) in Project Viva, DNAmAge and age acceleration were cross-sectionally associated with higher total serum IgE, and greater odds of atopic sensitization. Every 1-year increase in intrinsic epigenetic age acceleration was associated with a 1.22 (95% CI [1.07-1.39]), 1.17 (95% CI [1.03-1.34]), and 1.29 (95% CI [1.12-1.49]) higher odds of atopic sensitization, environmental and food allergen sensitization. DNAmAge and extrinsic epigenetic age acceleration were also cross-sectionally associated with current asthma at mid-childhood. DNAmAge and age acceleration at birth and early-childhood were not associated with mid-childhood allergy or asthma. The mid-childhood association between age acceleration and atopic sensitization were replicated in an independent dataset.
As the epigenetic clock may reflect the immuno-and-developmental components of biological aging, our study suggests pathways through which molecular epigenetic mechanisms of immunity, development and maturation may interact along the age-axis, and associate with childhood allergy and asthma by mid-childhood.