Epigenetic aging 4–10 years after a gestational diabetes mellitus pregnancy

Abstract

One study has revealed an association between GDM exposure and offspring age acceleration compared to non-GDM exposed offspring. This association has not been evaluated expansively. Our study seeks to expand this area of research to evaluate the association between exposure to a GDM pregnancy and accelerated epigenetic aging. This cohort included 137 mother-child dyads (GDM-OB = 66 mothers, 61 offspring; Normal Weight/NW = 71 mothers, 55 offspring) who gave birth 4–10 years before enrollment. Demographic characteristics and whole blood samples from mothers and offspring were collected. A MethylEPIC 850K array was performed. Epigenetic age and the residuals from age acceleration were calculated using the Horvath epigenetic clock. The mean epigenetic age of mothers in the GDM group was higher than the NW group (M = 48.4 ± 8.5; M = 43.4 ± 9.7; X2 = 15.8, P < .0001, respectively). Offspring of NW mothers had a higher epigenetic age than offspring of GDM mothers (M = 20.2 ± 7.7; M = 17.3 ± 8.4; X2 = 13.9, P = .0002, respectively). Mothers with a NW and GDM pregnancy had a strong positive correlation between chronological age and epigenetic age (r = 0.76, P = 1.8E-12; r = 0.72, P = <2.2E-16, respectively). NW and GDM offspring had moderate correlations between chronological age and epigenetic age (r = 0.43, P = .0011; r = 0.65, P = 1.3E-08, respectively). Mothers in the GDM group had a higher mean epigenetic age than mothers in the NW group. Offspring of NW Mothers had a higher average epigenetic age than offspring of GDM Mothers. Accelerated aging in pediatric populations remains an understudied area, enhancing the impact of quantification of methylation age vs. chronological age in mother-child dyads from our study.