In Utero Exposure to Cardiometabolic Complications and Epigenetic Age Acceleration in Late Adolescence — The Association Specialists
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In Utero Exposure to Cardiometabolic Complications and Epigenetic Age Acceleration in Late Adolescence (23764)

Eskedar Mekonnen 1 , Phillip Melton 2 , Sarah Cohen-Woods 3 , Julia Liu 1 , Tina Bianco-Miotto 4 , Jessica Grieger 1
  1. School of Medicine, College of Health, Adelaide, SA, Australia
  2. Menzies Institute for Medical Research, College of Health and Medicine, University of Tasmania, Hobart, Tasmania, Australia
  3. Flinders University Institute for Mental Health and Wellbeing, College of Education, Psychology, and Social Work, Flinders University, Adelaide, SA, Australia
  4. School of Agriculture, Food and Wine, College of Science, Adelaide, SA, Australia

Background: Prenatal exposure to cardiometabolic complications, such as gestational diabetes mellitus (GDM), pregnancy-induced hypertension (PIH), and high maternal BMI, may accelerate biological ageing in offspring, increasing their risk of chronic disease.

 

Methods: Data on GDM, PIH, and maternal BMI were obtained from the Raine Study. Whole blood samples from 1,192 offspring of Gen 1 at the 17-year follow-up were analysed to estimate eight epigenetic age clocks. Pearson correlation evaluated the relationship between epigenetic clocks and maternal pre-pregnancy BMI. Independent t-tests and ANOVA were used to examine differences in epigenetic age between exposed and non-exposed offspring to GDM, PE and maternal obesity, after adjusting for multiple testing. Linear regression modelled associations between epigenetic age acceleration and GDM, PE and maternal BMI.

 

Results: Maternal BMI positively correlated with offspring GrimAge and DunedinPACE. For each 1 kg/m² increase in maternal BMI, offspring demonstrated accelerated biological ageing, reflected by a 0.004-year increase in the pace of ageing (DunedinPACE), a 0.06-year increase in GrimAge, and a 0.004-year decrease in telomere age. In sex-stratified analyses, each 1 kg/m² increase in maternal BMI was associated with accelerated Hannum age, GrimAge, DunedinPACE, and telomere age in female offspring. No significant differences in epigenetic ageing measures were observed among offspring exposed to GDM or PIH.

 

Conclusions: Offspring exposed to maternal obesity show accelerated ageing, while no significant effects were observed from exposure to GDM or PIH. These findings highlight the importance of promoting a healthy pre-pregnancy weight to enhance biological longevity and mitigate the risk of chronic illnesses in offspring.