Boston Birth Cohort study finds that maternal pre-pregnancy obesity alters newborn DNA methylation, potentially increasing the risk of obesity in the child. The research targets high-risk U.S. demographics and could guide future interventions for childhood obesity.
By Vijay Kumar MalesuAug 27 2023Reviewed by Benedette Cuffari, M.Sc. In a recent study published in the journal BMC Medicine, researchers investigate the impact of maternal pre-pregnancy overweight or obesity on newborn cord blood deoxyribonucleic acid methylation and its potential role in intergenerational obesity risk in a high-risk United States demographic.
Despite suggestions that maternal obesity may cause epigenetic alterations that influence child obesity, there remains a lack of conclusive research supporting these claims. To date, only a few studies have linked maternal body mass index , fetal DNAm, and childhood BMI, whereas other studies have reported differing results and often overlooked notable risk factors like smoking.
BBC specifically targeted low birthweight and premature births for its study. Mothers provided data regarding their socio-demographics, lifestyle habits, and medical histories following delivery. The analytical methodology involved comparing the demographics of newborns to maternal pre-pregnancy BMI, identifying differentially methylated sites linked to maternal BMI, and executing mediation analyses. The mediation analysis aimed to determine the extent to which the influence of maternal BMI on child obesity risk was due to methylation at a specific locus.
Eight CpG sites corresponded to six genes and were significantly associated with maternal BMI. The highest hypermethylated difference for each single unit increase in maternal BMI was related to the tumor protein P53 inducible nuclear protein 1 gene. Other notable hypermethylated CpG sites were observed in the phosphatase and tensin homolog and KILLIN genes.
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