Maternal Obesity’s Impact on Newborn DNA and Childhood Obesity
Childhood obesity rates in the United States have been on the rise, with approximately 19.7% of children being affected. Maternal pre-pregnancy overweight or obesity (OWO) is a recognized risk factor for childhood obesity, especially in racial minorities. However, the link between maternal obesity and the risk of childhood obesity remains unclear, with conflicting results from previous studies.
To shed light on this topic, a recent study published in BMC Medicine investigated the impact of maternal pre-pregnancy obesity on newborn cord blood DNA methylation and its potential role in intergenerational obesity risk. The study focused on a high-risk demographic in the United States by utilizing data from the Boston Birth Cohort, which predominantly consists of urban and low-income minorities.
The study included 903 mother-child pairs, with cord blood samples collected from the newborns. DNA methylation was measured in these samples, and the children’s body mass index (BMI) was analyzed from birth to 18 years of age. Maternal pre-pregnancy BMI and smoking habits during pregnancy were also taken into account.
The findings revealed that there were eight specific DNA methylation sites associated with maternal BMI, corresponding to six genes. One of the genes, tumor protein P53 inducible nuclear protein 1 (TP53INP1), showed the highest hypermethylated difference with every increase in maternal BMI. Other hypermethylated sites were observed in the phosphatase and tensin homolog (PTEN) and KILLIN genes. Hypomethylated genes were found in newborns born to mothers with higher BMIs, including the alpha- and gamma-adaptin binding protein (AAGAB), alpha kinase 1 (ALPK1), and excision repair cross-complementation group 8 (ERCC8) genes.
Overall, 481 DNA methylation sites in newborns were associated with maternal BMI, with links to hematocrit, triglycerides, and tobacco use disorder. However, none of these sites had a significant effect on the association between maternal BMI and birth weight. On the other hand, 14 DNA methylation sites had a significant mediation effect on the association between maternal BMI and childhood obesity. These sites mediated the association between maternal BMI and offspring overweight/obesity at different ages, with mediation proportions ranging from 4.38% to 25.21%.
It is worth noting that maternal smoking did not have a significant mediation effect on methylation at any of the identified sites.
This study provides valuable insights into the potential epigenetic influences of maternal pre-pregnancy obesity on the risk of childhood obesity. By understanding these mechanisms, targeted interventions can be developed to address the intergenerational cycle of obesity. However, further research is needed, especially in underrepresented racial groups, to gain a comprehensive understanding of the epigenetic factors contributing to childhood obesity.
This study contributes to the growing body of evidence highlighting the importance of maternal health before pregnancy in shaping the health outcomes of future generations. By addressing maternal obesity, we can potentially reduce the risk of childhood obesity and promote healthier lives for our children.
