Background: Early life stress exposure in preterm infants may alter DNA methylation of NR3C1 and HSD11B2, disrupting neurobehaviors needed for oral feeding (PO) skill development.
Purpose: To (1) examine the feasibility of the study protocol; (2) describe early life stress, DNA methylation of NR3C1 and HSD11B2, and PO skill development; and (3) explore the association between DNA methylation of NR3C1 and HSD11B2 and infant characteristics, early life stress, and PO skill development.
Method: We employed a longitudinal descriptive pilot study (N = 10). Infant characteristics were collected from the infant's electronic medical record. Early life stress was assessed via the modified Neonatal Infant Stressor Scale. DNA methylation of NR3C1 exon 1F and HSD11B2 promoter regions was analyzed from the infant's buccal samples. PO skill development was evaluated using the Early Feeding Skills Assessment.
Results: Infants who experienced more acute and chronic stress during their neonatal intensive care unit hospitalization demonstrated higher DNA methylation at CpG 17 and 31 of the NR3C1 exon 1F and at CpG 4 and 28 of the HSD11B2 promoter regions. Infants with higher DNA methylation at these CpG sites also exhibited less optimal PO skill development and experienced longer transition from first to full PO.
Implications for practice and research: Our findings revealed relationships among early life stress, DNA methylation of NR3C1 and HSD11B2, and PO skill development in preterm infants. Future research is warranted to examine the multiomics pathways whereby early life stress influences the phenotypes of infant outcomes.
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