LAUSR

Over the past 5 to 10 years, the opioid epidemic has become a national crisis in the United States. This emergency has led also to an increase in in utero exposure to opioids, with a subsequent rise in neonatal abstinence syndrome (NAS) in infants, a devastating syndrome that causes withdrawal symptoms and requires extensive treatment. Epigenetic modifications have been identified as one molecular mechanism that may contribute to the lasting neurodevelopmental effects observed in children exposed to opioids in utero. The OPRM1 gene codes for the μ opioid receptor and is a strong candidate for sensitivity to opioids. Many human genetic studies have found associations between this gene and opioid-use disorders, and animal research supports the role of this gene, using a variety of drugrelated behavioral models. Previous work by Wachman et al provided evidence that higher methylation levels in the OPRM1 gene promoter were present in infants who required pharmacological intervention for treatment. Recently in this Journal, the investigators replicate their findings in a sample of 58 mother-infant dyads recruited in a separate cohort, from whom DNA was collected. Higher levels of DNA methylation at several CpG sites in the OPRM1 promoter were observed in those infants who required pharmacological treatment, as found in the previous study. In addition, higher levels of methylation at some CpG sites were associated with longer stay in the hospital for the infants. These results have important implications for understanding the molecular mechanisms contributing to NAS, and provide a novel direction for the development of future treatments that may be specifically targeted to certain individuals, based on genetic status.