Infant Mental Health Home Visiting Buffers the Effect of Methylation on Infants’ Socioemotional Health

• In Event: Parenting intervention

Abstract

Infants born to parents with childhood or current adversity are at heightened risk of negative socioemotional outcomes (Bale, 2014; Park et al., 2019). Recent research has sought to understand how early exposure to stress affects risk for health and mental health outcomes over the lifetime and across generations (DeSocio, 2018). Methylation of DNA is an epigenetic mechanism thought to be linked to environmental stress and adversity (DeSocio, 2018). Methylation can regulate gene transcription, changes throughout development and can be altered by changes in the environment. Methylation of the NRC31 gene that codes for glucocorticoid receptors (GRs) is among the most studied. Traditionally, methylation of the NRC31 gene is thought to suppresses the expression of GRs, thereby harming the feedback loop that reduces the hypothalamic-pituitary-adrenal (HPA) axis when cortisol levels remain too high for too long (DeSocio, 2018). Oberlander and colleagues (2008) found that prenatal exposure to maternal depression in the third trimester of pregnancy was associated with increased NRC31 methylation and increased salivary cortisol stress response at 3 months. High levels of cortisol are toxic to the developing brain, resulting in disruptions in the brain structures that regulate behavior and emotions (Bock et al., 2014). Methylation of NRC31 is associated with internalizing behavior in preschoolers (Parade et al., 2016).

Research on interventions that disrupt the intergenerational transmission of the negative effects of adversity are nascent. The Michigan Model of Infant Mental Health Home Visiting (IMH-HV) is a needs-driven dyadic intervention focused on improving the quality of the parent-child relationship. The current study sought to examine the effect of IMH-HV on the relationship between toddlers’ NRC31 methylation and their socioemotional competence in a randomized-controlled trial.

Participants included a sample of 44 parents and toddlers randomly assigned to receive 12 months of IMH-HV treatment or to a control group. Toddler socioemotional competence was measured via parental report using the Brief Infant-Toddler Social Emotional Assessment (BITSEA; Briggs-Gowan et al., 2004), a 44-item parent-report measure for children ages 12–35 months. At 12 months post-enrollment, saliva samples were collected from children using Oragene kits (DNA Genotek). Methylation of the exon 1F region of the glucocorticoid receptor, NRC31, was measured via pyrosequencing. Eight methylation sites were assayed, and percent methylation at each site was averaged for each child.

The overall regression model including child methylation, treatment, and an interaction term between methylation and treatment predicting child socioemotional competence was significant, F (3, 40) = 5.94, p = .05, R2 = .17. Moderation analysis revealed a significant interaction effect of IMH-HV treatment on the relationship between children’s methylation of NRC31 and their parent-reported socioemotional competence, F (1, 40) = 6.77, p = .013, R2 = .14). Simple slopes revealed that in the absence of treatment, methylation of NRC31 predicts lower socioemotional competence (b = -.37, p = .03). However, this effect is not seen for children in the treatment group (b = .33, p > .1), suggesting that IMH-HV treatment appears to buffer the effect of NRC31 methylation on children’s socioemotional outcomes.

Group Authors

Michigan Collaborative for Infant Mental Health Research

Authors

• Julie Ribaudo, University of Michigan - Ann Arbor
  Presenting Author

• Jamie Lawler, Eastern Michigan University

• Rebekah L. Petroff, University of Michigan

• Jaclyn M. Goodrich, University of Michigan

• Maria Muzik, University of Michigan - Ann Arbor

• Katherine L Rosenblum, University of Michigan - Ann Arbor