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Can Home Visiting Services Modify the Impact of Maternal Adversity on Infant DNA Methylation?

Sat, March 23, 9:45 to 11:15am, Hilton Baltimore, Floor: Level 2, Key 10

Integrative Statement

Early childhood home visiting (HV) programs aim to mitigate early parenting stress and establish early nurturing relationships and secure attachments. Undermining these efforts are the early adverse environments experienced by mothers and their children. The field has become increasingly aware of the transgenerational effects of parental adversity, and emerging evidence points to epigenetic mechanisms as having a role in ‘programming’ early risks. Prenatal and postnatal exposures to adversity may elicit functional changes in gene expression controlled by DNA methylation (DNAm), potentially leading to alterations in developmental trajectories. Research has demonstrated an association between maternal prenatal objective stress (e.g., physical hardship, traumatic experiences) and offspring DNAm of the SCG5 (Secretogranin V) gene, which encodes a chaperone protein widespread in neuroendocrine tissues. Further, early life adversity has been associated with DNAm of the SLC6A4 gene; this gene encodes the serotonin transporter with implications for depression. Although epidemiologic relationships have been demonstrated, it is unknown whether HV programs can impact early epigenetic responses (e.g., DNAm) to adversity, potentially promoting more resilient phenotypes.

In this presentation, we will describe results from Pregnancy and Infant Development study conducted in a large HV program in Cincinnati, Ohio. The dose of prenatal HV was hypothesized to modify (i.e., buffer) the relationships between (1) maternal adverse childhood experiences (ACEs)—as a measure of life-course hardship— and offspring DNAm in the SCG5 gene promoter and (2) maternal depressive symptoms and offspring DNAm in the SLC6A4 gene promoter. We followed a cohort of 53 mother-child pairs enrolled in HV. Mothers completed ACE and depression (EPDS) measures prenatally, and infant buccal samples were collected for pyrosequencing at 1-month post-partum. Multivariable general linear models were used to examine the association between maternal ACEs (≥3 versus <3 ACEs), depressive symptoms, and infant SCG5 and SLC6A4 DNAm expressed as M-values averaged across 4 and 8 CpG sites, respectively. We tested for an interaction between maternal exposure variables and prenatal HV (≥ the median of 10 versus 1-9 visits).

A significant interaction was observed between the levels maternal ACEs and prenatal HV in predicting the outcome of SCG5 DNAm (interaction term: -1.09, 95% Confidence Interval [CI]: -1.91, -0.28; p=0.028). Similarly, a significant interaction was observed in which the effect of depressive symptoms on infant SLC6A4 DNAm was modified by the level of prenatal HV (interaction term: -0.14, 95% CI: -0.22, -0.06; p=0.0006). Interpretations and limitations will be discussed.

In a home visited population, preliminary evidence indicates that maternal ACEs and depressive symptoms have a relationship with offspring SCG5 and SLC6A4 DNAm that differs based on dose of prenatal HV. Protective factors such as HV delivered at a high intensity may contribute to protective epigenetic responses and phenotypes. Although the analyses were limited in scope and programs cannot yet integrate this information into practice, the evidence draws attention to the benefit of early enrollment and deleterious factors such as maternal trauma and depression. Large-scale epigenome-wide analyses are needed to elucidate the DNAm patterns that may signify risk/resilience to negative intergenerational effects.

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