Association Between Maternal Adverse Childhood Experiences and Neonatal SCG5 DNA Methylation-Effect Modification by...

Area of Science:

• Epigenetics
• Developmental Psychology
• Neuroendocrinology

Background:

• Maternal childhood adversity and trauma can induce biological changes impacting offspring via epigenetic mechanisms like DNA methylation.
• Early life interventions, such as home visiting (HV) programs, may buffer these intergenerational effects.
• The secretogranin V (SCG5) gene plays a role in neuroendocrine function and may be a target of these epigenetic modifications.

Purpose of the Study:

• To investigate the association between maternal adverse childhood experiences (ACEs) and neonatal DNA methylation (DNAm) in the SCG5 gene.
• To examine whether prenatal home visiting (HV) modifies the relationship between maternal ACEs and offspring SCG5 DNAm.
• To explore intergenerational epigenetic inheritance in at-risk mother-child dyads.

Main Methods:

• A cohort of 53 mother-child pairs from the Pregnancy and Infant Development Study (Cincinnati, Ohio) was analyzed.
• Maternal ACEs were assessed via questionnaire during pregnancy.
• Infant buccal DNA methylation at four CpG sites in the SCG5 gene was measured 1 month postpartum; multivariable linear regression was employed.

Main Results:

• A higher number of maternal ACEs (more than 3) was significantly associated with lower offspring DNAm in the SCG5 gene (-5.79 percentage points).
• This association between maternal ACEs and neonatal SCG5 DNAm was significantly modified by the number of prenatal home visits received.
• Preliminary evidence indicates a differential relationship between maternal ACEs and offspring SCG5 DNAm based on the extent of prenatal HV.

Conclusions:

• Maternal adverse childhood experiences are associated with altered neonatal DNA methylation in the SCG5 gene.
• Prenatal home visiting may serve as a protective factor, modifying the epigenetic consequences of maternal adversity on offspring.
• These findings highlight the potential for early life interventions to mitigate the intergenerational transmission of stress-related epigenetic changes.