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Parental Conflict from Pregnancy Onward and Preadolescent Brain Development: The Mediating Role of Child Problem Behavior

Sat, March 23, 12:45 to 2:15pm, Baltimore Convention Center, Floor: Level 3, Room 322

Integrative Statement

Background: Research consistently suggests that parental conflict, has a negative impact on children’s development. Numerous studies have documented an impact of exposure to parental conflict on children’s immediate and long-term emotional responses, but why effects persist and when children are most vulnerable is less clear. As a potent stressor, parental conflict interferes with children’s abilities to regulate stress physiology and may be associated with brain development. However, neuroimaging assessments of children exposed to parental conflict have been limited. In this talk, we present evidence of how parental conflict in different childhood periods is related to pre-adolescent brain morphology. We hypothesized that children exposed to parental conflict early in life show differences in subcortical areas. We also test the mediating role of childhood emotional problems.
Methods: This study was embedded in Generation R, a population-based cohort followed from fetal life onwards. This study includes 2,615 children with parental conflict and neuroimaging data. Parental conflict was repeatedly assessed by the subscale General Functioning of the Family Assessment Device, a validated measure consisting of 12 items. Mothers completed the questionnaire at 20 weeks pregnancy, at child age 5 and 10 years, fathers assessed conflict prenatally and at age 10. High-resolution structural neuroimaging data were collected using a single 3-Tesla MRI system when children were 10 years old. Imaging data were processed through FreeSurfer. Child emotional problems were assessed with the Child Behavior Checklist at age 3 years by the mother. The prospective associations between parental conflict and child neuroimaging measures were determined with linear regressions and mixed models. We formally tested if child problem behavior explained the association of prenatal parental conflict and hippocampal volume with mediation models. Regression models were adjusted for potential confounders, including socioeconomic factors and maternal psychopathology. False discovery rate was utilized to correct for multiple comparisons.
Results: Prenatal parental conflict was associated with less gray matter B = -5.24 (95% CI: -10.1, -0.41, p =.034); and a smaller hippocampal volume B = -0.08 (95% CI: -0.13, -0.02, p = .004) in preadolescence. There was no evidence for an association of exposure to parental conflict at ages 5 and 10 years with brain morphology. Repeated measures analyses showed an interaction with time of conflict assessment; i.e. only effects of the prenatal assessment. Effect sizes were smaller for paternal ratings. The association of prenatal parental conflict with hippocampal volume was mediated by child problem behavior at age 3, however, the indirect effect explained approximately about 15% of the total effect.
Conclusions: This cohort study from fetal life forward suggests that high levels of prenatal parental conflict in early life are related to brain development during childhood. In particular the hippocampus development may be affected. This study cannot establish whether these associations result from prenatal or child exposure before age 5 years. These associations were partly mediated by child emotional problems, a well-documented consequence of parental conflict. Our results my help better understand why parental conflict has such long-term and persisting effects and underscore the importance of very early interventions.

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