Abstract
The prenatal period represents a critical time for brain growth and development. These rapid neurological advances render the fetus susceptible to various influences with life-long implications for mental health. Maternal distress signals are a dominant early life influence, contributing to birth outcomes and risk for offspring psychopathology. This prospective longitudinal study evaluated the association between prenatal maternal distress and infant white matter microstructure. Participants included a racially and socioeconomically diverse sample of 85 mother-infant dyads. Prenatal distress was assessed at 17 and 29 weeks' gestational age (GA). Infant structural data were collected via diffusion tensor imaging at 42-45 weeks' postconceptional age. Findings demonstrated that higher prenatal maternal distress at 29 weeks' GA was associated with increased fractional anisotropy (b = .283, t(64) = 2.319, p = .024) and with increased axial diffusivity (b = .254, t(64) = 2.067, p = .043) within the right anterior cingulate white matter tract. No other significant associations were found with prenatal distress exposure and tract fractional anisotropy or axial diffusivity at 29 weeks' GA, nor earlier in gestation.
Highlights
The developmental origins of health and disease (DOHaD) or the fetal origins of adult disease (FOAD) models posit that environmental exposures early in development, and during intrauterine life, have lasting implications for health and disease across the life span (Barker, 1990, 1994, 1994, 1995; Gluckman & Hanson, 2004)
This association between maternal distress at 29 weeks’ gestational age (GA) and higher fractional anisotropy in the right anterior cingulate remained after considering gestational age at birth (GAB), BW percentile, and income-to-needs ratio (INR) in the regression, b = .283, t (64) = 2.319, p = .024 (Figure 3a)
The DOHaD/FOAD hypothesis highlights the importance of fetal experiences for shaping developmental trajectories with long-term consequences for health and well-being
Summary
The developmental origins of health and disease (DOHaD) or the fetal origins of adult disease (FOAD) models posit that environmental exposures early in development, and during intrauterine life, have lasting implications for health and disease across the life span (Barker, 1990, 1994, 1994, 1995; Gluckman & Hanson, 2004). Prenatal maternal symptoms of distress predict later infant and child psychopathology and risk mechanisms even when maternal symptoms of distress are subclinical and below diagnostic categorical thresholds (Glynn, Howland, & Fox, 2018; O’Connor, Monk, & Fitelson, 2014; Sandman, Buss, Head, & Davis, 2015) These findings highlight the importance of investigating the intergenerational consequences of maternal distress from a transdiagnostic perspective as supported by the National Institute of Mental Health’s research domain criteria (RDoC) initiative (Gao et al, 2021; Insel et al, 2010). Accumulating evidence across experimental studies in rodents and observational studies in humans have demonstrated that postnatal stress exposure, when experienced during early life, is associated with variability in the structure and function of frontolimbic and temporal circuitry (for review see Chen & Baram, 2016; McLaughlin, Weissman, & Bitrán, 2019) These neural circuits are important for affective processing, including the evaluation of social stimuli and emotion regulation (Dannlowski et al, 2012; Hartley & Phelps, 2010). A recent longitudinal study of normative early childhood brain circuit maturation has reported widespread increases in fractional anisotropy, as well as decreases in radial diffusivity and axial diffusivity, between birth and 1 year of age for the major white matter tracts (Stephens et al, 2020)
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