Abstract

Individuals with prenatal alcohol exposure (PAE) exhibit neurological deficits associated with brain injury including smaller brain volumes. Additional risk factors such as lower socioeconomic status (SES) may also have an impact on brain development for this population. This study examined how brain volumes are related to SES in both neurotypically developing children and adolescents, and those with PAE. 3D T1-weighted MPRAGE images were acquired from 69 participants with PAE (13.0 ± 3.2 years, range 7.1–18.8 years, 49% female) and 70 neurotypical controls (12.4 ± 2.9 years, range 7.0–18.5 years, 60% female) from four scanning sites in Canada. SES scores calculated using Hollingshead’s Four-Factor Index of Social Status from current caregiver placement were not significantly different between groups, though more children with PAE had lower SES scores compared to controls. Psychometric data comprised 14 cognitive measures, including executive functioning, attention and working memory, memory, math/numerical ability, and word reading. All cognitive scores were significantly worse in children with PAE compared to controls, though SES was not correlated with cognitive scores in either group after correction for multiple comparisons. All 13 brain volumes were smaller in children with PAE compared to children in the control group. Higher SES was associated with larger hippocampus and amygdala volumes in controls, but there were no such associations in children with PAE. Direct evaluation of the interaction between SES and diagnostic group did not show a significant differential impact of SES on these structures. These findings support previous links between SES and brain volumes in neurotypically developing children, but the lack of such a relationship with SES in children with PAE may be due to the markedly smaller brain volumes resulting from the initial brain injury and postpartum brain development, regardless of later SES.

Highlights

  • Prenatal alcohol exposure (PAE) is associated with a range of lifelong physical, cognitive, and neurological impacts, and may result in a diagnosis of fetal alcohol spectrum disorder (FASD; Cook et al, 2016; Hoyme et al, 2016; Mattson et al, 2019)

  • socioeconomic status (SES) did not differ significantly across prenatal alcohol exposure (PAE) subgroups, though the SES range was somewhat restricted in the PAE-only subgroup (44 ± 13, range 28–66) compared to the fetal alcohol syndrome (FAS)/partial fetal alcohol syndrome (pFAS) (44 ± 16, range 17–66) and alcohol-related neurodevelopmental disorder (ARND) subgroups (42 ± 14, range 11–65)

  • Current caregiving arrangement differed significantly between groups, with most children in the control group (n = 69, 99%) living with their biological parent(s), compared to only 9% (n = 6) of those with PAE, and the rest residing in adoptive families (n = 42, 61%), foster care placements (n = 12, 17%), or with other legal guardians (n = 7, 13%)

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Summary

Introduction

Prenatal alcohol exposure (PAE) is associated with a range of lifelong physical, cognitive, and neurological impacts, and may result in a diagnosis of fetal alcohol spectrum disorder (FASD; Cook et al, 2016; Hoyme et al, 2016; Mattson et al, 2019). PAE can impact any stage of fetal development, with studies suggesting that structural impacts are associated with the developmental timing of exposure (see reviews by Jones, 2011; Mattson et al, 2019). PAE can trigger a range of additional impacts such as maternal hypoxia, oxidative stress, displacement or malabsorption of essential nutrients, and altered metabolism, all of which can further alter fetal brain development (for reviews see Goodlett and Horn, 2001; Young et al, 2014; del Campo and Jones, 2017). General population prevalence for FASD ranges from 2 to 5%, the disability is thought to occur more frequently in communities marked by socioeconomic disadvantage (May et al, 2014, 2018; Lange et al, 2017; Popova et al, 2019a,b)

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