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Background: Animal models have demonstrated that maternal nutrition can alter fetal vulnerability to prenatal alcohol exposure (PAE). Few human studies have examined the role of nutrition in fetal alcohol spectrum disorders (FASD)., Objectives: Our objectives were to examine whether fetal vulnerability to PAE-related growth restriction is modified by: 1) rate of gestational weight gain; or prenatal dietary intakes of 2) energy, 3) iron, or 4) choline., Methods: In a prospective longitudinal birth cohort in Cape Town, South Africa, 118 heavy-drinking and 71 abstaining/light-drinking pregnant women were weighed and interviewed regarding demographics, alcohol, cigarette/other drug use, and diet at prenatal visits. Infant length, weight, and head circumference were measured at 2 wk and 12 mo postpartum., Results: Heavy-drinking mothers reported a binge pattern of drinking [Mean = 129 mL (∼7.2 drinks)/occasion on 1.3 d/wk). Rate of gestational weight gain and average daily dietary energy, iron, and choline intakes were similar between heavy-drinking women and controls. In regression models adjusting for maternal age, socioeconomic status, cigarette use, and weeks gestation at delivery, PAE [ounces (30 mL) absolute alcohol per day] was related to smaller 2-wk length and head circumference and 12-mo length, weight, and head circumference z-scores (β = -0.43 to -0.67; all P values <0.05). In stratified analyses for each maternal nutritional measure (inadequate compared with adequate weight gain; tertiles for dietary energy, iron, and choline intakes), PAE-related growth restriction was more severe in women with poorer nutrition, with effect modification seen by weight gain, energy, iron, and/or choline for several anthropometric outcomes., Conclusions: Gestational weight gain and dietary intakes of energy, choline, and iron appeared to modify fetal vulnerability to PAE-related growth restriction. These findings suggest a need for screening programs for pregnant women at higher risk of having a child with FASD to identify alcohol-using women who could benefit from nutritional interventions., (© The Author(s) 2022. Published by Oxford University Press on behalf of the American Society for Nutrition.)

Background: Prenatal alcohol exposure (PAE) is associated with postnatal iron deficiency (ID), which has been shown to exacerbate deficits in growth, cognition, and behavior seen in fetal alcohol spectrum disorders. However, the mechanisms underlying PAE-related ID remain unknown., Objectives: We aimed to examine biochemical measures of iron homeostasis in the mother, placenta, neonate, and 6.5-month-old infant., Methods: In a prenatally recruited, prospective longitudinal birth cohort in South Africa, 206 gravidas (126 heavy drinkers and 80 controls) were interviewed regarding alcohol, cigarette, and drug use and diet at 3 prenatal visits. Hemoglobin, ferritin, and soluble transferrin receptor (sTfR) were assayed twice during pregnancy and urinary hepcidin:creatinine was assayed once. Infant ferritin and hemoglobin were measured at 2 weeks and 6.5 months and sTfR was measured at 6.5 months. Histopathological examinations were conducted on 125 placentas and iron transport assays (iron regulatory protein-2, transferrin receptor-1, divalent metal transporter-1, ferroportin-1, and iron concentrations) were conducted on 63., Results: In multivariable regression models, prenatal drinking frequency (days/week) was related to higher maternal hepcidin and to sequestration of iron into storage at the expense of erythropoiesis in mothers and neonates, as evidenced by a lower hemoglobin (g/dL)-to-log(ferritin) (ug/L) ratio [mothers: raw regression coefficient (β) = -0.21 (95% CI: -0.35 to -0.07); neonates: β = -0.15 (95% CI: -0.24 to -0.06)]. Drinking frequency was also related to decreased placental ferroportin-1:transferrin receptor-1 (β = -0.57 for logged values; 95% CI: -1.03 to -0.10), indicating iron-restricted placental iron transport. At 6.5 months, drinking frequency was associated with lower hemoglobin (β = -0.18; 95% CI: -0.33 to -0.02), and increased prevalences of ID (β = 0.09; 95% CI: 0.02-0.17) and ID anemia (IDA) (β = 0.13; 95% CI: 0.04-0.23). In causal inference analyses, the PAE-related increase in IDA was partially mediated by decreased neonatal hemoglobin:log(ferritin), and the decrease in neonatal hemoglobin:log(ferritin) was partially mediated by decreased maternal hemoglobin:log(ferritin)., Conclusions: In this study, greater PAE was associated with an unfavorable profile of maternal-fetal iron homeostasis, which may play mechanistic roles in PAE-related ID later in infancy., (© The Author(s) 2021. Published by Oxford University Press on behalf of the American Society for Nutrition.)

In recent years a number of semi-automated and automated segmentation tools and brain atlases have been developed to facilitate morphometric analyses of large MRI datasets. These tools are much faster than manual tracing and demonstrate excellent test-retest reliabilities. Reliabilities of automated segmentations relative to "gold standard" manual tracings have, however, been shown to vary by brain region and in different cohorts. It remains uncertain to what extent smaller brain volumes and potential changes in grey/white matter contrasts in paediatric brains impact on the performance of automated methods, and how pathology may influence performance. This study examined whether using data from automated FreeSurfer segmentation would alter our ability, compared to manual segmentation, to detect prenatal alcohol exposure (PAE)-related volume changes in subcortical regions and the corpus callosum (CC) in pre-adolescent children. High-resolution T1-weighted images were acquired, using a sequence optimized for morphometric neuroanatomical analysis, on a Siemens 3T Allegra MRI scanner in 71 right-handed, 9- to 11-year-old children (27 fetal alcohol syndrome (FAS) and partial FAS (PFAS), 25 non-syndromal heavily exposed (HE) and 19 non-exposed controls) from a high-risk community in Cape Town, South Africa. Data from timeline follow-back interviews administered to the mothers prospectively during pregnancy were used to quantify the amount of alcohol (in ounces absolute alcohol per day, AA/day) that the children had been exposed to prenatally. Volumes of corpus callosum (CC) and bilateral caudate nuclei, hippocampi and nucleus accumbens (NA) were obtained by manual tracing and automated segmentation using both FreeSurfer versions 5.1 and 6.0. Reliability across methods was assessed using intraclass correlation (ICC) estimates for consistency and absolute agreement, and Cronbach's α. Ability to detect regions showing PAE effects was assessed separately for each segmentation method using ANOVA and linear regression of regional volumes with AA/day. Our results support findings from other studies showing excellent reliability across methods for easy-to-segment structures, such as the CC and caudate nucleus. Volumes from FreeSurfer 6.0 were smaller than those from version 5.1 in all regions except the right caudate, for which they were similar, and right hippocampus and CC, for which they were larger. Despite poor absolute agreement between methods in the NA and hippocampus, all three segmentation methods detected dose-dependent volume reductions in regions for which reliabilities on ICC consistency across methods reached at least 0.70, namely the CC, and bilateral caudate nuclei and hippocampi. PAE-related changes in the NA for which ICC consistency did not reach this minimum were inconsistent across methods and should be interpreted with caution. This is the first study to demonstrate in a pre-adolescent cohort the ability of automated segmentation with FreeSurfer to detect regional volume changes associated with pathology similar to those found using manual tracing., (Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.)

Prenatal alcohol exposure (PAE) is associated with a range of physical, cognitive, and behavioral problems, particularly in arithmetic. We report ERP data collected from 32 infants (mean age = 6.8 mo; SD = 0.6; range = 6.1-8.1; 16 typically developing [TD]; 16 prenatally alcohol-exposed) during a task designed to assess error detection. Evidence of error monitoring at this early age suggests that precursors of the onset of executive control can already be detected in infancy. As predicted, the ERPs of the TD infants, time-locked to the presentation of the solution to simple arithmetic equations, showed greater negative activity for the incorrect solution condition at middle-frontal scalp areas. Spectral analysis indicated specificity to the 6-7 Hz frequency range. By contrast, the alcohol-exposed infants did not show the increased middle-frontal negativity seen in the TD group nor the increased power in the 6-7 Hz frequency, suggesting a marked developmental delay in error detection and/or early impairment in information processing of small quantities. Overall, our research demonstrates that (a) the brain network involved in error detection can be identified and highly specified in TD young infants, and (b) this effect is replicable and can be utilized for studying developmental psychopathology at very early ages., (Copyright © 2019 The Author(s). Published by Elsevier Ltd.. All rights reserved.)