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Review
. 2022 May 9;80(6):1568-1579.
doi: 10.1093/nutrit/nuab119.

Effects of nutrition and gestational alcohol consumption on fetal growth and development

Vishal D Naik  1 , Jehoon Lee  2 , Guoyao Wu  3 , Shannon Washburn  2 , Jayanth Ramadoss  1   4
Affiliations
Review

Effects of nutrition and gestational alcohol consumption on fetal growth and development

Vishal D Naik et al. Nutr Rev. .

Abstract

Fetal alcohol exposure can lead to a range of developmental disorders, including impaired fetal growth and development of multiple organ systems. These disorders are grouped under the term fetal alcohol spectrum disorders (FASDs). Adequate nutrition and a conducive intrauterine environment are essential for healthy fetal development. Nutrient deficiencies resulting from inadequate maternal nutrient ingestion may be compounded by alcohol-induced altered nutrient metabolism, placental clearance, and malabsorption. Alcohol-induced alteration of the intrauterine environment is the main source of developmental deficits and nutritional insufficiencies can worsen the effects on fetal development. In this review, we discuss studies examining the collective and interactive effects of nutrition (specifically iron, selenium, vitamin A, thiamine, zinc, folate, vitamin B12, choline, and amino acids) relative to gestational alcohol consumption and its effects on fetal growth and development. We also summarize scientific reports that tested potential benefits of micronutrient supplementation in animal models of fetal alcohol spectrum disorders and in humans. In summary, the deleterious effects of alcohol exposure in relation to nutrient homeostasis further validate that avoidance of alcohol consumption during pregnancy is the most effective way to mitigate the teratogenic effects of alcohol.

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Figures

Figure 1
Figure 1
Reduced iron status and body growth in rat offspring of iron-deficient (ID) dams. (A–D) ID offspring are anemic at postnatal day (P) 10, but iron repletion normalizes their iron status by P35. Hematocrit (A), hemoglobin (B), liver iron (C), and brain iron (D) in iron-sufficient (IS) or ID offspring at P10 and/or P35. Dashed lines indicate the normal reference range for nonpregnant adults and do not fully apply to growing animals (n = 5–13 rats per treatment group at each time point). (E, F) Effect of maternal ID and postnatal alcohol on body weight of P10 and P35 male (E) and female (F) pups treated with indicated alcohol dose (n ≥ 22 rats per treatment group per sex). (G, H) Alcohol significantly diminished male (G) and female (H) whole brain weight on P10 and P35, which was not further altered by iron status (n ≥ 5 rats per treatment group per sex). *Significantly different from age-matched IS pups receiving the same alcohol dose; †significantly different from age-matched animals receiving 0 g/kg alcohol within the same iron status. Abbreviation: Alc, alcohol. Adapted from Rufer et al
Figure 2
Figure 2
Ovine fetal ultrasonographic parameters on gestational day (GD) 76. Values are reported as mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001. Adapted with permission from Sawant et al
Figure 3
Figure 3
The ethanol–glutamine model illustrating putative maternal amino acid homeostatic responses to an acute challenge of ethanol after chronic exposure. The kidney acts as a major sink for glutamine during ethanol-induced acidosis. Increased renal extraction of plasma glutamine results in decreased availability of arginine and citrulline, whose syntheses are glutamine dependent. Acidemia-induced elevations in renal glutamine SNAT3 transporter expression result in increased renal uptake of histidine and asparagine. In the muscle, ethanol-induced acidosis upregulates the transamination of branched-chain amino acids (BCAAs) with α-ketoglutarate to form glutamate and branched-chain α-ketoacids (BCKAs) and also directly stimulates the oxidative catabolism of BCKAs, leading to decreased plasma levels of BCAAs. Adapted with permission from Ramadoss et al
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