Fetal Alcohol-Related Postnatal Growth Restriction Is Independent of Infant Feeding Practices and Postnatal Alcohol

Alexia C Edwards1,2, Sandra W Jacobson3,4,5, Marjanne Senekal4

  • 1Departments of Emergency Medicine and Pediatrics, Institute of Human Nutrition, Columbia University Vagelos College of Physicians and Surgeons, New York, NY 10032, USA.

Nutrients
|July 11, 2023
PubMed

Insights

Prenatal alcohol exposure (PAE) causes growth restriction. This study found that infant feeding practices and postnatal alcohol exposure did not influence this growth restriction, indicating a direct teratogenic effect of PAE.

Area of Science:

  • Obstetrics and Gynecology
  • Pediatrics
  • Public Health

Background:

  • Prenatal alcohol exposure (PAE) is a known cause of fetal growth restriction.
  • The influence of postnatal nutrition and breast milk alcohol exposure on growth deficits remains unclear.

Purpose of the Study:

  • To compare infant feeding practices between heavy drinkers and controls.
  • To investigate if feeding practices confound fetal alcohol growth restriction.
  • To determine the impact of postnatal alcohol exposure via breast milk on infant growth.

Main Methods:

  • Recruited pregnant women (heavy drinkers and controls) in Cape Town, South Africa.
  • Assessed alcohol and substance use, and infant feeding practices (e.g., breastfeeding, formula feeding).
  • Measured infant anthropometry (weight, length, head circumference) from 2 weeks to 5 years.

Main Results:

  • No significant differences in breastfeeding duration, exclusivity, formula feeding, or complementary feeding practices were observed between groups.
  • PAE was consistently associated with poorer postnatal anthropometry across all measured time points.
  • Postnatal alcohol exposure through breast milk did not impact anthropometry after accounting for PAE.

Conclusions:

  • Fetal alcohol-related growth restriction is not explained by differences in infant feeding practices or postnatal alcohol exposure.
  • The observed growth deficits are likely a direct teratogenic consequence of prenatal alcohol exposure.