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Published on: December 14, 2014
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.
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.
Abstract:
Prenatal alcohol exposure (PAE) causes growth restriction that worsens in the first year of life. However, the roles of postnatal nutrition in fetal alcohol growth restriction and the impact of postnatal alcohol exposure via breastmilk on growth remain unknown. We aimed to compare infant feeding practices during the first 6.5 months of life between heavy drinkers and abstainers/light drinkers, to examine whether these practices play confounding roles in fetal alcohol growth restriction, and to determine the impact of postnatal alcohol exposure via breastmilk on growth. Eighty-seven heavy-drinking pregnant women and 71 abstainers/light drinkers (controls) were recruited prenatally from antenatal clinics in Cape Town, South Africa. Demographic background and alcohol, cigarette, marijuana, and methamphetamine use during pregnancy were assessed pre- and postnatally. Infant feeding practices were assessed at 6.5 months postpartum using the USDA Infant Feeding Questionnaire. Infant weight, length, and head circumference were measured at 2 weeks, 6.5 and 12 months, and 5 years. Neither prenatal nor postnatal alcohol consumption was related to the duration of breastfeeding, exclusive breastfeeding, exclusive formula, or mixed feeding. Complementary feeding practices were remarkably similar between exposure groups. PAE was related to all postnatal anthropometry measures at all age points, independent of infant feeding practices. Postnatal alcohol exposure via breastmilk was unrelated to any anthropometry outcome after control for PAE. In conclusion, fetal alcohol-related postnatal growth restriction was not attributable to differences in postnatal infant feeding practices or postnatal alcohol exposure and is thus likely a direct teratogenic effect of PAE.
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