Fetal Alcohol-Related Postnatal Growth Restriction Is Independent of Infant Feeding Practices and Postnatal Alcohol Exposure in a Prospective South African Birth Cohort

Author:

Edwards Alexia C.12,Jacobson Sandra W.345ORCID,Senekal Marjanne4ORCID,Dodge Neil C.3,Molteno Christopher D.5,Meintjes Ernesta M.4,Jacobson Joseph L.34,Carter R. Colin14

Affiliation:

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

2. Adult & Pediatric Intensive Care Units, State University of New York Downstate Medical Center, Brooklyn, NY 11203, USA

3. Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, MI 48201, USA

4. Department of Human Biology, University of Cape Town Faculty of Health Sciences, Cape Town 7925, South Africa

5. Department of Psychiatry and Mental Health, University of Cape Town Faculty of Health Sciences, Cape Town 7925, South Africa

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.

Funder

NIH/NIAAA

Lycaki-Young Fund

Publisher

MDPI AG

Subject

Food Science,Nutrition and Dietetics

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