Fetal Alcohol Growth Restriction Is Not Attributable to Infant Feeding Practices in a Prospective Birth Cohort in Cape Town, South Africa

Abstract

ObjectivesPrenatal alcohol exposure is the most common preventable cause of neurodevelopmental deficits worldwide and causes growth restriction that worsens in the first year of life. Fetal alcohol growth restriction has been shown to be a marker for severity of alcohol-related neurocognitive deficits. However, the role of postnatal nutrition in fetal alcohol growth restriction remains unknown. The aims of this study were to compare infant feeding practices (e.g., breastfeeding, formula feeding, complementary foods) between heavy drinkers and controls and to examine whether these practices play confounding roles in fetal alcohol growth restriction. Methods123 heavy drinking pregnant women and 86 controls were recruited at their first antenatal clinic visit in Cape Town, South Africa. Demographic background and alcohol, cigarette, marijuana, and methamphetamine use during pregnancy were assessed prenatally. Infant feeding practices were assessed at 6.5 mo postpartum using the USDA Infant Feeding Questionnaire. Infant weight, length and head circumference were measured at 2 wk and 6.5 and 12 mo. Potential confounders were those related to growth outcomes at p < .10 in univariate regression models. ResultsThere were no differences between heavy drinkers and controls in duration of breastfeeding, exclusive breastfeeding, or formula or mixed feeding. Although heavy drinkers were slightly more likely to have given their infants porridge, eggs, red meat, chicken, fish, and fries, complementary feeding practices were otherwise remarkably similar between drinkers and controls. In regression models adjusting for potential confounders (maternal age, cigarette use, socioeconomic status (SES)), frequency of prenatal drinking (days/wk) was related to smaller weight- (B = –.33(–.53, –.13)), length- (B = –.36(–.53, –.18)), and head circumference-for-age (B = –.22(–.40, –.03)) z-scores at 12 mo. These relations were not altered by controlling for breastfeeding, formula feeding, or complementary foods. ConclusionsInfant feeding practices among heavy drinkers and controls were very similar in this low-SES cohort. Fetal alcohol growth restriction was not attributable to differences in infant feeding practices and is thus likely a teratogenic effect of PAE. Funding SourcesNIH/NIAAA; MI Lycaki-Young Fund.