R Colin Carter1, Marjanne Senekal2, Christopher P Duggan3, Neil C Dodge4, Ernesta M Meintjes2, Christopher D Molteno3,5,6, Joseph L Jacobson2,4, Sandra W Jacobson2,4,6. 1. Institute of Human Nutrition and Departments of Emergency Medicine and Pediatrics, Columbia University Vagelos College of Physicians and Surgeons and NYP Morgan Stanley Children's Hospital, New York, NY, USA. 2. Department of Human Biology, University of Cape Town Faculty of Health Sciences, Cape Town, South Africa. 3. Division of Gastroenterology, Hepatology, and Nutrition, Boston Children's Hospital, Boston, MA, USA. 4. Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, MI, USA. 5. Departments of Nutrition and Global Health and Population, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 6. Department of Psychiatry and Mental Health, University of Cape Town Faculty of Health Sciences, Cape Town, South Africa.
Abstract
BACKGROUND: Animal models have demonstrated that maternal nutrition can alter fetal vulnerability to prenatal alcohol exposure (PAE). Few human studies have examined the role of nutrition in fetal alcohol spectrum disorders (FASD). OBJECTIVES: Our objectives were to examine whether fetal vulnerability to PAE-related growth restriction is modified by: 1) rate of gestational weight gain; or prenatal dietary intakes of 2) energy, 3) iron, or 4) choline. METHODS: In a prospective longitudinal birth cohort in Cape Town, South Africa, 118 heavy-drinking and 71 abstaining/light-drinking pregnant women were weighed and interviewed regarding demographics, alcohol, cigarette/other drug use, and diet at prenatal visits. Infant length, weight, and head circumference were measured at 2 wk and 12 mo postpartum. RESULTS: Heavy-drinking mothers reported a binge pattern of drinking [Mean = 129 mL (∼7.2 drinks)/occasion on 1.3 d/wk). Rate of gestational weight gain and average daily dietary energy, iron, and choline intakes were similar between heavy-drinking women and controls. In regression models adjusting for maternal age, socioeconomic status, cigarette use, and weeks gestation at delivery, PAE [ounces (30 mL) absolute alcohol per day] was related to smaller 2-wk length and head circumference and 12-mo length, weight, and head circumference z-scores (β = -0.43 to -0.67; all P values <0.05). In stratified analyses for each maternal nutritional measure (inadequate compared with adequate weight gain; tertiles for dietary energy, iron, and choline intakes), PAE-related growth restriction was more severe in women with poorer nutrition, with effect modification seen by weight gain, energy, iron, and/or choline for several anthropometric outcomes. CONCLUSIONS: Gestational weight gain and dietary intakes of energy, choline, and iron appeared to modify fetal vulnerability to PAE-related growth restriction. These findings suggest a need for screening programs for pregnant women at higher risk of having a child with FASD to identify alcohol-using women who could benefit from nutritional interventions.
BACKGROUND: Animal models have demonstrated that maternal nutrition can alter fetal vulnerability to prenatal alcohol exposure (PAE). Few human studies have examined the role of nutrition in fetal alcohol spectrum disorders (FASD). OBJECTIVES: Our objectives were to examine whether fetal vulnerability to PAE-related growth restriction is modified by: 1) rate of gestational weight gain; or prenatal dietary intakes of 2) energy, 3) iron, or 4) choline. METHODS: In a prospective longitudinal birth cohort in Cape Town, South Africa, 118 heavy-drinking and 71 abstaining/light-drinking pregnant women were weighed and interviewed regarding demographics, alcohol, cigarette/other drug use, and diet at prenatal visits. Infant length, weight, and head circumference were measured at 2 wk and 12 mo postpartum. RESULTS: Heavy-drinking mothers reported a binge pattern of drinking [Mean = 129 mL (∼7.2 drinks)/occasion on 1.3 d/wk). Rate of gestational weight gain and average daily dietary energy, iron, and choline intakes were similar between heavy-drinking women and controls. In regression models adjusting for maternal age, socioeconomic status, cigarette use, and weeks gestation at delivery, PAE [ounces (30 mL) absolute alcohol per day] was related to smaller 2-wk length and head circumference and 12-mo length, weight, and head circumference z-scores (β = -0.43 to -0.67; all P values <0.05). In stratified analyses for each maternal nutritional measure (inadequate compared with adequate weight gain; tertiles for dietary energy, iron, and choline intakes), PAE-related growth restriction was more severe in women with poorer nutrition, with effect modification seen by weight gain, energy, iron, and/or choline for several anthropometric outcomes. CONCLUSIONS: Gestational weight gain and dietary intakes of energy, choline, and iron appeared to modify fetal vulnerability to PAE-related growth restriction. These findings suggest a need for screening programs for pregnant women at higher risk of having a child with FASD to identify alcohol-using women who could benefit from nutritional interventions.
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