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Tracking the effects of prenatal alcohol exposure through to 9 years of age

Although studies of alcohol's effects on fetal growth have consistently demonstrated deficits that persist through infancy, the data on long-term postnatal growth from human studies have been inconsistent. A new study of the effects of heavy prenatal alcohol exposure (PAE) on growth and body composition throughout childhood has found growth restrictions that persist through to nine years of age, as well as a delay in weight gain during infancy, both of which were exacerbated by iron deficiency.

Results will be published in the November 2012 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

"This study is the first to examine the effects of heavy PAE on growth in a single cohort over time using a more rigorous single statistical model with repeated measures for each outcome," said R. Colin Carter, an instructor of pediatrics at Harvard Medical School as well as corresponding author for the study. "Our research adds to prior findings of fetal alcohol-related growth restriction in childhood by demonstrating that the effects of alcohol exposure on somatic growth are largely determined in utero. In addition, this study is the first to examine the effects of PAE on percent body fat."

Carter and his colleagues recruited two groups of pregnant women at their initiation of prenatal care at an urban obstetrical clinic in Cape Town, South Africa: 85 heavy-drinking women, defined as two or more drinks/day or four or more drinks/occasion, and 63 abstaining and light-drinking women, defined as less than one drink/day and no binge drinking. The women were interviewed during their pregnancies about alcohol, smoking, drug use, and demographics. Their children had their length/height, weight, and head circumference measured at 6.5 and 12 months, and again at five and nine years of age.

"We found that children born to women who drank heavily during pregnancy had reductions in weight, height, and head circumference when compared with children without heavy PAE," said Carter. "This alcohol-related growth restriction was present in early infancy and persisted through to nine years of age. What is important is that these effects were exacerbated by iron deficiency in infancy. By contrast, iron deficiency at five years of age and food security did not impact the effects of alcohol on growth. Infants with heavy PAE also had a delay in weight gain at 12 months of age. In addition, the most alcohol-affected children, those with fetal alcohol syndrome (FAS) and partial FAS (PFAS), had leaner body composition when compared with children without these diagnoses."

The persistence of smaller weight, height, and head circumference, an indicator of brain growth, suggest that these effects may be permanent and are potentially markers of later cognitive development, said Carter. "These effects may be detrimental to the children as growth deficits have been shown to be related to other health problems, such as lower IQ," he said. "Furthermore, the effects of alcohol on growth were much more severe if the child had iron deficiency anemia as an infant, a condition that is common in the US and worldwide."

Carter and his colleagues will continue to study the origins of the iron deficiency that they found. "In previous analyses, we found that iron deficiency anemia in infancy appeared to be a direct effect of PAE," he said. "Other data suggest that this fetal alcohol-related infant iron deficiency is due to alcohol-induced disruptions in fetal iron stores, that is, maternal alcohol use appears to interfere with the accumulation of iron by the fetus in utero, even in women who are not themselves iron deficient."

Carter added that these findings support the use of growth restriction as a marker for PAE. "We saw a postnatal delay in weight gain at 12 months, which may have relevance for postnatal nutritional interventions," he said. "The leaner body composition seen in children with FAS or PFAS could be attributable to decreased nutritional intake, for example, total energy or protein, increased metabolic needs, for example, from increased catabolism or physical activity, or a deficit in nutrient utilization in alcohol-exposed children. It is not clear whether the low body fat seen in these most affected children might be amenable to interventions that bolster nutrition, which are effective in other diseases such as cystic fibrosis, metabolic disorders, and intestinal diseases."

In summary, noted Carter, any drinking during pregnancy is not advised, especially heavy or binge drinking. "Our findings show that heavy drinking during pregnancy leads to marked growth restrictions at birth and that these effects persist through childhood," he said. "Heavy drinking during pregnancy also leads to a delay in weight gain in infancy. The effects of heavy drinking during pregnancy on growth are markedly worse if the child has iron deficiency anemia during infancy. Lastly, children with FAS or PFAS are leaner than children without these diagnoses."

Contact: R. Colin Carter, M.D.
Children's Hospital Boston

Alcoholism: Clinical & Experimental Research

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