Iodine deficiency in pregnancy and the effects of maternal iodine supplementation on the offspring: a review

Abstract

The World Health Organization (WHO) recently increased their recommended iodine intake during pregnancy from 200 to 250 μg/d and suggested that a median urinary iodine (UI) concentration of 150–249 μg/L indicates adequate iodine intake in pregnant women. Thyrotropin concentrations in blood collected from newborns 3–4 d after birth may be a sensitive indicator of even mild iodine deficiency during late pregnancy; a < 3% frequency of thyrotropin values > 5 mU/L indicates iodine sufficiency. New reference data and a simple collection system may facilitate use of the median UI concentration as an indicator of iodine status in newborns. In areas of severe iodine deficiency, maternal and fetal hypothyroxinemia can cause cretinism and adversely affect cognitive development in children; to prevent fetal damage, iodine should be given before or early in pregnancy. Whether mild-to-moderate maternal iodine deficiency produces more subtle changes in cognitive function in offspring is unclear; no controlled intervention studies have measured long-term clinical outcomes. Cross-sectional studies have, with few exceptions, reported impaired intellectual function and motor skills in children from iodine-deficient areas, but many of these studies were likely confounded by other factors that affect child development. In countries or regions where < 90% of households are using iodized salt and the median UI concentration in school-age children is < 100 μg/L, the WHO recommends iodine supplementation in pregnancy and infancy.