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IODINE STATUS AND CONGENITAL HYPOTHYROIDISM IN THE USA

$363,661N01FY2017HDNIH

Nysdoh/Health Research, Inc., Menands NY

Investigators

Abstract

Iodine is an essential nutrient required for the production of thyroid hormones. Consequences of severe iodine deficiency include goiter, hypothyroidism, cretinism, intellectual impairment and increased pregnancy loss, due to inadequate production of thyroid hormones. The recommended daily iodine intake is 150 ug/day in the general adult population, and 250 ug/day among pregnant and lactating women. Pregnancy increases iodine requirements in the mother by increasing maternal thyroid hormone requirements and renal iodine excretion, and because the fetal thyroid gland requires iodine from the mother. Recent studies of pregnant women in the United States show a decline in median urinary iodine concentrations from 327 ug/L in 1971-1974 to 129 ug/L in 2005-2010, indicating that more than half of all pregnant women in the United States are iodine deficient. The etiology of congenital hypothyroidism in areas where pregnant women suffer from severe iodine deficiency is well known. Because the fetus is totally dependent on maternal iodine for thyroid hormone production, it is virtually a given that a newborn with inadequate iodine status and congenital hypothyroidism has the condition because of low maternal iodine concentration. It is not known, however, whether the level of iodine deficiency present in US pregnant women Is sufficiently severe to cause congenital hypothyroidism. Measuring iodine concentrations in blood samples from newborns that have congenital hypothyroidism and from unaffected control newborns will provide us with a better sense of whether current maternal iodine concentrations in the US are affecting the fetus.

View original record on NIH RePORTER →