Abstract

Iodine is an essential component of thyroid hormones thyroxine (T4) and triiodothyronine (T3) that play a fundamental role in brain development and maturation. During gestation, the maternal thyroid has to increase the synthesis of thyroid hormones since the mother is the principal source of T4 and iodine for the fetus and of iodine during lactation. This doubles the needs of maternal iodine intake to 250–300 µg per day. After starvation, iodine deficiency remains the most frequent cause worldwide of preventable mental retardation in children. Severe iodine deficiency results in wide spectrum of disorders including cretinism. Mild iodine deficiency causes maternal hypothyroxinemia, which affects pregnant women even in apparently iodine-sufficient areas. Maternal hypothyroxinemia often goes unnoticed because T3 levels remain within the normal range and thyrotropin (TSH) is not increased. Recent epidemiological data have found that mild maternal hypothyroxinemia during the first month of pregnancy increases the risk of neurodevelopmental abnormalities in children. Experimental data in animal models have shown altered brain cortical cytoarchitecture in pups born to hypothyroxinemic dams. To prevent iodine deficiency during gestation and lactation, the World Health Organization (WHO) recommends a supplement of 250 µg iodine per day for every expectant woman, in addition to the use of iodized salt in households and a diet comprising iodine rich foods. The importance of iodine supplementation to ensure adequately elevated T4 levels in all women considering conception and during pregnancy and lactation is discussed and fully recommended.

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