Endocrine Abstracts

Iodine deficiency (ID) is a public health problem and has considerable consequences other than endemic goiter, known as iodine deficiency disorders (IDD). Neonatal hypothyroidism, growth retardation, and cretenism are the results of severe ID. Neuronal migration and myelination of fetal brain requires iodine. Thus, insufficient iodine intake during pregnancy may cause permanent fetal brain damage. ID in prenatal period and early childhood has unfavorable effects on cerebral development. The duration and severity of maternal ID were suggested to be associated with worse clinical outcomes. Iodine requirement which is 150 µg/d increases toover 250 µg/d during pregnancy. On the other hand, the effect of mild-moderate ID on the long term neuromotor development of fetus is not well established. Severe ID in pregnancy is also thought to be a risk factor for pregnancy outcome, such as stillbirth , miscarriage, preterm delivery, and birth of small-for-gestational weight babies. Although ID can be easily prevented by quite inexpensive iodization strategies, it continues to be the most important cause of irreversible but also preventable mental retardation worldwide. However this strategy alone is inefficient during the pregnancy and lactation period. World Health Organization (WHO) recommends 250 µg/d iodine intake for pregnant and lactating women whereas routine supplementation programs with iodized salt provides about 100 -150 µg/d. Thus, routine iodine containing supplements are much recommended in the United States and Europe but current data indicates that it has not become much widespread.