Iodine intake is essential for the production of thyroid hormone. Iodine deficiency remains a public health problem in many regions around the world. Iodine deficiency can present as a spectrum of disorders depending on the degree of severity. Pregnant and lactating women are particularly vulnerable to iodine deficiency disorders because of their increased iodine requirements. Severe maternal iodine deficiency has been associated with cretinism or impaired neuro development in children as well as obstetric complications. Universal salt iodization has been shown to prevent these disorders in severely iodine deficient areas. Recently,observational studies have demonstrated an association between mild-to-moderate iodine deficiency and poorer cognitive out-comes in children. 

    Adequate dietary iodine intake is essential for thyroid hormone synthesis . During pregnancy thyroid hormone production increases by 50%, which increases daily iodine requirements .Increased activity of type 3 deiodinase in the placenta increases the degradation of thyroxine (T4) to the inactive form reverse triiodothyroinine (T3). In addition, higher glomerular filtration rates lead to a 30-50% increase in the renal excretion of iodide beginning in the late first trimester and persisting throughout pregnancy . When iodine intake is adequate, the thyroid gland is able to adapt to the demands of pregnancy. However, in areas of iodine deficiency total iodine stores decline progressively during the course of pregnancy, as reflected by urinary iodine concentrations (UIC) . In individuals with iodine deficiency, pregnancy may result in depletion of intrathyroidal iodide stores, which in turn may lead to hypothyroxinemia, increased thyroid stimulating hormone (TSH) levels, and increased thyroid volume . Iodine requirements remain elevated in women who are breastfeeding because lactating breast tissue expresses the sodium iodide symporter, which actively concentrates iodine in breast milk . The World Health Organization (WHO) and United States Institute of Medicine (IOM) have made recommendations for iodine intakes which address the differing needs preconception, during pregnancy and postpartum. The WHO recommends 150  μg/day iodine intake for nonpregnant adults, increasing to 250  μg/day in pregnancy and lactation . The US IOM similarly recommends iodine intakes of 150  μg/day in nonpregnant adults, 220  μg/day during pregnancy, and 290  μg/day while lactating .

     Women with severe iodine deficiency in pregnancy are at increased risk for obstetric complications including miscarriage, stillbirth, congenital anomalies, and perinatal mortality . Studies in regions of severe iodine deficiency have demonstrated an association with late pregnancy fetal loss and post-partum death . Children in the most severely iodine deficient populations (where women ingest <20-25 ug iodine/day) may be born with cretinism (characterized by severe intellectual impairment,deaf mutism and motor spasticity) . Because thyroid hormone is essential for normal fetal neu-rodevelopment, iodine deficiency during pregnancy is also associated with adverse neuro-developmental effects. Thyroid gland embryogenesis is largely complete around 10-12 weeks of gestation. At around 18-20 weeks gestation pituitary TSH can be detected in the fetal serum, and fetal thyroid hormone production begins . Consequently, in the first half of gestation, fetal neuro-development depends on the maternal T4 that crosses the placenta. In regions in which there is severe iodine insufficiency, both maternal and fetal hypothyroxinemia can occur. Without adequate thyroid hormone to stimulate neuronal migration and myelination of the fetal brain, irreversible neurological damage has been reported.

     Adequate nutritional iodine intake is critically important for fetal neuro development. The iodine status of vulnerable populations, including pregnant and lactating women, should be carefully monitored.