A raw material required for thyroid synthesis.

Ingested iodine is converted to iodide and absorbed.

Dietary intake is necessary for the production of thyroid hormones.

Iodine deficiency affects 1.9 2 billion people worldwide.

Dietary iodine requirements increase during pregnancy due to increased thyroid hormone production, increased renal iodine losses, and fetal requirements.

Dietary requirements are increased with the lactation to the concentration of iodine in breast milk.

Minimum daily requirement for normal thyroid function is 150 microgm in the U.S.

Recommended dietary allowance is 220 µg per day during pregnancy and 290 µg per day during lactation.

Average daily dietary intake in the U.S. is 500 microgm.

Kosher salt an sea salt do not contain iodine.

Normal plasma iodide (I-) level is about .3 microgm/dL and is distributed in approximately 25L.

Principally taken up by the thyroid gland to make thyroid hormone and the kidneys which excrete it into the urine.

About 120 microgm enters the thyroid daily.

The thyroid secretes 80 microgm as iodine in T3 and T4.

A substrate for thyroid hormone synthesis and is actively transported into the thyroid fully to the cells by an iodine symporter.

Iodine is oxidized and bound covalently to the tyrosyl residues of thyroglobulin.

The coupling of iodinate tyrosyl residues results in the formation of T4 and T3, which are stored within the colloid space.

Forty microgm of iodide diffuses daily into the extracellular fluid.

T3 and T4 are metabolized in the liver and other tissues with release of 60 microgm of iodide per day into the extracellular fluid.

Some thyroid hormone derivatives are excreted in the bile and some of the iodine in these products are reabsorbed in the enterohepatic circulation with a net loss of iodide in the stool of approximately 20 mcg per deciliter.

The total amount of iodide that enters the extracellular fluid is 600 mcg per day: 20% of this iodide enters the thyroid and 80% is excreted in the urine.

Deficiency in pregnancy can lead to decreased maternal thyroxine and include maternal and fetal goiters, cretinism, intellectual impairments, neonatal hypothyroidism, increased pregnancy loss and infant mortality.

Decreases in maternal T4 associated with mild iodine deficiency may lead to impaired cognitive function in children, and is the leading cause of preventable intellectual disability worldwide.

Urine iodine values are used to screen for iodine deficiency in populations.

There is diurnal and day-to-day variation in urinary iodine excretion, so identifying specific individuals at risk for deficiency is not possible.

Median urinary iodine values for pregnant women is between 150 and 249 mcg/L.

Median urinary iodine levels in pregnant women have undergone a 50% decline.

Iodine intake in the US has decreased by half between the 1970s and the 1990s, and the most recent median urinary iodine level study for pregnant women revealed only 125 mcg/L, suggesting that mild Iodine deficiency occurs in pregnant US women (Caldwell KL et al).

Because of the decreased median urinary iodine concentration in United States, and the importance of iodine during pregnancy, it is recommended that patients who are pregnant, lactating, or planning a pregnancy should ingest dietary supplements containing 150 µg of potassium iodide per day.

The Endocrine Society advocates that all daily prenatal multivitamins should contain 150-200 µg of potassium iodide.

A total iodine intake of as much as 500-1100 µg per day is considered safe in pregnancy.

Almost 50% of prenatal multivitamins in the US contain no iodide, and an estimated 20% of pregnant women use iodine containing supplements.

Iodine supplementation in pregnancy results in increased maternal urine iodine concentrations, decreased maternal and neonatal thyroid volumes, and decreased neonatal thyroglobulin levels.

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