Iodine is as an essential constituent of the thyroid hormones thyroxine 3,5,3',5' tetraiodothyronine (T4) and 3,5,3' triiodothyronine (T3). Iodine deficiency impairs normal growth and development due to inadequate production of T3 and T4. The classic sign of iodine deficiency is an enlarged thyroid gland, which in combination with other symptoms begets hypothyroidism. Some patients with hypothyroidism develop an extremely large thyroid, or goiter.

Iodine deficiencies in the U.S. and other developed countries are rare, due to the introduction of iodized salt and generally iodine-rich soil. Iodine deficiency disorders (IDDs) are evident at all ages, but particularly noticeable during periods of rapid growth, such as during the fetal and neonatal stages and during infancy. Iodine deficiency during pregnancy is associated with a greater incidence of stillbirths, abortions, and congenital abnormalities. Endemic cretinism occurs with an iodine intake of below 25 mcg per day and is characterized by mental deficiency, deaf mutism, and spastic diplegia. In infants and children, hypothyroidism related to iodine deficiency results in retardation of physical and mental development.

In adults, iodine deficiency results in reduced mental function, depression, and apathy. In developing countries, more than 1 billion persons are estimated to be at risk of IDDs.

The thyroid gland contains about 70 to 80% of the approximately 15 mg to 20 mg of iodine in the body. The rest is distributed throughout the body, especially in the ovaries, muscles, and blood. Iodine is rapidly absorbed through the gut and excreted by the kidney.

• Fresh saltwater shellfish and seafood
• Iodized salt
• Foods grown in iodine-rich soil
• Milk (depending on the iodine in the cow's diet)
• Iodized bread

Iodized salt contains 76 mcg iodine per gram of salt.

• Iodized salt
• Topical iodine

To maintain normal thyroid function, and to correct iodine-deficiency hypothyroidism

Fibrocystic breast disease: There is some evidence to suggest that subclinical hypothyroidism and/or iodine deficiency may be causative factors in fibrocystic breast disease (FBD). Levothyroxin treatment has been shown to cause rapid pain relief in patients with mastodynia (breast pain) due to FBD. A review of three clinical studies on iodine replacement therapy (sodium iodide, protein-bound iodide, and molecular iodine) in FBD revealed that patients respond best to molecular iodine. Patients treated with molecular iodine had subjective and objective improvement in symptoms and fewer side effects than patients treated with sodium iodide. Iodine deficiency may increase the sensitivity of breast cells to estrogen. This estrogen hypersensitivity causes the breast ducts to produce small cysts that eventually results in fibrosis.

Breast cancer: There is some evidence to suggest that iodine may be an important element for normal breast tissue growth and development. Iodine-deficient breast tissues show changes in RNA/DNA ratios and estrogen receptor proteins, and are more susceptible to carcinogen action and promotion of lesions. Furthermore, studies on women with atypical breast tissue and malignancy has revealed increased radioactive iodine uptake.

Vaginitis: Iodine, used topically as a douche, has been shown to be effective at treating vaginitis. Povidone iodine (betadine) has been shown to be effective at treating vaginitis caused by yeast (candida), fungal, and protozoa (trichomonas) infections. Women treated with povidine iodine cleansing kits, after insertion of intrauterine contraceptive devices (IUDs), had significantly less cervical bacterial growth than untreated women. Further studies are needed to determine if this effect may minimize the risk of pelvic infection during and immediately after insertion of IUDs. Excessive iodine use should be avoided to prevent suppression of thyroid function.

The RDAs for iodine are as follows.

Infants:

• 0 to 6 months: 40 mcg
• 6 to 12 months: 50 mcg

Children:

• 1 to 3 years: 70 mcg
• 4 to 6 years: 90 mcg
• 7 to 10 years: 120 mcg

Adolescents and Adults:

• 11+ years: 150 mcg
• Pregnant females: 175 mcg
• Lactating females: 200 mcg

The measures above are typically surpassed in dietary intake in the U.S. and other developed countries, making supplementation unnecessary.

The following are potential side effects of iodine treatment or oversupplementation: iodine-induced hyperthyroidism; hypothyroidism; autoimmunity (Hashimoto and Graves' types); increased incidence of papillary cancers.

Iodine-induced thyrotoxicosis occurs most commonly in individuals treated with iodinated radiocontrast agents and with the antiarrhythmic drug amiodarone. Kelp tablets (mean iodine dose 21.5 g) have also been shown to cause thyrotoxicosis in some cases.

Daily intake of 2,000 mcg iodine may be potentially toxic.

Excess iodine intake may cause hypothyroidism in euthyroid individuals from high iodine intake areas or those with a history of lymphocytic thyroiditis, treated Graves' disease, or subtotal thyroidectomy. Conversely, excess iodine may induce hyperthyroidism in areas of iodine deficiency and in older patients with nodular goiter. Excess iodine has also been shown to cause both hypo- and hyperthyroidism in euthyroid individuals with a previous episode of thyroid dysfunction due to recombinant interferon-alpha treatment for viral hepatitis B and C.

It may be harmful to ingest more iodine than is typically consumed per day (260 to 600 mcg) from table salt.

Routine thyroid function tests should be conducted on infants treated with topical antiseptic iodine due to the potential for iodine toxicity.

Goitrogens (such as turnips, cabbage, mustard, soybeans, cassava root, peanuts, pine nuts) block iodine uptake in the gastrointestinal tract.

Although no clinically significant interactions between iodine and conventional medications are known to have been reported in the literature to date, this supplement should be used with caution in patients taking thyroid medications (PDR 1999).

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