Iodine Deficiency Treatment & Management

Updated: Jul 15, 2018
  • Author: Stephanie L Lee, MD, PhD; Chief Editor: George T Griffing, MD  more...
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Approach Considerations

Treatment of iodine deficiency

Correction of an individual's iodine deficiency should be instituted at a level recommended by the US Institute of Medicine (IOM) and the World Health Organization (WHO). In a nonpregnant adult, 150 mcg/day is sufficient for normal thyroid function.

Consultation with an endocrinologist should be considered when the etiology of thyroid abnormalities is unclear. Thyroidectomy may be indicated for patients with compressive symptoms of a large goiter.


At a population level, iodine deficiency disorder (IDD) can be prevented by the iodization of food products or the water supply. In practice, this is usually achieved by iodization of salt. An alternative in some developing countries has been the periodic injection of iodized oil supplements. [15, 19]

Iodine treatment-related hyperthyroidism

The primary complication of iodine therapy for IDD is the development of hyperthyroidism. This may occur, especially in patients older than 45 years, because of the hyperfunctioning areas of autonomy that tend to develop in patients with long-standing iodine-deficient goiters. [30]

A Danish study investigating the incidence of hyperthyroidism associated with Denmark's iodine fortification program found that, based on the incident use of antithyroid medication in various parts of the country, the incidence of hyperthyroidism was greater among persons who had suffered from moderate iodine deficiency than it was among those who had had only a mild deficiency. [31] In the moderately deficient population, the incident use of antithyroid medication increased the most in persons younger than 40 years or older than 75 years. Four years after iodine fortification began, the incidence of hyperthyroidism apparently began to decline, returning to prefortification rates in most population groups by the end of 6 years.


Sources of Iodine Replacement

Iodine replacement should be based on the recommendations of IOM and WHO. In an adult, 150 mcg/day is sufficient for normal thyroid function. Replacement of iodine is most easily achieved by requesting that the patient use iodized salt in his or her cooking and at the table or an iodine-containing daily multiple vitamin. Other dietary sources of iodine include milk, egg yolks, and saltwater fish. Not all daily or prenatal multiple vitamins contain iodine, but those that do, typically contain 150 mcg of iodine per tablet.

While a person who follows a vegan diet still might consume iodized salt, only 70% of salt sold from US supermarket shelves currently is iodized. Other major sources of US dietary iodine are saltwater fish, milk and milk products, and eggs. These food items are not included in a true vegan diet. [22]

The Institute of Medicine (IOM) recommended dietary allowance (RDA) is 220 mcg/day of iodine for pregnant women. Not all daily or prenatal multiple vitamins contain iodine, but those that do, typically contain 150 mcg of iodine per tablet. The IOM recommends 290 mcg/day for lactating women and 90-120 mcg/day for children aged 1-11 years. The adequate intake for infants is 110-130 mcg/day.

The American Thyroid Association and the Endocrine Society [32, 33] have recommended that lactating women take vitamins containing 150 mcg of iodide daily to supplement their dietary intake of iodide. This recommendation stems from NHANES reports of low individual maternal urinary iodide concentrations in women of childbearing age and pregnant women, although it is not clear that lactating women in the United States are at risk for iodine deficiency. [34]

Infant formula is required by the FDA to contain minimum and maximum calorie-based iodine of 5 and 75 mcg/100 kcal. If an infant formula does not contain at least the minimum amount of each of the nutrients required by the FDA, it is subject to recall. [35]

In developing countries, eradication of iodine deficiency has been accomplished by adding iodine drops to well water or by injecting people with iodized oil.

Using highly concentrated pharmaceutical agents such as a saturated solution of potassium iodide (SSKI), which has a concentration of 35,000-50,000 mcg/drop, is impractical and potentially dangerous.


Treatment of Nontoxic Goiters Caused by Iodine Deficiency

Long-term dietary iodine replacement at levels recommended by IOM and WHO may decrease the size of iodine-deficient goiters in very young children and pregnant women and is indicated for all patients with iodine deficiency. [6] Generally, long-standing goiters associated with iodine deficiency disorder respond with only small amounts of shrinkage after iodine supplementation, and patients are at risk for developing hyperthyroidism. Patients do not routinely require specific therapy unless the goiter is large enough to cause compressive symptoms (eg, tracheal obstruction, thoracic inlet occlusion, hoarseness).


Exogenous levothyroxine (L-T4) can also be used to decrease goiter size but generally is not effective in adults and older children. Supplemental L-T4, when added to the T3 and T4 secretion by the autonomous nodules in the endemic goiter, may cause thyrotoxicosis. Long-term L-T4 therapy that results in the suppression of the TSH level to below-normal levels may have deleterious effects on cardiac and bone health; therefore, L-T4 therapy is no longer routinely administered to patients with goiter.

Radioactive iodine

Radioactive iodine (iodine-131 [131I]) has been used, primarily in Europe, to decrease thyroid volume in patients with euthyroid goiters (40-60% volume reduction). In the United States, 131I is the most common treatment for toxic multinodular goiters associated with hyperthyroidism. Risks associated with 131I therapy include permanent hypothyroidism.


The standard of care for large goiter associated with obstructive symptoms such as dough, stridor, and dysphagia is thyroidectomy. If the goiter extends into the anterior mediastinum, surgery is the recommended treatment even without obstructive symptoms. After the surgery, the patient will need levothyroxine replacement therapy.