Adapted from: Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes.
National Academy Press, Washington, D.C.; 2001.
Assessment of Iodine Status
A population’s iodine status is evaluated by four means: urinary iodine concentration (UI), population rate of goiters, serum TSH, and serum thyroglobulin. Although UI is a good gauge of a population’s iodine status, individuals can vary greatly on their UI status on repeated samples.
An individual’s iodine status can be determined by three or more random UI readings on non-consecutive days or by 24-hour urinary iodine assessments. Alternative practitioners have used 24-hour iodine challenge tests and skin iodine absorption tests. 24-hour urinary challenge tests require the patient to ingest a one-time, high-dose of iodine orally. The premise of this test is based on the assumption that if there is a deficiency the body will “consume” the iodine and less will be measured in the urine. This testing is based on the inaccurate assumption that nearly all of the ingested iodine dose would be eliminated in 24-hours in a state of iodine sufficiency. Urinary iodine output does change as iodine intake changes, but only after many months.20
The iodine skin test was most thoroughly studied many years ago. In 1932, researchers found that 75-80% of iodine applied to the skin evaporates into the air within 24-hours.21 The remaining fraction does absorb and may have biological activity, yet the absorption is identical on live or dead skin and the rate is identical regardless of direction of application to dead skin. Therefore no mechanism is known that increases iodine absorption through the skin when there is a deficiency.22
American Iodine Status
The largest body of data on iodine intake among Americans comes from the National Health and Nutrition Examination Surveys (NHANES) I and II. These surveys have revealed that the overall intake of iodine among American adults has been decreasing significantly over the last several decades. Average levels found in the NHANES I from 1971-1974 compared with the NHAMES III from the late 1988-1994 has shown that iodine intake has decreased by over 50% among all ages, races genders, and socioeconomic statuses. This worrisome trend was largely reversed in the 2002 study, which showed a significant reversal of the trend. Nearly all Americans consume enough to offset goiters, yet 16% of the critical pregnant population, and 8% of the non-pregnant population may be at risk for IDD.23,24
Non Nutritional Medical Uses of Iodine
Like most new medicines, iodine went through a stage of being enthusiastically used for a variety of conditions. Early on it was found to be an effective topical antiseptic and internal mucolytic. Later emergent uses included use as an imaging contrast agent, as a constituent of anti-arrhythmic drugs, and as a treatment for fibrocystic breast disease. As the toxicology of iodine became more predictable, all of these uses have been abandoned or greatly diminished.25
TOXICITY OF IODINE
The main sources of toxic iodine exposure are:
•Drugs and supplements such as amiodarone (Cordarone®, Pacerone®), oral potassium iodide (SSKI), Lodoral®;
•Salt fortification quality control issues, mostly in third world countries;
•Secondary exposure to iodine as a water purifying agent;
•Exposure from use of iodine as a contrast agent.
Iodine toxicity can occur in three different ways: from simple chronic overexposure; from an increase of iodine in a population with a previously stable but low intake; or from a single bolus dose. It is important to note that those with historical iodine deficiencies (even slight) and those with latent thyroid antibodies, are especially susceptible to iodine toxicity.26
Individuals from populations lacking iodine in their diet can manifest toxicity with additional doses as low as 50-100 μg daily. While this is possible, toxicities are more common with consumption of higher levels in excess of 1000-1100 μg daily for months.
Iodine toxicity disrupts thyroid function by causing a combination of goiters, nodules, hypothyroidism, or hyperthyroidism. Iodide induced thyrotoxicosis, the Jod-Basedow phenomenon, can be induced with even moderate doses of iodide in individuals with low intakes of iodine. High doses of iodine, such as those used in iodine based radiocontrast agents have been documented to cause the Jod-Basedow phenomenon. Conversely, hypothyroidism may occur if the Wolff-Chaikoff effect, in which there is a protective shut down of thyroid hormone synthesis in the presence of too much iodine, fails to be self limiting.
Patients exposed to isolated very large amounts of radiographic contrast dyes or the drug amiodarone also are prone to manifest abrupt side effects, especially hyperthyroidism. This is the most common mechanism of onset for toxic nodular goiter in older males.
Chronic iodine intake generally above 5000 μg daily can also cause non-thyroidal symptoms including a metallic taste in the mouth, increased salivation, gastrointestinal side effects, and acneiform skin lesions.26 Given the efficient renal clearance of iodine, non-thyroidal side effects tend to be self-limiting. The most troubling thing about thyroidal iodine side effects is that permanent damage to thyroid function can be done through provocation of latent antibodies to thyroid proteins. Of course, once the autoimmune process is started, it is often not reversible.
Safe Upper limit
The Institute of Medicine has established the following Tolerable Upper Intake Levels (ULs) for iodine:
•1-3 years: 900 μg;
•4-8 years: 300 μg;
•9-13 years: 600 μg;
•14-18 years: 900 μg
•19 years and older: 1100 μg;
•Pregnant women 14-18 years: 900 μg;
•Pregnant women 19 years and older: 1100 μg;
•Lactating women 14-18 years: 900 μg;
•Lactating women 19 years and older: 1100 μg.
CONCLUDING REMARKS
Proponents of Pharmacologic Iodine
Revisionist claims have been made over the last few years regarding ideal iodine intake. An argument has been put forth that since iodine has various pharmacologic effects at dose well above established levels for optimal thyroid function, then these very high doses must be physiologically essential. The proponents call on results from iodine challenge tests as proof of a deficiency existing in all or nearly all who are tested. The proposed doses are contained in a product called Lodoral®, which ranges in potency from 12500-50000 μg of iodine per tablet. These levels are 12.5-50-fold above the 1000-1100 μg. safe UL established by the WHO and the International Council on Iodine Deficiency Diseases.
Numerous problems exist with the premises of this position. Firstly, whilst it is true that nutrients may have medically useful effects when used in doses above amounts needed