Department of Medicine, University of Virginia Health Sciences Center Charlottesville, Virginia 22908
Address all correspondence and requests for reprints to: John T. Dunn, Department of Medicine, University of Virginia Health Sciences Center, Box 511, Charlottesville, Virginia 22908.
![]() |
Introduction |
---|
![]() |
The need for iodine |
---|
Iodine may have effects independent of the thyroid. Clinical studies suggest that fibrocystic breast disease is sensitive to iodine nutrition and improves when supplemented, particularly with iodine (I2) rather than iodide (1). An experimental model in iodine-deficient rats showed mammary lobular hyperplasia that improved with I2 but not with I- treatment (2). The dimensions of this additional pathway of iodine metabolism are not yet clear, but it deserves following.
![]() |
Optimal iodine intake |
---|
About 90% of iodine is eventually excreted in the urine. The median urinary iodine concentration in casual samples, expressed as micrograms per liter (µg/L), is currently the most practical biochemical laboratory marker of community iodine nutrition. It is more useful and much simpler than measuring 24-h samples or calculating urinary iodine/creatinine ratios. Recommendations by the International Council for the Control of Iodine Deficiency Disorders, WHO, and UNICEF (4) set 100 µg/L as the minimal urinary iodine concentration for iodine sufficiency; this figure corresponds roughly to a daily intake of 150 µg iodine. The upper limit for safe iodine intake is uncertain and varies widely among individuals and populations, as discussed below. Intakes up to 1 mg iodine per day are safe for most people, and much higher amounts are usually tolerated without problem.
![]() |
Consequences of too little iodine |
---|
Endemic goiter is the first and most visible sign of iodine deficiency. The thyroid enlarges as an adaptation to the threat of inadequate hormone, a reaction mediated by TSH stimulation and perhaps other growth factors. In mild iodine deficiency, this response may be adequate to preserve euthyroidism, but at the cost of an enlarged thyroid and the attendant risks of neck compression and eventual hyperfunctioning autonomous nodules with hyperthyroidism. An insufficient adaptation in adults produces hypothyroidism with its usual clinical stigmata. The damage is greater when iodine deficiency provokes hypothyroidism during fetal or early life, because thyroid hormone is necessary for proper development of the central nervous system, particularly its myelination. Individuals who were hypothyroid at this critical period frequently have permanent mental retardation, which cannot be corrected by later administration of thyroid hormone or iodine. Child survival is also threatened by iodine deficiency, and several studies show that neonatal mortality decreases, sometimes by 50% or more, when the deficiency is corrected (8).
Almost one third of the worlds population lives in areas of iodine deficiency and risks these consequences. Most of these people are in developing countries, but many in the large industrialized countries of Europe are also affected. Correcting this public health problem is the goal of a massive global campaign that is showing remarkable progress so far. But despite its importance to most other countries, iodine deficiency receives little attention in the United States because its elimination years ago has been widely assumed.
![]() |
Consequences of iodine excess |
---|
Iodine intake appears causally related to autoimmune thyroid disease (9). Injection of thyroglobulin into experimental animals induces a thyroiditis similar to human autoimmune thyroiditis, and the immunological response is more vigorous with iodine-rich thyroglobulin (11). Administration of iodine to goitrous humans provoked a reversible thyroiditis and antibody elevation in some (12). Epidemiological studies have shown that an increased incidence of autoimmune thyroid disease frequently parallels an increased dietary iodine intake (13).
The amount of dietary iodine also influences the type and incidence of thyroid cancer. In experimental work with rats and mice, iodine deficiency is associated with the appearance of both papillary and follicular cancer. In areas that corrected previously established iodine deficiency (e.g. Argentina and Austria), the incidence of papillary thyroid cancer increased, whereas that of follicular cancer decreased (13). Epidemiological studies show a general correlation of dietary iodine with the presence of occult papillary cancer, ranging from 9% on autopsies in iodine-deficient Poland to 36% in iodine-enriched Finland (14).
![]() |
Trends in United States iodine nutrition |
---|
Americans obtain iodine from many sources besides salt (17). Agriculturists learned in the early part of the century that iodine supplements improve the health and productivity of domestic animals, for the same reasons it benefits people. Dairy products, eggs, and meat frequently contain high but variable amounts of iodine, depending on its content in animal feeds. Additionally, iodophors are used somewhat unevenly in the dairy industry, and some of the iodine from teat dips is absorbed and finds its way into milk and meat. About 40 yr ago, iodate was introduced in the commercial baking industry as a bread stabilizer, significantly increasing the iodine intake of the American population. Recently this practice has declined. A common food coloring, erythrosine, contains large amounts of iodine; much of it may not be bioavailable, but it still appears in most analyses of urinary iodine. Iodine is also widely used as a radiocontrast medium, in medicines such as amiodarone and topical antiseptics, and for water purification. Many multivitamin preparations contain 150 µg of iodine per tablet. Some people consume additional amounts from kelp or other so-called health foods. Of these many sources, most are unrecognized and none are regulated. Except for iodized salt, the amount of iodine from each is governed by social and commercial forces rather than by their public health impact, and changes usually occur without any public notification or awareness.
In this environment of uncontrolled iodine exposure, the report of Hollowell et al. is very timely. The median urinary excretion of 145 µg/L iodine for the United States is nearly optimal. It implies an iodine intake of about 200 µg/day, comfortably above the recommended minimum. The authors express particular concern about women of childbearing age, although the median is still in the adequate range. Their most important finding is the decrease by more than 50% from the overall median of 321 µg/L reported in the National Health and Nutritional Examination Surveys 1 from the 1970s. Possible reasons for this decline include changes in national food consumption patterns and food industry practices. Attempts at monitoring intake by analysis of standardized meals, despite many limitations, generally confirm this downward trend in iodine intake. For example, the Total Diet Study of the U.S. Food and Drug Administration reported an iodine intake of 373 µg for 2 yr olds in the 19821991 period compared with 621 µg in 19741982 (18).
![]() |
Implications from current data |
---|
We can learn from the history of other countries. In the 1950s, Guatemala had severe iodine deficiency. Then the country developed a model salt iodization program and by 1972 could claim the eradication of endemic goiter. Following that, the program lapsed, monitoring of iodized salt became lax, and endemic goiter reappeared (19). Similar failures of initially successful programs occurred in Colombia, Thailand, and Mexico. In each, the problem could have been avoided by appropriate monitoring. Many previously deficient countries are now reaching iodine sufficiency, certainly a major achievement, but most still have weak or nonexistent plans for long-range monitoring. In others, e.g. the United Kingdom, iodine sufficiency has been achieved by silent prophylaxis, under circumstances somewhat similar to those in the United States but without iodized salt (20). Both countries lack any regular monitoring system, and thus can fail to recognize suboptimal iodine nutrition, either too much or too little.
![]() |
Recommendations for the future |
---|
1. Insist on adequate monitoring of urinary iodine levels in future national nutrition surveys, to detect further trends. As of this writing, NHANES 4 is being programmed, and does not include surveying for urinary iodine concentration, apparently for lack of funding priority. This shortsighted omission should be corrected. Only effective monitoring will adequately detect further trends in iodine nutrition and permit appropriate recommendations for adjustment.
2. Relate the urinary iodine data of Hollowell et al. to other measures of iodine nutrition. Iodine deficiency increases the serum thyroglobulin, the serum TSH, the thyroidal radioiodine uptake, and the incidence of transient hypothyroidism in neonatal screening programs. Data for most of these measures are being routinely collected. The questions should be asked: Have any of them changed with the apparent decrease in iodine intake?
3. Motivate endocrinologists and other relevant professionals to take an active interest in monitoring U.S. iodine nutrition and responding to the results. Endocrinologists see and treat the effects of iodine on the thyroid. They occupy a stable niche in the health system, and are more likely to have an enduring interest in iodine supply and its consequences than are public health officials, government agencies, or the commercial sector. Thyroid specialists and their organizations are leading the drive for optimal iodine nutrition in Austria, Germany, Italy, and Switzerland. In contrast, the interest among U.S. endocrinologists is tepid. The findings of Hollowell et al. warn against complacency. We and our professional societies, particularly The Endocrine Society and the American Thyroid Association, clearly need to do more to see that our fellow citizens get the right amount of iodine.
Received July 20, 1998.
![]() |
References |
---|