1Abbreviations: H2O2, hydrogen peroxide; ICCIDD, International Council for the Control of Iodine Deficiency Disorders; KI, potassium iodide; MCT8, monocarboxylate transporter 8; NIS, sodium iodide symporter; T3, triiodothyronine; T4, thyroxine; TPO, thyroid peroxidase; TRH, thyrotropin-releasing hormone; TSH, thyroid-stimulating hormone; UNICEF, United Nations Children’s Fund; WHO, World Health Organization.
OVERVIEW
The only established role of iodine in humans is to be a component of thyroid hormones. The hormones are essential for development and growth, and severe iodine deficiency may lead to developmental brain damage (1). Moreover, thyroid hormones participate in regulation of the daily activity of probably every single cell.
Appropriate thyroid hormone levels for the current state of every cell are obtained through several complicated systems. Iodine exerts strong autoregulatory effects on the thyroid gland to accommodate thyroid iodine utilization to daily needs for hormone production, despite large variations in iodine supply. Over time, activation of iodine autoregulatory mechanisms may lead to thyroid functional abnormalities in many individuals. Thus, the epidemiology of thyroid disease in a population is associated with the iodine intake level, even if neither regular severe iodine deficiency nor excess is present.
HISTORICAL BACKGROUND
The history associated with iodine has been that of the iodine deficiency diseases endemic goiter and cretinism. Iodine discovery is credited to Bernard Courtois in 1811, and the first use of iodine for treatment of goiter was published in 1820 by Coindet (2, 3) in Geneva. The use of iodine in high doses for medical purposes in the early nineteenth century led to the first reports of clinical thyrotoxicosis after intake of iodine (4).
A landmark in progress was the trial performed in Ohio between 1917 and 1922 by Marine and Kimball in 4495 school children; results of this trial showed profound effects of iodine supplements on goiter frequencies (5). Voluntary iodized salt prophylaxis was introduced in Michigan in 1924.
During the same period, Hunziker, from iodine-deficient Switzerland, observed that as little as 100 µg iodine per day was effective in preventing goiter, and in 1922, voluntary iodine prophylaxis was introduced in parts of Switzerland (6).
Despite considerable knowledge on the prevention of iodine deficiency, developmental brain damage caused by iodine deficiency occurred in many parts of the world until recent decades. The formation in 1985 of the International Council for the Control of Iodine Deficiency Disorders (ICCIDD; http://www.ICCIDD.org) (7) and its subsequent activities in collaboration with the World Health Organization (WHO) and The United Nations Children’s Fund (UNICEF) improved the situation, but further efforts are necessary.
DIETARY SOURCES
The dietary sources of iodine vary with the country and population sector. Data from the United States were reviewed by Pearce (8). In countries such as the United States with an extensive intake of dairy products, these foods are often the most important source. Iodine is concentrated in milk (see later), and the iodine content of dairy products is often relatively high because of the iodine in supplements given to dairy cows. Before the Danish iodization of salt, iodine in dairy products contributed 44% of iodine intake, whereas iodine in fish products contributed 15% (9).
Countries where iodine-rich kelp products constitute a significant part of the diet (Japan, Korea) have a generally high iodine intake (10, 11), much higher than the internationally recommended levels (see later). Groundwater iodine content is low in most places. High levels may be caused by leaching of iodine-containing humic substances into aquifers, presumably from old sea bottom deposits (12, 13).
A dietary iodine source that is difficult to control is iodine from chemicals used by the food industry for other purposes. The most prominent example is the use of iodate in the baking industry in the United States, although this practice has become less common. Nonetheless, some types of bread may contain more than the recommended daily intake of iodine in a single slice, without any notification to the consumer (14). The decrease in the use of iodate by the baking industry is probably one of the main causes for the fall in median urinary iodine concentration in the US population from 320 µg/L in 1971 to 1974 (excessive; Table 13.1) to 145 µg/L in 1988 to 1994 (within recommended levels). In 2001 to 2002, it was 168 µg/L (15), and in 2003 to 2004 it was 160 µg/L (16).
The use of iodine-containing medications, radiographic contrast agents, or disinfectants may lead to very high iodine intakes in some individuals.
Multivitamins may contain iodine, often 150 µg per tablet. This is an important source of iodine intake in some populations.
A major source of iodine intake in many countries is iodized salt, to prevent iodine deficiency disorders (17). Programs differ among countries. In the United States, the iodine content of iodized salt is relatively high (45 mg of iodine/kg salt [45 ppm]), albeit with large variations among samples of salt (18), but the use of iodine is voluntary and is limited to 70% of household salt (8). Switzerland uses lower amounts of iodine in salt (20 ppm) (19), but the frequency of use is high; 95% of household salt and 70% of salt used by the food industry are iodized. In some countries, such as Denmark, the use of iodized salt is obligatory for some purposes (table salt, bread production, but not other types of food) (20), to obtain more uniform distribution of iodine intake in the population.
RECOMMENDED INTAKES
Both international and national organizations have made similar recommendations on iodine intake. Because approximately 90% of iodine in diet is excreted by the kidney, and because iodine nutrition is mostly assessed by urinary iodine measurement, recommendations are often given for urinary iodine excretion values. The recommendations given by the WHO, UNICEF, and ICCIDD (1) are outlined in Table 13.1.
TABLE 13.1 WORLD HEALTH ORGANIZATION, UNITED NATIONS CHILDREN’S FUND, AND INTERNATIONAL COUNCIL FOR THE CONTROL OF IODINE DEFICIENCY DISORDERS EPIDEMIOLOGIC CRITERIA FOR ASSESSING IODINE NUTRITION BASED ON MEDIAN URINARY IODINE CONCENTRATIONS
a Applies to adults, but not to pregnant and lactating women. Comment: In adults, a median nonfasting urinary iodine concentration of 100 µg/L would correspond to a urinary iodine excretion of 150 µg/24 hour (71). Because small amounts of iodine are excreted in feces and sweat, intake of iodine would be 10% higher than urinary iodine excretion. The intakes recommended by the World Health Organization, United Nations Children’s Fund, and International Council for the Control of Iodine Deficiency Disorders are as follows: <5 years of age, 90 µg; 6 to 12 years, 120 µg; >12 years, 150 µg; pregnancy and lactation, 250 µg/day. Iodine 1 µg/L corresponds to 7.88 nmol/L.
b For lactating women and for children <2 years of age, a median urinary iodine concentration of 100 µg/L can be used to define adequate iodine intake, but no other categories of iodine intake are defined. Although lactating women have the same requirement as pregnant women, the median urinary iodine is lower because part of iodine is excreted in breast milk.
c The term “excessive” means in excess of the amount required to prevent and control iodine deficiency. Comment: If iodine intake of the population is in general adequate with a median urinary iodine excretion of 100 to 200 µg/L in representative groups, the daily iodine intake and thyroid stores of iodine will be sufficient to cover the needs during pregnancy and lactation (23).
From World Health Organization, United Nations Children’s Fund, International Council for the Control of Iodine Deficiency Disorders. Assessment of Iodine Deficiency Disorders and Monitoring Their Elimination: A Guide for Programme Managers. 3rd ed. Geneva: World Health Organization, 2007:1-99, with permission.
The iodine take recommendations of the Food and Nutrition Board of the US Institute of Medicine (21) are shown in Table 13.2. These recommendations are for iodine intakes of population groups to minimize the risk of disease and for average intakes of individuals over a period of time. The recommendations are not for evaluation of individuals on a daily basis. Because of the adaptive capacities of the thyroid, most individuals adapt to days of very low or high iodine intake without incident.
TABLE 13.2 RECOMMENDATIONS ON DIETARY INTAKES OF IODINE BY THE FOOD AND NUTRITION BOARD OF THE INSTITUTE OF MEDICINE
a RDA, recommended dietary allowance: the average daily intake that meets the estimated iodine needs of almost all (97.5 %) individuals in the group.
b AI, adequate intake: the iodine intake that appears to sustain normal thyroid structure and function in the group. Data are insufficient to establish an RDA.
c UL, tolerable upper intake level: the highest level of daily iodine intake that is likely to pose no risk of adverse health effects for almost all individuals in the group.
From Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes: Iodine. Washington, DC: National Academy Press, 2001:258-89, with permission.
The Public Health Committee of the American Thyroid Association recommends that women living in the United States and Canada receive dietary supplements that contain 150 µg iodine during pregnancy and lactation to cover the increase in need of iodine during these periods (22). Detailed recommendations on iodine intake during pregnancy and lactation have been published by WHO/UNICEF/ICCIDD (23) (see Table 13.1).
EFFECTS OF IODINE IN THE HUMAN BODY
The effects of iodine in the human body can be regarded as belonging to one of three groups:
1. Effects of deficient production of thyroid hormone caused by iodine deficiency.
2. Autoregulatory effects of iodine on the thyroid gland.
3. Extrathyroidal effects of iodine that are mostly of theoretic importance in need of final proof.
The central role of iodine is to be part of the hormones produced in the thyroid gland. Avoidance of iodine deficiency is especially important in pregnancy, to prevent developmental brain damage in the fetus.
The autoregulatory effects of iodine on the thyroid gland tend to compensate for a low iodine supply by increasing the activity of processes involved in utilization of iodine for thyroid hormone production. Other autoregulatory processes rapidly shut down thyroid utilization of iodine after intake of excess iodine. Thus, the thyroid gland normally keeps thyroid hormone production stable despite large changes in iodine supply. The price for the complex ability to compensate for these variables is a tendency to develop thyroid disease. Because the thyroid processes activated by low and high iodine intake are different, the pattern of thyroid disease in a population depends on the level of iodine intake (24).
Extrathyroidal effects and handling of iodine have received less focus. The exception is the processes involved in transport of iodine from the mother to the breast-fed child, and to some degree also from the mother to the fetus through the placenta. This iodine is necessary for thyroid hormone production by the fetal and infant thyroid.
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