Longevity Medical Review
Iodine: the Next Vitamin D?
by Lara Pizzorno, MDiv, MA, LMT
Part I: Americans at High Risk for Iodine Insufficiency
Abstract
Despite the widely held assumption that Americans are iodine-sufficient due to the availability of iodized salt, the U.S. population is actually at high risk for iodine insufficiency. Iodine intake has been decreasing in the U.S. since the early 70s as a result of changes in Americans' food and dietary habits, including the facts that iodized salt is infrequently used in restaurant and processed foods, and iodized salt sold for home use may provide far less than the amount of iodine listed on the container's label. The widespread dispersal of perchlorate, nitrate and thiocyanate (competitive inhibitors of iodide uptake) in the environment blocks absorption of the little iodine Americans do consume, further compounding the problem.
In adults, iodine is necessary not only for the production of thyroid hormones, thus affecting systemic metabolism, but is now recognized to play a protective role against fibrocystic breast disease and breast cancer. In addition, a relationship has been hypothesized between iodine deficiency and a number of other health issues including other malignancies, obesity, attention deficit hyperactivity disorder (ADHD), psychiatric disorders, and fibromyalgia.
Analogous to the case of vitamin D, a nutrient for which the 400 IU RDI, although capable of preventing rickets, has been proven inadequate for this pro-hormone's numerous other functions in the body, the iodine RDI for adults of 150 mcg/day (220 mcg/day for pregnant women), while sufficient to prevent goiter (and cretinism), is inadequate for the promotion of optimal fetal brain development or optimal health in adults. Intake of 3-6 mg/day, an amount commonly consumed in Japan without increased incidence of autoimmune thyroiditis or hypothyroidism, may be necessary to support not only thyroid hormone production, but iodine's important antioxidant functions in the breast and other tissues in which this trace mineral is concentrated.
Part I of this article discusses the numerous factors that place Americans at high risk for iodine insufficiency. Part II reviews iodine's roles in the body, the relationship of iodine insufficiency to the above mentioned pathologies, available options in laboratory assessments of iodine levels, optimal intake, preferential forms of supplementation, and cofactors necessary for optimal iodine utilization.
Introduction
Iodine deficiency, defined as urinary iodine excretion <100 mcg/L, is widespread not only in developing countries, but in European countries including Germany, France, Italy and Belgium, and, despite the assumption that Americans are iodine-sufficient, in the U.S. as well.1,2
The 2001-2002 National Health and Nutrition Examination Survey (NHANES) revealed that iodine intake as measured by urinary iodine dropped ~50% from median levels of 320 mcg/L during the period of 1971-1974 to 1988-1994, to 165 mcg/L in 2001-2002. Among women of childbearing age (15-44 years), a group that may serve as "canaries in the coal mine" as they are more closely monitored due to the risk of cretinism associated with maternal iodine deficiency, the statistics were even worse—36% of women of childbearing age were not consuming sufficient dietary iodine (150 mcg/L), and 15% of them had urinary iodine levels (the standard means of evaluating iodine levels in the body) <50 mcg/L. The WHO defines iodine deficiency as a urinary iodine excretion <100 mcg/L; <50 mcg/L indicates moderate to severe deficiency.1,3,4 This situation appears to be worsening; the most recent NHANES (2003-2004) found a urinary iodine level <100 mcg/L in 29 +/-3.0%; <50 mcg/L in 11.3 +/- 1.8%; and <20 mcg/L in 2.4 +/- 1.2% of the U.S. population as a whole, including 15.1 =/- 3.2% of women of reproductive age.5 More recent data (2007) assessing iodine levels in the breast milk of lactating mothers in Boston revealed 47% contained insufficient amounts of iodine to meet infant requirements.6 These statistics clearly indicate that the U.S. population is at increasing risk for iodine deficiency.
Factors Contributing to Americans' Risk for Iodine Deficiency
Changes in Food Production and Dietary Habits
Milk, and therefore dairy products, used to be a reliable source of iodine, but their content of the trace mineral has greatly decreased due to changes in the dairy industry, which has phased out the use of iodine-based disinfectants and reduced the use of iodine in feed supplements. When checked in 1989-1990, the average iodine content of U.S. whole cow's milk had plummeted from a high of 602 (+/-184) mcg/L in 1978 to 155 (+/-19) mcg/L in 1990. In 2002, when researchers in Boston measured the iodine content of cow's milk from 5 separate processing plants (sold as 18 brands of milk in local grocery stores), samples contained as little as 88 mcg/L, about half the amounts typically present in 1990 and only 15% of those seen in 1978.7,8 Furthermore, both children and adults consume much less milk today than in past decades.9,10,11
Bread was once a reliable source of iodine because of the use of iodate-based bread conditioners to prolong shelf life. Due to concerns about high bread iodine content in the 1960s, however, most commercial bakeries stopped using iodate bread conditioners, replacing them with bromate-based "flour improvers." (Not only has the use of potassium bromate significantly reduced iodine intake in the U.S., but potassium bromate is a carcinogen, triggering thyroid follicular cell tumors, renal cell tumors, and mesotheliomas of the peritoneum in rats.12,13,14
The research conducted on dietary sources of iodine in Boston in 2002 also measured iodine content in 20 brands of bread, 17 of which contained an average of 10.1 mcg/slice, despite ingredient labeling that indicated use of iodate. Three brands contained an average of 300 mcg/slice, but only one of these breads indicated use of an iodate conditioner. So, while some breads may still be a good source of iodine, the consumer has no way of knowing which ones, nor how much is provided.8
Sea vegetables, such as kelp, dulse, hijiki, and nori, are an excellent source of iodine (¼ cup [dry weight] supplies 415 mcg). Their frequent use in Japanese cuisine is responsible for an average daily iodine intake estimated to range from 5,280 to 13,800 mcg (i.e., ~5-14 mg/day) among the Japanese.1 Sea vegetables, however, are not frequent American fare. Nori, the sea vegetable most frequently consumed seaweed by Americans due to its use in sushi, provides minimal amounts of iodine, much less than that found in any of the other seaweeds. Additionally, sea vegetables have a high affinity for heavy metals, so unless certified organic, they may be grown in polluted waters from which they will absorb not only healthful minerals, but contaminants such as arsenic, lead, cadmium and/or mercury.15
Iodine Content of Edible Seaweeds16
Seaweed
Iodine (mg/8g*)
Kombu/kelp (Lamanaria)34
Wakame (Undari )3.2
Nori (Porphyra umbilicalis)**0.94
Dulse (Palmaria)5.1
Hijiki (Hisikia)5.03
*8 mg = typical serving size in Asian cuisine**A full flat sheet of nori (Porphyra tenera), used to make sushi, contains ~ 0.1 mg of iodine This leaves iodized salt as the major source of dietary iodine for the majority of the U.S. population. Unfortunately, relying on salt to meet iodine requirements may not be effective for a number of reasons.
Americans have been told to limit salt intake, and many are taking the advice to heart. Because excessive sodium intake can increase hypertension risks, many agencies now promote reducing salt intake. The American Heart Association recommends that healthy American adults reduce their sodium intake to less than 2,300 mg (about 1 teaspoon)/day. A 1995 survey found 58% of men and 68% of women reported never or rarely using ordinary table salt.17 More recently, the American Medical Association has suggested that the FDA remove salt from the Generally Recognized as Safe list.18
Even individuals not actively limiting salt intake may not be getting much iodine along with their sodium. Research published in the January 2008 issue of Environmental Science and Technology indicates iodized salt in the U.S. is unlikely to contain the amount specified on the label, and even if it did, virtually all of the salt used in prepared foods in the U.S. is not iodized. 7
According to product labels, all U.S. iodized salt contains 45 mcg of iodine per gram, which translates to 400 mcg per teaspoon19, but when University of Texas researchers analyzed 88 samples of iodized table salt from 40 states, 53% of samples contained less. Iodine values in freshly opened, top-of-the container samples averaged 44.1 mcg/kg; however, actual values ranged from as little as 12.7 to 129 mcg/kg. And the amount of iodine within each can was not homogenous, but varied as much as 3.3 times among the 5 samples taken at different depths from the same container. Iodine was also found to decrease greatly during high humidity storage, although light or heat had little effect. At 80 and 90% relative humidity (e.g., in many areas of the U.S. during the summer months or in salt container set on the counter and exposed to steam during cooking any time of the year), the corresponding half-lives of iodine are 7.25 and 3.4 days. Even at low humidity (30-45% relative humidity), iodine loss has been reported to be 58.5% over 3.5 years. In sum, even if consuming iodized salt, we have no reliable idea of how much iodine is actually provided, and the longer a container of salt has been in use, particularly if exposed to humidity, the more likely its iodine content has significantly decreased.7
Of equal or greater concern, the use of iodized salt is not mandatory either in restaurants or in food processing in the U.S., and processed and restaurant food dominates the American diet. Americans are eating out a lot (an average of 4.9 meals a week for households earning $75,000/year),20 and even when eating at home, often rely on prepared processed foods. The American Heart Association estimates that 75% of the sodium Americans consume is from processed foods like tomato sauce, soups, condiments, canned foods and prepared mixes, i.e., it is non-iodized.21
So, despite the fact that the prepared food typically consumed by Americans contains high levels of sodium, with very few exceptions, that sodium is unaccompanied by iodine. Restaurants, fast-food outlets, and food processors claim they fear iodized salt might change the flavor of their products, a concern that turns out to be unsupported by fact. In 2006, UNICEF invited delegates from the Republic of Moldova to Switzerland, where all salt for both human and animal consumption must be iodized, to convince them to use iodized salt in food production. Iodine deficiency is common in Moldova where, every year, approximately 27,000 newborn babies suffer from brain damage as a result—a tragedy that has convinced lawmakers to mandate the use of iodized salt in all processed foods. Delegates visited food factories where they found that the addition of iodine to Swiss bread, baked goods, and world-renowned cheeses caused no change in the taste or consistency of these foods. Unfortunately, however, no such program exists in the U.S.22
Iodine Uptake Inhibitors—Perchlorate, Nitrate, Thiocyanate—are Ubiquitous
Iodides are absorbed via a transport protein called the sodium-iodide symporter (NIS), the thyroid cell-surface protein responsible for ferrying iodide from the plasma into the thyroid. NIS is found in the gastric mucosa and other tissues that utilize and concentrate iodine, including mammary tissue, the salivary gland, and cervix.1 Perchlorate, in its form as an ammonium salt (not all perchlorates are ammonium bound, some are bound to potassium), is manufactured primarily for use as a rocket propellant, in explosives manufacture, and formerly, as a pharmaceutical, is also present in nitrate fertilizers, and is a highly potent competitive inhibitor for NIS transport with 30 times higher affinity for human NIS than iodine. (Use of perchlorate to treat hyperthyroidism was withdrawn in the United States because of severe adverse effects [aplastic anemia and agranulocytosis]; however, it is still used in some countries for the treatment of thyrotoxicosis and hypothyroidism induced by the antiarrhythmic drug, amiodarone).23,24,25,26,27
Disposal of perchlorate has resulted in significant contamination of groundwater throughout the western United States where perchlorate (at levels over 4 ppb) contaminates the drinking water of ~11 million people, which has caused concern at the Environmental Protection Agency. High levels of perchlorate have also been found in the U.S. food supply with perchlorate contamination documented in grain, fruit, vegetables, forage crops for livestock, and even in dietary supplements and flavor enhancing ingredients.25,28,29,30,31 In a recent study, perchlorate was detected in 20 of 31 dietary supplements tested, with the highest level (10 mcg/g) found in a supplement recommended for women as a prenatal nutritional supplement.32 Given these facts, it is not surprising that human milk has been found to contain five times the perchlorate levels (10.1 mcg/L) of cow's milk (2 mcg/L).33
Recent evidence that perchlorate contamination of food and water is a widespread phenomenon has let to attempts to evaluate its effects on thyroid function in the general population. Analysis of the NHANES 2001-2002 revealed relationships between urinary perchlorate levels, urinary iodine levels, serum TSH, and serum T4 levels in adult men and women.31
Among women in the NHANES subset, 36% had low urine iodine levels (<100 mcg/L), which, since the NHANES subset is representative of the general population, translates to 2.2 million women nationwide. Perchlorate contamination, as little as 5 ppb, was associated with elevations of TSH and decreased serum T4 in the entire subset of 1,111 women, regardless of their iodine status. In women with low urine iodine levels (<100 mcg/L , which indicates iodine deficiency), perchlorate levels of 5 ppb were associated with a 16% decrease in T4 levels and elevation of TSH levels, consistent with inhibition of iodide uptake. In women with urine iodine levels <100 mcg/L, the group at highest risk of insufficient iodine for thyroid hormone production, exposure to 5 ppb perchlorate could theoretically result in subclinical hypothyroidism. (Subclinical hypothyroidism is currently defined as an elevated TSH with T3 and T4 levels within normal reference ranges.)31,34
Nitrate and Thiocyanate, Possibly More Significant NIS Competitors than Perchlorate
In addition to perchlorate, two other competitors for NIS, nitrate and thiocyanate, also acquired through drinking water and food, negatively impact iodine uptake, and because of their higher prevalence, may be much more significant than perchlorate. The iodine uptake inhibitory effects of nitrate and thiocyanate—as defined by their legally accepted maximal contaminant levels in drinking water— far exceed that of the currently debated reference dose for perchlorate of 0.0007 mg/k/day in drinking water.35
Nitrate is ubiquitous in food. It occurs naturally (e.g., in green beans, carrots, squash, spinach, and beets), is added as a preservative (in meat and fish), and finds its way into the food supply as a contaminant resulting from organic and mineral fertilizers. Analysis of winter iceberg lettuce purchased in Santa Cruz County, CA, in 1998, found an average of 973 mg of nitrate per kg of fresh weight. As a result of the agricultural use of nitrogen-containing organic and mineral fertilizers, nitrate is also common in surface and ground sources of drinking water.35
A survey of 5,500 private water supplies from 9 Midwestern states found 13% had nitrate concentrations >10 mg/L, the federal maximum contaminant level. Two million families are estimated to drink water from private wells that fail to meet the federal drinking-water standard for nitrate. In urban areas, municipal wastewater-treatment discharges on surrounding farmland aggravate the problem.36 Hypertrophy of the thyroid gland has been noted at nitrate levels exceeding 50 mg/L. School children living in a community in Slovakia, where drinking-water wells contained high nitrate levels (>50 mg/L), were found to have enlarged thyroid glands and signs of subclinical thyroid disorder (thyroid hypoechogenicity37 [low intensity echoes] by ultrasound [seen in Hashimoto's thyroiditis and Graves disease], increased TSH levels, positive thyroperoxidase antibodies).38
Dietary thiocyanate also inhibits iodine uptake by the NIS. Brassica family vegetables contain compounds that can be converted to thiocyanates in the gut; however, cooking reduces the thiocyanate (and nitrate) content of vegetables, plus only about 50% of the thiocyanate produced in the gut is bioavailable. Cigarette smoking, however, is a significant source of thiocyanate in the body. Recent studies in the U.S. have found that thiocyanate concentrations in the breast milk of smokers were fourfold higher than those of non-smokers, and iodine content in the breast milk of smoking mothers was twofold reduced, likely due to the thiocyanate's competitive inhibition for NIS in the mammary gland. Thiocyanate has a half-life of approximately 6 days, compared to 8 and 5 hours for perchlorate and nitrate respectively.35 Lastly, research suggests a synergistic effect of perchlorate with thiocyanate resulting in significantly more damage to thyroid function than either compound alone in iodine-deficient individuals. Data from the 2001-2002 NHANES revealed that in women with urinary iodine levels <100 mcg/L, the association between perchlorate and decreased T4 was 66% greater than in non-smokers. These results suggest that thiocyanate in cigarette smoke interacts with perchlorate at commonly occurring perchlorate exposures to negatively impact thyroid function to a much greater degree in individuals with urinary iodine levels <100 mcg/L.39 Little or no data are available on the daily-required dose of dietary iodine to withstand inhibition of NIS iodine—uptake by perchlorate, nitrate and thiocyanate present in American's drinking water, food and exposure to cigarette smoke.35
Conclusion
The combination of changes in food production and American dietary habits have significantly decreased iodine consumption in the U.S. The majority of Americans may not even be meeting RDI recommendations for iodine, which given our unremitting, widespread, and increasing exposure to a variety of iodine uptake inhibitors, are likely insufficient for the promotion of optimal brain development or adult thyroid function.
In adults, iodine is necessary not only for the production of thyroid hormones, but has recently been recognized to play a protective role against fibrocystic breast disease and breast cancer. A relationship has also been suggested between iodine deficiency and a number of other health issues including other cancers, obesity, attention deficit hyperactivity disorder (ADHD), psychiatric disorders, and fibromyalgia.
Part II of this article will suggest revising the RDIs to levels that consider these factors and are based on our recently developed understanding of iodine's varied roles in the body and the relationship of iodine insufficiency to the above mentioned pathologies. Available options in laboratory assessments of iodine levels, preferential forms of iodine supplementation, and cofactors necessary for optimal iodine utilization will also be discussed.
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