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October 2009

Iodine-deficiency disorders.

2 billion individuals worldwide have insufficient iodine intake, with those in south Asia and sub-Saharan Africa particularly affected. Iodine deficiency has many adverse effects on growth and development. These effects are due to inadequate production of thyroid hormone and are termed iodine-deficiency disorders. Iodine deficiency is the most common cause of preventable mental impairment worldwide. Assessment methods include urinary iodine concentration, goitre, newborn thyroid-stimulating hormone, and blood thyroglobulin. In nearly all countries, the best strategy to control iodine deficiency is iodisation of salt, which is one of the most cost-effective ways to contribute to economic and social development. When iodisation of salt is not possible, iodine supplements can be given to susceptible groups. Introduction of iodised salt to regions of chronic iodine-deficiency disorders might transiently increase the proportion of thyroid disorders, but overall the small risks of iodine excess are far outweighed by the substantial risks of iodine deficiency. International efforts to control iodine-deficiency disorders are slowing, and reaching the third of the worldwide population that remains deficient poses major challenges.

Lancet. 2008 Oct 4;372(9645):1251-62

Urinary iodine concentration: United States National Health And Nutrition Examination Survey 2001-2002.

Urine iodine has been measured in the US population by the National Health and Nutrition Examination Survey (NHANES) since 1971. A downward trend was noted between NHANES I (320 +/- 6 microg/L in 1971-1974) and NHANES III (145 +/- 3 microg/L in 1988-1994). This report presents data from NHANES 2001-2002 that indicates that the US median urine iodine (UI) level has stabilized since the initial drop between NHANES I and NHANES III. The median UI concentration in the US population in NHANES 2001-2002 was found to be 167.8 microg/L (95% confidence interval [CI] 159.3-177.6). The NHANES 2001-2002 data confirm the current stability of the U.S. iodine intake and continued adequate iodine nutrition for the country.

Thyroid. 2005 Jul;15(7):692-9

Iodine nutrition: iodine content of iodized salt in the United States.

Adequacy of iodine nutrition in the United States has lately been of concern. A major source of dietary iodine for the US population is iodized salt. The US Food and Drug Administration (USFDA) recommends 60-100 mg Kl/kg salt, equivalent to 46-76 mg l/kg salt. All U.S. iodized salt contains 45 mg l/kg according to labels. We collected samples of table salt from freshly opened containers from US volunteers. A sample was sent to us when the can was first purchased. Subsets of volunteers sent further samples when the salt container became half-empty through normal use and a further final sample when the container was nearly finished. We also looked at iodine distribution homogeneity within individual containers, loss of iodine from salt upon exposure to humidity and sunlight, and upon short-term heating (dry and in solution) as may be encountered in cooking. Measurements were made in 0.01% w/v salt solutions by induction coupled plasma-mass spectrometry with 72Ge as an internal standard. The median and mean (+/-sd) I content in freshly opened top-of-the-can salt samples was 44.1 and 47.5 +/- 18.5 mg/kg (n=88, range 12.7-129 mg l/kg) and geometric mean and standard deviation of 44.70 and 1.41. Forty-seven of 88 samples fell below the USFDA recommended I content while 6 exceeded it. The homogeneity in a single can of salt varied greatly: in 5 samples taken from the same container from different depths, the iodine content varied by as little as 1.2x (8.3% coefficient of variance (CV)) to as much as 3.3x (49.3% CV) from one container/brand to another. Iodine is significantly lost upon high humidity storage but light or dry heat has little effect. There is much recent literature on iodine sufficiency and uptake inhibitors; there is also much misinformation and disinformation. We review the relevant literature and discuss our results with reference to the United States.

Environ Sci Technol. 2008 Feb 15;42(4):1315-23

Iodine: deficiency and therapeutic considerations.

Iodine deficiency is generally recognized as the most commonly preventable cause of mental retardation and the most common cause of endocrinopathy (goiter and primary hypothyroidism). Iodine deficiency becomes particularly critical in pregnancy due to the consequences for neurological damage during fetal development as well as during lactation. The safety of therapeutic doses of iodine above the established safe upper limit of 1 mg is evident in the lack of toxicity in the Japanese population that consumes 25 times the median intake of iodine consumption in the United States. Japan’s population suffers no demonstrable increased incidence of autoimmune thyroiditis or hypothyroidism. Studies using 3.0- to 6.0-mg doses to effectively treat fibrocystic breast disease may reveal an important role for iodine in maintaining normal breast tissue architecture and function. Iodine may also have important antioxidant functions in breast tissue and other tissues that concentrate iodine via the sodium iodide symporter.

Altern Med Rev. 2008 Jun;13(2):116-27

Iodine content of various meals currently consumed by urban Japanese.

Various meals being currently consumed by urban Japanese were determined for iodine. The meal samples were collected in 1982 and 1984. The habitual daily home meals of 4 middle-aged Japanese living in urban areas contained 45-1,921 micrograms (mean; 362, 361, 429, and 1,023 micrograms, respectively) of iodine per day. The regular meals served in two university hospitals contained 95-287 micrograms (mean; 195 micrograms) and 89-4,746 micrograms (mean; 1,290 micrograms) of iodine per day, respectively, and the diets for diabetes mellitus contained 59-144 micrograms (mean; 96 micrograms) of iodine per day. In the daily meals containing iodine exceeding ca. 300 micrograms, some kinds of seaweeds and, in some cases, several foods containing a red food color with low iodine bioavailability, erythrosine, provided a large portion of iodine. The iodine contents of refectory meals in a university were 47-203 micrograms (mean; 113 micrograms) per meal and those of lunches in two elementary schools were 25-31 micrograms (mean; 27 micrograms) and 18-43 micrograms (mean; 36 micrograms) per lunch, respectively. These results suggest that the current daily iodine intake of urban Japanese is not great and that erythrosine elevates the iodine content of meals.

J Nutr Sci Vitaminol (Tokyo). 1986 Oct;32(5):487-95

Iodine replacement in fibrocystic disease of the breast.

OBJECTIVE: To determine the response of patients with fibrocystic breast disease to iodine replacement therapy. DESIGN: Review of three clinical studies beginning in 1975: an uncontrolled study with sodium iodide and protein-bound iodide; a prospective, control, crossover study from iodide to molecular iodine; and a prospective, control, double-blind study with molecular iodine. SETTING: University affiliated breast-treatment clinics. PATIENTS: Study 1: 233 volunteers received sodium iodide for 2 years and 588 received protein-bound iodide for 5 years. Study 2: the treatment of 145 patients from study 1 treated with protein-bound iodide for several months who still had symptoms was switched to molecular iodine 0.08 mg/kg; 108 volunteers were treated initially with molecular iodine. Study 3: 23 patients received molecular iodine, 0.07 to 0.09 mg/kg body weight; 33 received an aqueous mixture of brown vegetable dye and quinine. The numbers in study 2 increased over the review period so that 1,365 volunteers were being treated with molecular iodine by 1989. INTERVENTIONS: All patients in study 3 had pre- and post-treatment mammography and measurement of serum triiodothyronine, thyroxine and thyroid-stimulating hormone levels. MAIN OUTCOME MEASURES: Subjective evaluation—freedom from pain—and objective evaluation—resolution of fibrosis. RESULTS: Study 1: 70% of subjects treated with sodium iodide had clinical improvement in their breast disease, but the rate of side effects was high; 40% of patients treated with protein-bound iodide had clinical improvement. Study 2: 74% of patients in the crossover series had clinical improvement, and objective improvement was noted in 72% of those who received molecular iodine initially. Study 3: in the treatment group 65% had subjective and objective improvement; in the control group there was a subjective placebo effect in 33% and an objective deterioration of 3%. CONCLUSIONS: The fibrocystic breast reacts differently to sodium iodide, protein-bound iodide and molecular iodine. Molecular iodine is nonthyrotropic and was the most beneficial.

Can J Surg. 1993 Oct;36(5):453-60

Effects of kelp supplementation on thyroid function in euthyroid subjects.

OBJECTIVE: To study the effects of ingestion of two different doses of supplemental kelp on the thyroid function of healthy euthyroid subjects. METHODS: We conducted a double-blind prospective clinical trial involving 36 healthy euthyroid subjects, who were randomly assigned to receive placebo (4 alfalfa capsules per day), low-dose kelp (2 kelp capsules and 2 alfalfa capsules per day), or high-dose kelp (4 kelp capsules per day) for 4 weeks. Thyrotropin (thyroid-stimulating hormone or TSH), free thyroxine, and total triiodothyronine were assessed at weeks 0, 4, and 6. Response to thyrotropin-releasing hormone stimulation, urinary iodine excretion, and basal metabolic rate were determined at weeks 0 and 4. RESULTS: TSH concentrations did not differ significantly between week 0 and week 4 in the placebo group (P = 0.16) but increased significantly in both the low-dose kelp (P = 0.04) and high-dose kelp (P = 0.002) groups. Free thyroxine concentrations decreased slightly but significantly after 4 weeks of placebo but were unchanged in the low-dose and the high-dose kelp groups. In contrast, total triiodothyronine levels did not differ significantly after 4 weeks of placebo or low-dose kelp therapy but were significantly decreased after high-dose kelp therapy (P = 0.04). Similarly, the thyrotropin-releasing hormone stimulation test showed no significant change in poststimulation TSH after 4 weeks in the placebo or low-dose kelp groups but revealed a significantly increased response after high-dose kelp therapy (P = 0.0002). The 24-hour urinary iodine excretion showed dose-dependent increases in the two kelp study groups. Basal metabolic rate did not change significantly in any study group during the 4-week study period. All thyroid laboratory values returned to baseline 2 weeks after cessation of kelp supplementation, except for TSH in the high-dose kelp group, which was significantly decreased. CONCLUSION: Short-term dietary supplementation with kelp significantly increases both basal and poststimulation TSH. These findings corroborate previous studies on the effects of supplemental iodide given to euthyroid subjects for a similar period. Further studies are needed to determine whether long-term kelp supplementation would cause clinically significant thyroid disease.

Endocr Pract. 2003 Sep-Oct;9(5):363-9

Electrolyte loss in sweat and iodine deficiency in a hot environment.

The authors studied electrolyte loss from profuse sweating in soccer-team players and evaluated the relationship between this source of iodine loss and iodine deficiency. Thirteen male soccer-team players and 100 sedentary students from the same high school were evaluated for 8 d, during which the players were training. The authors analyzed 208 sweat samples to determine losses of iodine, sodium, potassium, and calcium in sweat. Excretion of urinary electrolytes by the subjects was also measured. The mean losses of iodine, sodium, potassium, and calcium in sweat following a 1-hr game were 52 microg, 1,896 mg, 248 mg, and 20 mg, respectively; the ratios of sweat loss to urinary daily loss of the four electrolytes were 0.75, 0.2, 1.88, and 0.92, respectively. Urinary iodine was significantly (p < .02) lower than the normal level of 50 microg/gm creatinine in 38.5% of the soccer players, compared with 2% of the sedentary students. Forty-six percent of the players had Grade I goiter, compared with a mere 1% of the sedentary students (p < .01). The results of the study suggest that loss of iodine through profuse sweating may lead to iodine deficiency, and loss of electrolytes through sweating may have a dietary significance for heat-stressed individuals or for individuals who perform heavy workloads.

Arch Environ Health. 2001 May-Jun;56(3):271-7

A review of iodine toxicity reports.

This article summarizes case reports, population studies, and experimental studies from the literature concerning adverse effects of exposure to iodine from the mid-1880s to 1988. Exposure to excessive iodine through foods, dietary supplements, topical medications, and/or iodinated contrast media has resulted in thyroiditis, goiter, hypothyroidism, hyperthyroidism, sensitivity reactions, or acute responses for some individuals. Reports of maternal iodine exposure during pregnancy or lactation affecting newborn or nursing infants are cited. Susceptibility to excess iodine is discussed as well as the relationship between dose and response. It is concluded that some individuals can tolerate very high levels of iodine with no apparent side effects and that iodine intakes less than or equal to 1,000 mg/day are probably safe for the majority of the population, but may cause adverse effects in some individuals. Determination of maximum tolerable levels of iodine intake will require human experimental studies at levels between 0.150 and 1,000 mg/day for normal subjects, subjects with autonomous thyroid tissue, and iodine-sensitive subjects.

J Am Diet Assoc. 1990 Nov;90(11):1571-81

Thyrotropin levels and risk of fatal coronary heart disease: the HUNT study.

BACKGROUND: Recent studies suggest that relatively low thyroid function within the clinical reference range is positively associated with risk factors for coronary heart disease (CHD), but the association with CHD mortality is not resolved. METHODS: In a Norwegian population-based cohort study, we prospectively studied the association between thyrotropin levels and fatal CHD in 17,311 women and 8,002 men without known thyroid or cardiovascular disease or diabetes mellitus at baseline. RESULTS: During median follow-up of 8.3 years, 228 women and 182 men died of CHD. Of these, 192 women and 164 men had thyrotropin levels within the clinical reference range of 0.50 to 3.5 mIU/L. Overall, thyrotropin levels within the reference range were positively associated with CHD mortality (P for trend = .01); the trend was statistically significant in women (P for trend = .005) but not in men. Compared with women in the lower part of the reference range (thyrotropin level, 0.50-1.4 mIU/L), the hazard ratios for coronary death were 1.41 (95% confidence interval [CI], 1.02-1.96) and 1.69 (95% CI, 1.14-2.52) for women in the intermediate (thyrotropin level, 1.5-2.4 mIU/L) and higher (thyrotropin level, 2.5-3.5 mIU/L) categories, respectively. CONCLUSIONS: Thyrotropin levels within the reference range were positively and linearly associated with CHD mortality in women. The results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal CHD.

Arch Intern Med. 2008 Apr 28;168(8):855-60