Iodine intake

It is difficult to define the normal range of iodine intake in humans, and despite efforts to provide iodine supplementation in many geographic areas of the world, endemic iodine deficiency and attendant goiter remain a world health problem (147). Exposure to excess iodine may sometimes lead to the development of thyroid disease. This unusual type of iodide-induced goiter has been found, for example, in 10% of the population of a Japanese island where fishermen and their families consume large quantities of an iodine-rich seaweed and have an iodine intake as high as 200 mg/d (148). 

In older patients with goiter due to iodine deficiency there is a risk of provoking hyperthyroidism by increasing iodine intake (p. 247) During chronic maximal stimulation, thyroid follicles can become independent of TSH stimulation ( autonomic tissue"). If the iodine supply is increased, thyroid hormone production increases while TSH secretion decreases due to feedback inhibition. The activity of autonomic tissue, however, persists at a high level thyroxine is released in excess, resulting in iodine-induced hyperthyroidism. 

Urinary Iodine Excretion (UIE) provides the best single measurement of iodine intake of the population and Should be used for initial and follow up assessment. For epidemiological studies, population and not individual levels are is required. To achieve this 40 casual samples from a particular group can be collected (may be collected from schoolchildren at the same time as the goiter is assessed). The values are expressed as a median. Median UIE in the population below 100 pg/1 indicate iodine deficiency. Thus median UIE 10 pg/1 means no deficiency, 50-99 pg/1 indicates mild, 20 9 pg/1 moderate, and <20 pg/1 severe IDD. 

A normal rate of thyroid hormone synthesis depends on an adequate dietary intake of iodine. Iodine is naturally present in water and soil, although some soils contain very low amounts. As a result, seafood is a more reliable source of iodine than crop plants. Approximately 1.6 billion people in more than 100 countries live in areas where natural sources of dietary iodine intake are marginal or insufficient. A minimum of 60 j.g of elemental iodine is required each day for thyroid hormone synthesis, and at least 100 j.g/day is required to eliminate thyroid follicular cell hyperplasia and thyroid enlargement (i.e., iodine deficiency goiter). 

T4, T3, MIT, and DIT are stored outside the cell in the follicular colloid in peptide linkage within the Tg molecules. In normal humans on an iodine-sufficient diet, Tg makes up approximately 30% of the mass of the thyroid gland and represents a 2- to 3-month supply of hormone. The total amount of iodine contained as T4, T3, MIT, and DIT within Tg varies with the dietary iodine intake. 

An adequate dietary intake of iodine is essential to prevent hypothyroidism. In many areas of the world, dietary iodine intake is insufficient and must be supplemented. There is another element in which a dietary intake may be insufficient that is also associated with thyroid hormone metabolism. This element is... 

Allegrini, M., Pennington, J. A. T. and Tanner, J. T. 1983. Total diet study Determination of iodine intake by neutron activation analysis. J. Am. Diet. Assoc. 83, 18-24. 

The complexity of the interaction between iodine intake and autoimmune thyroid disease has been highlighted by reports of evidence that iodide (compared with thyroxine) induces thyroid autoimmunity in patients with endemic (iodine deficient) goiter (43), while in those with pre-existing thyroid autoimmunity, evidenced by the presence of antithyroid (thyroid peroxidase) antibodies, administration of iodine in an area of mild iodine deficiency led to subclinical or overt hypothyroidism (44). 

Because of reports of severe hyperthyroidism after the introduction of iodized salt in two severely iodine-deficient African counties (Zimbabwe and the Democratic Republic of the Congo), a multicenter study has been conducted in seven countries in the region to evaluate whether the occurrence of iodine-induced hyperthyroidism after the introduction of iodized salt was a generalized phenomenon or corresponded to specific local circumstances in the two affected countries (46). Iodine deficiency had been successfully eliminated in all of the areas investigated and the prevalence of goiter had fallen markedly. However, it was clear that some areas were now exposed to iodine excess as a result of poor monitoring of the quality of iodized salt and of the iodine intake of the population. In these areas, iodine-induced hyperthyroidism occurred only when iodized salt had been recently introduced. 

Laurberg P. Iodine intake—what are we aiming at J Clin Endocrinol Metab 1994 79(l) 17-9. 

Solomon BL, Evaul JE, Burman KD, Wartofsky L. Remission rates with antithyroid drug therapy continuing influence of iodine intake Ann Intern Med 1987 107(4) 510-2. 

Laurberg P, Bulow Pedersen I, Knudsen N, Ovesen L, Andersen S. Environmental iodine intake affects the type of nonmalignant thyroid disease. Thyroid 2001 ll(5) 457-69. 

Susceptibility factors genetic (unoperated or palliated cyanotic congenital heart disease beta-thalassemia major) sex (conflicting results) altered physiology (iodine intake, conflicting results)... 

Two neonates who had been given intravenous amiodarone as fetuses at 26 and 29 weeks and whose mothers had also taken it orally developed hypothyroidism (83). The authors suggested that low dietary iodine intake by the mothers may have contributed, by enhancing the Wolff-Chaikoff effect. 

Alderman, G. Stranks, M.H. (1967) The iodine content of bulk herd milk in summer in relation to estimated dietary iodine intake of cows. Journal of Science in Food Agriculture, 8, 151-3. 

It has been known for a long time that some foodstuffs, eg, turnips and rutabaga, are goitrogenic because of the presence of progoitrin. This substance is hydrolyzed to goitrin, or (5)-5-vinjI-2-oxazohdinethione [500-12-9] (14), which is goitrogenic when iodine intake is low. 

Tajiri J, Higashi K, Morita M, Umeda T, Sato T. Studies of hypothyroidism in patients with high iodine intake. J CUn Endocrinol Metab 1986 63(2) 412-17. 

Martino E, Safran M, Aghini-Lombardi F, Rajatanavin R, Lenziardi M, Fay M, Pacchiarotti A, Aronin N, Macchia E, Haffajee C, et al. Environmental iodine intake and thyroid dysfunction during chronic amiodarone therapy. Ann Intern Med 1984 101(l) 28-34. 

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