Thyroid diseases iodine intake

Iodine is an essential component of thyroid hormone either low or high intake may lead to thyroid disease. Currently, intake of seaweed, a low-calorie food containing sufficient calcium, potassium, iron and vegetable fibers, has been recommended for the prevention of ischemic heart diseases, cerebrovascular diseases, dys-hpidemia, diabetes mellitus, hypertension, metabofic syndrome and obesity, as well as for osteoporosis and iron-deficiency anemia (Mizukami et ai, 1993). Besides, salt has been iodized, and as a result, iodine intake has increased throughout the world (Zhao et ai, 1998). 

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). 

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). 

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. 

Iodide concentrations higher than normal inhibit iodination of tyrosine, an effect that is useful in the treatment of thyroid disease. Inadequate iodine intake results in diffuse enlargement of the thyroid (goiter). 

Large amounts of thioq anate are generated in people with a high intake of cyanide from tobacco smoking, from cyanide in food, or from industrial pollution of the environment with cyanide. Thiocyanate may also be directly consumed with certain foods. Thiocyanate is a competitive inhibitor of the sodium iodide symporter (NIS) at thiocyanate levels normally found in blood. Thereby, it worsens iodine deficiency by inhibition of thyroidal iodide accumulation and by inhibition of iodide transport into breast milk for infant nutrition. Cessation of smoking, reduction of industrial pollution and improved diet will reduce the role of thiocyanate in thyroid disease. In individuals exposed to high levels of thiocyanate, adverse effects may be prevented by an increase in iodine intake. 

Unpublished results from the Danish Investigation of Iodine Intake and Thyroid Diseases before iodine fortification was introduced. Results are median values with 25th and 75th percentiles in parentheses. 

Data from the Danish Investigation of Iodine Intake and Thyroid Diseases based on a FFQ before iodine fortification was introduced in Denmark. Food with a low iodine content was not included, iodine intake from other sources is a little underestimated and iodine from milk, fish and eggs consequently a little overestimated. Rasmussen efa/., (2002). 

Iodine intake level (based on UI) affects the type of benign thyroid disease (Laurberg et ai, 2001). A number of studies (Laurberg et ai, 2001 Suzuki et al., 1975 Stanbury et ai, 1998) indicated the following specific associations a high iodine intake causes endemic goiter (Suzuki etai, 1975). Aswitch from low to sufficient iodine... 

Thyroid disorders are common in all populations, but the occurrence and the pattern of disease depend on the iodine intake of the population. The association between iodine intake level and the risk of disease is U-shaped, as both low and high iodine intakes are associated with an increase in the risk of thyroid problems. The curve is nonsymmettical with the most serious problems associated with iodine deficiency, which should be corrected. However, the iodine intake should only be brought to the level where iodine deficiency disorders are avoided. Optimally, the iodization program should be planned to keep population iodine intake within a relatively narrow range around the recommended level. 

Prevention of disease by modification of risk factors is important in many areas of medicine. For optimal planning and execution of prevention programs it is important to know the dose—response relationship between the risk factor that is modified and the disease that is to be prevented. Such a relationship may take several forms (Rose, 1992 Laurberg et ai, 2001). For example, there seems to be a more or less linear association between irradiation of the thyroid in childhood and later development of thyroid cancer. Irradiation of the thyroid in childhood should be as low as possible. The relationship between iodine intake and the risk of disease is more complicated. Even if the most severe problems are seen when iodine intake is insufficient, a high iodine intake may also lead to disease. The relationship is U-formed (Laurberg et ai, 2001) (Figure 47.1). 

Figure 47.3 Nosological types of hyperthyroidism with different iodine intake levels. Relative frequency of the four most common nosological types of hyperthyroidism in Iceland, with relatively high iodine intake from consumption of fish and high iodine content of dairy products, and from East Jutland, Denmark, with mild-to-moderate iodine deficiency. MNTG, multinodular toxic goiter GD, Graves disease STA, solitary toxic thyroid adenoma SAT, subacute thyroiditis. Data from Laurberg et al., (1991).

Based on such evidence on iodine-induced disease in individual patients, it would be expected that an increase in population iodine intake would lead to an increase in the incidence and prevalence of certain thyroid disorders. To evaluate this in more detail, and to obtain information on the level of iodine intake where such an increase will take place, epidemiological studies are necessary. As shown in Table 47.1 there is evidence to suggest that a number of abnormalities may be more common when iodine intake becomes high. However, in general the evidence is less strong, compared with the evidence for less disease with eradication of iodine deficiency (Table 47.1), and the sum of burdens is lower (Figure 47.1). 

The mechanism leading to more hypothyroidism with higher iodine intake has not been fully elucidated. A high iodine load to the thyroid leads to inhibition of many thyroidal processes involved in hormone synthesis and secretion. Normally the thyroid will escape from this inhibition via downregulation of NIS and a subsequent fall in thyroidal iodide uptake (Eng et al., 1999). Apparently, this escape process is not fuUy effective in many people, especially people with a partly defective function of the thyroid because of thyroid autoimmunity or previous thyroid disease. 

Iodine deficiency with impairment of thyroid hormone production may have severe consequences. To compensate for the low iodine supply that was previously highly prevalent in the world, complex mechanisms have been developed in the thyroid gland. On the one hand, mechanisms are able to accumulate and utilize even very small supplies of iodine. On the other hand, the thyroid immediately reacts to a sudden load of iodine to avoid overproduction of thyroid hormone. As usual when complex mechanisms are involved, this leads to a risk of malfunction — and disease. To minimize such a risk at the level of the population, iodine intake is best kept within a relatively narrow range around the recommended level. 

Thyroid disorders are common in all populations, but the occurrence and the pattern of disease depend on the iodine intake of the population. 

Note The tabie shows associations between various ways to measure iodine intake and thyroid voiume in the same popuiation (Rasmussen etal., 2002). Thyroid voiume is inciuded as a dependent variabie and a measure of iodine intake as an independent variabie in a muitipie iinear regression modei. Each measure of iodine intake is inciuded in a separate modei. Other dependent variabies in the modeis inciude city, age and gender group, smoking (daiiy smoker or not daiiy smoker), drinking (>8 drinks/week or <8 drinks per week), and thyroid disease in the famiiy. P < 0.001 for aii these variabies. Subjects being treated for thyroid disease n = 77) were not inciuded in the anaiyses. Estimated 24-h iodine excretion iodine-to-creatinine ratio muitipiied by the expected daiiy creatinine excretion for the given individuai. 

Autoimmunity, abnormal iodine supply and neoplasia are the three common mechanisms behind thyroid diseases in a population. Further studies are needed to obtain information on the interplay between iodine intake and thyroid autoimmunity. This may allow optimal prevention of thyroid disease by adjusting iodine intake in the individual and in the population. 

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