Abstract
Thyroid cancer (TC) is the most common endocrine malignancy and in most countries, incidence rates are increasing. Although differences in population iodine intake are a determinant of benign thyroid disorders, the role of iodine intake in TC remains uncertain. We review the evidence linking iodine intake and TC from animal studies, ecological studies of iodine intake and differentiated and undifferentiated TC, iodine intake and mortality from TC and occult TC at autopsy, as well as the case–control and cohort studies of TC and intake of seafood and milk products. We perform a new meta-analysis of pooled measures of effect from case–control studies of total iodine intake and TC. Finally, we examine the post-Chernobyl studies linking iodine status and risk of TC after radiation exposure. The available evidence suggests iodine deficiency is a risk factor for TC, particularly for follicular TC and possibly, for anaplastic TC. This conclusion is based on: a) consistent data showing an increase in TC (mainly follicular) in iodine deficient animals; b) a plausible mechanism (chronic TSH stimulation induced by iodine deficiency); c) consistent data from before and after studies of iodine prophylaxis showing a decrease in follicular TC and anaplastic TC; d) the indirect association between changes in iodine intake and TC mortality in the decade from 2000 to 2010; e) the autopsy studies of occult TC showing higher microcarcinoma rates with lower iodine intakes; and f) the case control studies suggesting lower risk of TC with higher total iodine intakes.Electronic supplementary materialThe online version of this article (doi:10.1186/s13044-015-0020-8) contains supplementary material, which is available to authorized users.
Highlights
Thyroid cancer (TC) is the most common endocrine malignancy and in most countries, incidence rates have been steadily increasing over the past few decades, in women
The relevance of the thyroid tumors produced in these animal experiments to human lesions is uncertain: most of the studies induced profound iodine deficiency and excess more severe than found in human diets, and, in general, the follicular tumors show a pattern of morphology and behavior different from human thyroid cancers
This hypothesis is consistent with the findings of increased Follicular thyroid cancer (FTC) and anaplastic thyroid cancer (ATC) in populations with severe endemic goiter, because serum thyroid-stimulating hormone (TSH) is increased in moderateto-severe iodine deficiency in an effort to maintain euthyroidism [16]
Summary
Thyroid cancer (TC) is the most common endocrine malignancy and in most countries, incidence rates have been steadily increasing over the past few decades, in women. Animal studies Thyroid cancer in animals fed iodine deficient or iodine excessive diets In female rats, provision of iodine deficient diets for 6 to 20 months increases serum TSH and causes thyroid tumors in 54–100 % of animals, mainly follicular adenomas and follicular carcinomas [25,26,27,28]. Risk of adverse health consequences (iodine-induced hyperthyroidism, autoimmune thyroid disease) but in DHPN-treated rats, both iodine deficiency and excess increased thyroid follicular tumors, with iodine deficiency having a markedly stronger effect (Fig. 1a). To study the effects of iodine deficiency early in life on subsequent susceptibility to thyroid carcinogens, an iodine-free diet was fed to lactating rats and their weaned offspring until postnatal week 7, and the offspring were exposed to DHPN [35], but this did not significantly increase thyroid tumors. These data suggest both long-term iodine deficiency and excess are insufficient to stimulate thyroid carcinogenesis, but both promote thyroid carcinogenesis induced by radiation
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