Relevance of iodine intake as a reputed predisposing factor for thyroid cancer

Abstract

Iodine is a trace element that is essential for the synthesis of thyroid hormone. Both chronic iodine deficiency and iodine excess have been associated with hypertrophy and hyperplasia of follicular cells, attributed to excessive secretion of TSH. This may be associated to thyroid cancer risk, particularly in women. Experimental studies have documented thyroid cancer induction by elevation of endogenous TSH, although in a small number of animals. Iodine deficiency associated with carcinogenic agents and chemical mutagens will result in a higher incidence of thyroid malignancy. Inadequate low iodine intake will result in increased TSH stimulation, increased thyroid cell responsiveness to TSH, increased thyroid cell EGF-induced proliferation, decreased TGFβ 1 production and increased angiogenesis, all phenomena related to promotion of tumor growth. Epidemiological studies associating iodine intake and thyroid cancer led to controversial and conflicting results. There is no doubt that introduction of universal iodine prophylaxis in population previously in chronic iodine-deficiency leads to a changing pattern of more prevalent papillary thyroid cancer and declining of follicular thyroid cancer. Also anaplastic thyroid cancer is practically not seen after years of iodine supplementation. Iodine excess has also been indicated as a possible nutritional factor in the prevalence of differentiated thyroid cancer in Iceland, Hawaii and, more recently, in China. In conclusion: available evidence from animal experiments, epidemiological studies and iodine prophylaxis has demonstrated a shift towards a rise in papillary carcinoma, but no clear relationship between overall thyroid cancer incidence and iodine intake.

The influence of the environment on the development of thyroid tumors: a new appraisal

“…However, the role of iodine intake in the increasing incidence of thyroid cancer is still a matter of debate. In fact, iodine deficiency is associated with an increased risk of FTC, whereas chronically high iodine intake may increase the risk of PTC (Knobel & Medeiros-Neto 2007). Biographical data, tumor characteristics, and treatment and outcome for 190 patients with DTC from 1970 to 2000 were reviewed retrospectively by Dijkstra et al (2007).…”

“…They found a significant increase in the incidence of PTC, which may be related to increasing dietary iodine intake. Conversely, inadequate low iodine intake will result in increased thyroid-stimulating hormone (TSH) stimulation, increased thyroid cell responsiveness to TSH, increased thyroid cell epidermal growth factor-induced proliferation, decreased transforming growth factor beta 1 (TGFb1) production and increased angiogenesis, all phenomena related to promotion of tumor growth (Knobel & Medeiros-Neto 2007; Fig. 2).…”

Thyroid Disruptors: How They Act and How We React

“…Despite the widespread use of excess iodide in many places, a few apparently normal subjects with normal thyroid function prior to iodide exposure develop thyroid dysfunction, as previously reviewed (Markou et al 2001). Many studies indicate that even a small change in the level of iodine intake by a population will lead to a reduced frequency of some thyroid disorders, including goiter, follicular cancer and thyroid nodules; however, other types of disease, such as autoimmune thyroiditis and papillary carcinomas, will become more common (Knobel and Medeiros-Neto 2007;Ward et al 2007). Despite the evidence provided by previous studies, it is still controversial whether completely normal subjects may develop thyroid function disturbances when exposed to large doses of iodide, since there are some evidences that increased iodine intake is not associated with thyroid dysfunction (Markou et al 2001;Nauman and Wolff 1993) The only population in the world in which excessive intake of iodine had been described as a main cause of disease lived in some coastal areas of the Japanese island Hokkaido (Suzuki et al 1965).…”

Iodine and differentiated thyroid cancer: Pathogenetic and therapeutic implications

“…2,[4][5][6][7][8] There are many factors, such as ethnicity, selenium and goitrogen or carcinogen intake that complicate studies linking changes in DTC rates to iodine intake. 3 Although there continues to be disagreement on whether iodine intake determines the absolute prevalence of DTC, there is strong evidence that such intake influences its form of presentation with follicular thyroid carcinoma predominating in areas of dietary iodine deficiency while the papillary form is most common where iodine intake is replete or excessive 5,9 (Table 1). Furthermore, a shift towards the papillary form occurs when a population has undergone a programme of iodine prophylaxis.…”

“…The relationship between iodine nutrition and DTC pathogenesis is complex, arising from the fundamental observation that anything that stimulates thyroid growth such as TSH, has the potential ability to promote growth and neoplastic transformation in predisposed thyroid follicular cells. [1][2][3] One of the other major factors in the pathogenesis of thyroid cancer is previous irradiation. 16 The mechanisms through which events leading to PTC are initiated is uncertain but RET/PTC rearrangements as well as RAS, PAX 8 and PPAR  mutations have been implicated.…”