35
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Iodine intake as a risk factor for thyroid cancer: a comprehensive review of animal and human studies

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          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 material

          The online version of this article (doi:10.1186/s13044-015-0020-8) contains supplementary material, which is available to authorized users.

          Related collections

          Most cited references163

          • Record: found
          • Abstract: not found
          • Article: not found

          Korea's thyroid-cancer "epidemic"--screening and overdiagnosis.

            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            High prevalence of BRAF mutations in thyroid cancer: genetic evidence for constitutive activation of the RET/PTC-RAS-BRAF signaling pathway in papillary thyroid carcinoma.

            Thyroid papillary cancers (PTCs) are associated with activating mutations of genes coding for RET or TRK tyrosine kinase receptors, as well as of RAS genes. Activating mutations of BRAF were reported recently in most melanomas and a small proportion of colorectal tumors. Here we show that a somatic mutation of BRAF, V599E, is the most common genetic change in PTCs (28 of 78; 35.8%). BRAF(V599E) mutations were unique to PTCs, and not found in any of the other types of differentiated follicular neoplasms arising from the same cell type (0 of 46). Moreover, there was no overlap between PTC with RET/PTC, BRAF, or RAS mutations, which altogether were present in 66% of cases. The lack of concordance for these mutations was highly unlikely to be a chance occurrence. Because these signaling proteins function along the same pathway in thyroid cells, this represents a unique paradigm of human tumorigenesis through mutation of three signaling effectors lying in tandem.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Increasing incidence of differentiated thyroid cancer in the United States, 1988-2005.

              Studies have reported an increasing incidence of thyroid cancer since 1980. One possible explanation for this trend is increased detection through more widespread and aggressive use of ultrasound and image-guided biopsy. Increases resulting from increased detection are most likely to involve small primary tumors rather than larger tumors, which often present as palpable thyroid masses. The objective of the current study was to investigate the trends in increasing incidence of differentiated (papillary and follicular) thyroid cancer by size, age, race, and sex. Cases of differentiated thyroid cancer (1988-2005) were analyzed using the National Cancer Institute's Surveillance Epidemiology and End Results (SEER) dataset. Trends in incidence rates of papillary and follicular cancer, race, age, sex, primary tumor size ( 4 cm), and SEER stage (localized, regional, distant) were analyzed using joinpoint regression and reported as the annual percentage change (APC). Incidence rates increased for all sizes of tumors. Among men and women of all ages, the highest rate of increase was for primary tumors or =4 cm among men (1988-2005: APC, 3.7) and women (1988-2005: APC, 5.70) and for distant SEER stage disease among men (APC, 3.7) and women (APC, 2.3). The incidence rates of differentiated thyroid cancers of all sizes increased between 1988 and 2005 in both men and women. The increased incidence across all tumor sizes suggested that increased diagnostic scrutiny is not the sole explanation. Other explanations, including environmental influences and molecular pathways, should be investigated.
                Bookmark

                Author and article information

                Contributors
                +41-44-632-8657 , michael.zimmermann@hest.ethz.ch
                valeria.galetti@hest.ethz.ch
                Journal
                Thyroid Res
                Thyroid Res
                Thyroid Research
                BioMed Central (London )
                1756-6614
                18 June 2015
                18 June 2015
                2015
                : 8
                : 8
                Affiliations
                [ ]Laboratory of Human Nutrition, Department of Health Sciences and Technology, ETH Zürich, Schmelzbergstrasse 7, LFV D21, CH-8092 Zürich, Switzerland
                [ ]Laboratory of Human Nutrition, Department of Health Sciences and Technology, ETH Zürich, Schmelzbergstrasse 7, LFV E14, CH-8092 Zürich, Switzerland
                Article
                20
                10.1186/s13044-015-0020-8
                4490680
                25685198
                b994963d-9a0c-4955-9261-14fa854e9e0f
                © Zimmermann and Galetti. 2015

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 27 May 2015
                : 8 June 2015
                Categories
                Review
                Custom metadata
                © The Author(s) 2015

                Endocrinology & Diabetes
                iodine deficiency,iodine excess,iodine status,iodized salt,iodine supplement,urinary iodine,goiter,nodule,thyroid cancer

                Comments

                Comment on this article