NATURE REVIEWS | ENDOCRINOLOGY ADVANCE ONLINE PUBLICATION | 1 Sydney School of Public Health, Room 307, Edward Ford Building, The University of Sydney, Sydney 2006, Australia (M. Li). The Sydney Thyroid Clinic, Westmead Specialist Centre, 16–18 Mons Road, Westmead 2145, Australia (C. J. Eastman). Correspondence to: M. Li mu.li@sydney.edu.au The changing epidemiology of iodine deficiency Mu Li and Creswell J. Eastman Abstract | Globally, about 2 thousand million people are affected by iodine deficiency. Although endemic goitre is the most visible sign of iodine deficiency, its most devastating consequence is brain damage causing mental retardation in children. The relationship between iodine deficiency and brain damage was not clearly established until the 1980s when the term iodine deficiency disorders (IDDs), which encompass a spectrum of conditions caused by iodine deficiency, was introduced. This paradigm shift in the understanding of the clinical consequences of iodine deficiency led to a change in iodine deficiency assessment. The median urinary iodine excretion level has been recommended as the preferred indicator for monitoring population iodine deficiency status since 2001. The 2007 WHO urinary iodine data in schoolchildren from 130 countries revealed that iodine intake is still insufficient in 47 countries. Furthermore, about one-third of countries lack national estimates of the prevalence of iodine deficiency. The picture that has emerged from available data worldwide over the past two decades is that IDDs are not confined to remote, mountainous areas in developing countries, but are a global public health problem that affects most countries, including developed countries and island nations. The recognition of the universality of iodine deficiency highlights the need to develop and apply new strategies to establish and maintain sustainable IDD elimination and strengthen regular monitoring programmes. Li, M. & Eastman, C. J. Nat. Rev. Endocrinol. advance online publication 3 April 2012; doi:10.1038/nrendo.2012.43 Introduction Endemic goitre has been synonymous with iodine defi- ciency for a long time. Countries were often divided geo- graphically into endemic and nonendemic areas on the basis of goitre prevalence. Control efforts were directed towards curing or reducing goitre. With growing clini- cal and public health research, it became clear that the consequences of iodine deficiency go far beyond those of goitre and thyroid disease. 1 In 1983, the term iodine defi- ciency disorders (IDDs) was coined to emphasize that iodine deficiency can affect human beings at all stages of the life cycle and have a broad spectrum of adverse effects, including mental and physical impairment, dis- turbed thyroid function and goitre (Table 1). 2 Children from 2 months to 15 years of age born in areas of mod- erate to severe iodine deficiency can lose up to 13.5 IQ points. 3,4 At a population level, iodine deficiency has a negative impact on a country’s overall health and pro- ductivity and hinders its socioeconomic development. 5 The recognition that iodine deficiency is a major public health problem throughout the world has led to a global acceleration of efforts to combat this deficiency. Despite the progress of IDD elimination programmes, more than 2 thousand million people worldwide are still at risk of insufficient iodine intake. 6,7 In developing countries, 38 million newborn babies per year are not protected from the devastating consequences of iodine deficiency. 8 The problem, however, is not confined to developing countries. Iodine deficiency has been found in highly developed countries where it had been considered to have been eliminated or not exist. This Review exam- ines the paradigm shift in iodine deficiency control strat- egies over the past few decades and the effect of these changes on the assessment and prevalence trends of iodine deficiency worldwide. The article also highlights the evidence for iodine deficiency in developed countries gathered in the past decade and emphasizes the impor- tance of public health policy to support sustainable IDD elimination and surveillance programmes. Pathophysiology of iodine deficiency Thyroid iodine metabolism Dietary iodine is readily absorbed from the gastrointes- tinal tract and reaches the circulation in the form of iodide. Iodide is mostly cleared from the circulation by the thyroid gland and kidney. 9 During pregnancy and lactation, the mammary gland also concentrates and excretes iodine in breast milk. 10 The recommended daily iodine intakes by the WHO, UNICEF and International Council for the Control of Iodine Deficiency Disorders (ICCIDD), 11 and by the American Institute of Medicine 12 are shown in Table 2. In the thyroid gland, iodide is converted back to iodine and concentrated in the follicular cell. The thy- roid contains approximately 70–80% of the total iodine of a healthy adult body (~15–20 mg). 9,13 In the iodine- sufficient human, the thyroid takes up ~10% of the iodine from the circulation, whereas in states of chronic iodine deficiency thyroid iodine uptake can be >80%. 14,15 Iodine is an integral constituent of the thyroid hormones T 4 and T 3 . Iodine is incorporated into tyrosine residues of the thyroglobulin molecule and stored in the colloid Competing interests The authors declare no competing interests. REVIEWS © 2012 Macmillan Publishers Limited. All rights reserved