The objective of this paper is to review the global effort to eliminate iodine deficiency and its impact on public health. Iodine is an essential component of hormones produced by the thyroid gland. Iodine deficiency has multiple adverse effects in humans due to inadequate thyroid hormone production that are termed the iodine deficiency disorders. The major adverse effect is impaired cognition in children. The WHO's first estimate of the global prevalence of goitre in 1960 suggested that 20–60 % of the world's population was affected, with most of the burden in low- and middle-income countries. Iodine deficiency was identified as a key global risk factor for impaired child development where the need for intervention was urgent. This spurred a worldwide effort to eliminate iodine deficiency led by a coalition of international organisations working closely with national governments and the salt industry. In most countries, the best strategy to control iodine deficiency is carefully monitored iodisation of salt. The reach of current iodised salt programmes is remarkable: in 2018, 88 % of the global population used iodised salt. The number of countries with adequate iodine intake has nearly doubled over the past 20 years from 67 in 2003 to 118 in 2020. The resulting improvement in cognitive development and future earnings suggests a potential global economic benefit of nearly $33 billion. Iodine programmes are appealing for national governments because the health and economic consequences are high and can be easily averted by salt iodisation, a low-cost and sustainable intervention.

The present study aimed to evaluate the status of iodine nutrition and thyroid function in adults, to understand the distribution of thyroid disease in people with autoimmune thyroid disease (AITD) in different water iodine areas and to explore the relationship between serum iodine, urine iodine and thyroid function in people with AITD. A cross-sectional survey was conducted in areas of Shandong Province with different water iodine levels, and subsequently 1225 adults were enrolled from iodine-deficient (ID), iodine-adequate (IA) and iodine-excess (IE) areas. Urinary iodine, water iodine, salt iodine, serum iodine and thyroid function were measured. According to the urine iodine concentration, the ID and IA areas were defined as iodine sufficient and the IE area as iodine excessive. Urine iodine, serum iodine, free thyroxine (FT4) and thyroid-stimulating hormone (TSH) levels were comparatively higher in the IE area. The positive rate of thyroglobulin antibody (19·1 %) and the prevalence of AITD (21·8 %) were higher in the ID areas; the prevalence of subclinical hypothyroidism was lowest in the ID areas (7·3 %) and highest in the IE area (16·3 %). Among the AITD population, urinary iodine concentration, free triiodothyronine, FT4 and TSH had a non-linear correlation with serum iodine; abnormal TSH level, serum iodine concentration > 110 µg/l and goitre were risk factors for AITD in adults, especially females. Our data collectively suggest that universal salt iodisation has improved the iodine nutritional status of the population in ID areas in China. Non-step-by-step iodine fortification may induce the transformation of thyroid autoimmune diseases from recessive-to-dominant in susceptible people. Moreover, enhanced monitoring of thyroid function in people with AITD is important.

Low urinary iodine concentration (UIC) is associated with dyslipidaemia in adults but is not well characterised in adolescents. Because dyslipidaemia is a cardiovascular risk factor, identifying such an association in adolescents would allow for the prescription of appropriate measures to maintain cardiovascular health. The present study addresses this question using data in the 2001–2012 National Health and Nutrition Examination Survey for 1692 adolescents aged 12–19 years. Primary outcomes were UIC, cardiometabolic risk factors and dyslipidaemia. Data for subjects categorised by low and normal UIC and by sex were analysed by univariate and multivariate logistic regression. Treating UIC as the independent variable, physical activity level, apoB and lipid profiles differed significantly between subjects with low and normal UIC. Subjects with low UIC had a significantly greater risk of elevated total cholesterol (TC) (95 % CI 1·37, 2·81), elevated non-HDL (95 % CI 1·33, 2·76) and elevated LDL (95 % CI 1·83, 4·19) compared with those with normal UIC. Treating UIC as a dependent variable, the risk of low UIC was significantly greater in those with higher apoB (95 % CI 1·52, 19·08), elevated TC (≥4·4mmol/l) (95 % CI 1·37, 2·81) and elevated non-HDL (≥3·11mmol/l) (95 % CI 1·33, 2·76) than in those with normal UIC. These results show that male and female adolescents with low UIC tend to be at greater risk of dyslipidaemia and abnormal cardiometabolic biomarkers, though the specific abnormal parameters differed between sexes. These results may help to identify youth who would benefit from interventions to improve their cardiometabolic risk.

Universal salt iodisation (USI) has been successfully implemented in China for more than 15 years. Recent evidence suggests that the definition of ‘adequate iodine’ (100–199 µg/l) be revised to ‘sufficient iodine’ (100–299 µg/l) based on the median urinary iodine concentration (MUI) in school-age children. The objective of this study was to determine the prevalence of thyroid dysfunction in populations after long-term salt iodisation and examine whether the definition of adequate iodine can be broadened to sufficient iodine based on the thyroid function in four population groups. A cross-sectional survey was conducted in six provinces in the northern, central and southern regions of China. Four population groups consisting of 657 children, 755 adults, 347 pregnant women and 348 lactating women were recruited. Three spot urinary samples were collected over a 10-d period and blood samples were collected on the 1st day. In the study, among the adults, pregnant women and lactating women, the prevalence rates of elevated thyroglobulin antibody and thyroid microsomal antibody levels were 12·4, 8·5 and 7·8 %, and 12·1, 9·1 and 9·1 %, respectively. Abnormally high thyroid dysfunction prevalence was not observed after more than 15 years of USI in China because the thyroid dysfunction rates were all <5 %. The recommended range should be cautiously broadened from adequate iodine to sufficient iodine according to the MUI of school-age children considering the high levels of hormones and antibodies in the other populations. Adults, particularly pregnant women positive for thyroid antibodies, should be closely monitored.

I is an important mineral for health, required for the production of key thyroid hormones, which are essential for cellular metabolism, growth and physical development. Hence, adequate I is crucial at all stages of life, but imperative during pregnancy for fetal brain development and during a child’s early life for neurodevelopment. Within Ireland, limited information exists on population I intakes and status. Therefore, the purposes of the present analysis were to estimate dietary I intakes and to analyse urinary iodine (UI) status using the cross-sectional National Adult Nutrition Survey 2008–2010 and the most recent Irish Total Diet Study. Median I intakes in the total population (n 1106) were adequate with only 26 % of the population being classified as below the estimated average requirement (EAR). Milk consumption was the major source of I in the diet, contributing 45 % to total intake. Likewise, median UI concentrations (107 µg/l) indicated ‘optimal’ I nutrition according to the WHO cut-off points. In our cohort, 77 % of women of childbearing age (18–50 years) did not meet the EAR recommendation set for pregnant women. Although I is deemed to be sufficient in the majority of adult populations resident in Ireland, any changes to the current dairy practices could significantly impact intake and status. Continued monitoring should be of priority to ensure that all subgroups of the population are I sufficient.

I deficiency is still a worldwide public health problem, with children being especially vulnerable. No nationwide study had been conducted to assess the I status of Spanish children, and thus an observational, multicentre and cross-sectional study was conducted in Spain to assess the I status and thyroid function in schoolchildren aged 6–7 years. The median urinary I (UI) and thyroid-stimulating hormone (TSH) levels in whole blood were used to assess the I status and thyroid function, respectively. A FFQ was used to determine the consumption of I-rich foods. A total of 1981 schoolchildren (52 % male) were included. The median UI was 173 μg/l, and 17·9 % of children showed UI<100 μg/l. The median UI was higher in males (180·8 v. 153·6 μg/l; P<0·001). Iodised salt (IS) intake at home was 69·8 %. IS consumption and intakes of ≥2 glasses of milk or 1 cup of yogurt/d were associated with significantly higher median UI. Median TSH was 0·90 mU/l and was higher in females (0·98 v. 0·83; P<0·001). In total, 0·5 % of children had known hypothyroidism (derived from the questionnaire) and 7·6 % had TSH levels above reference values. Median TSH was higher in schoolchildren with family history of hypothyroidism. I intake was adequate in Spanish schoolchildren. However, no correlation was found between TSH and median UI in any geographical area. The prevalence of TSH above reference values was high and its association with thyroid autoimmunity should be determined. Further assessment of thyroid autoimmunity in Spanish schoolchildren is desirable.

I deficiency can lead to detrimental effects, particularly in neonates and young infants. The aim of this study was to explore whether postpartum maternal urinary I can be used to estimate the I status of newborns. In this cross-sectional study conducted in Tehran, lactating mothers and newborns, within 3–5 d postpartum, were randomly selected. Urine samples were collected from each mother and newborn, and a heel-prick blood sample was obtained from all newborns as part of the routine national newborn screening programme. According to the WHO criteria, median urinary I concentration (UIC) <100 µg/l and frequency over 3 % of thyroid stimulating hormone (TSH) >5 mIU/l was considered as I insufficiency. A total of 147 postpartum women and neonates, aged 27·8 (sd 5·3) years and 4·2 (sd 0·6) d, respectively, completed this study. The median UIC was 68·0 (interquartile range (IQR) 39·4–133·5) and 212·5 (IQR 92·3–307·3) µg/l in postpartum mothers and newborns, respectively. The median neonatal TSH was 1·00 (IQR 0·50–1·70) mIU/l. There was no significant difference in the neonatal UIC and TSH of infants whose mothers had deficient and sufficient urinary I. In the multiple linear regression, neonatal UIC value was associated with maternal urinary I (P=0·048) and parity (P=0·039); a significant association was observed between neonatal TSH and infant sex (P=0·038) and birth weight (P=0·049). The findings of our study demonstrate that, despite postpartum mothers being mildly I deficient, I status of their infants was adequate as assessed by UIC and TSH values. It seems factors other than maternal urinary I may influence the I status in newborns.

The objective of the present study was to assess the impact of providing small-quantity lipid-based nutrient supplements (SQ-LNS) on the I status of young Burkinabe children. In total, thirty-four communities were assigned to intervention (IC) or non-intervention cohorts (NIC). IC children were randomly assigned to receive 20 g lipid-based nutrient supplements (LNS)/d containing 90 µg I with 0 or 10 mg Zn from 9 to 18 months of age, and NIC children received no SQ-LNS. All the children were exposed to iodised salt through the national salt iodization programme. Spot urinary iodine (UI), thyroid-stimulating hormone (TSH) and total thyroxine (T4) in dried blood spots as well as plasma thyroglobulin (Tg) concentrations were assessed at 9 and 18 months of age among 123 IC and fifty-six NIC children. At baseline and at 18 months, UI, TSH and T4 did not differ between cohorts. Tg concentration was higher in the NIC v. IC at baseline, but this difference did not persist at 18 months of age. In both cohorts combined, the geometric mean of UI was 339·2 (95 % CI 298·6, 385·2) µg/l, TSH 0·8 (95 % CI 0·7, 0·8) mU/l, T4 118 (95 % CI 114, 122) nmol/l and Tg 26·0 (95 % CI 24·3, 27·7) µg/l at 18 months of age. None of the children had elevated TSH at 18 months of age. Marginally more children in NIC (8·9 %) had low T4 (<65 nmol/l) compared with the IC (1·6 %) (P=0·052). Salt samples (n 106) were collected from randomly selected participants and assessed by titration for I content, which was on average 37 (sd 15) ppm (range 5–86 ppm); 95 % of households had adequately iodised salt (I>15 ppm). A reduction of SQ-LNS I content could be considered in settings with similarly successful salt iodisation programmes.

Areas with low, adequate and excessive I content in water co-exist in China. Limited data are currently available on I nutrition and thyroid disease in lactating women and their breast-fed infants with different I intakes. This study aimed to evaluate I nutrition in both lactating women and their infants and the prevalence of thyroid disease in areas with different levels of I in water. From January to June 2014, a total of 343 healthy lactating women (excluding those taking anti-thyroid drugs or I supplements within a year of the study, consuming seafood at the time of the study or those diagnosed with congenital thyroid disease) from Beihai in Guangxi province and Jiajiazhuang, Yangcheng, Jicun and Pingyao townships in Shanxi province were selected. Compared with the I-sufficient group, median urinary I concentrations in both lactating women and infants as well as breast milk I levels were significantly lower in the I-deficient group (P<0·001). The prevalence of thyroid disease in lactating women, particularly subclinical hypothyroidism, was higher in the I-excess group than in the I-sufficient group (P<0·05). In areas with excessive water I content, high thyroid peroxidase antibody and high thyroglobulin levels were risk factors for abnormal thyroid-stimulating hormone levels. Our data collectively suggest that excessive I intake potentially causes subclinical hypothyroidism in lactating women. Moreover, enhanced monitoring of I status is important to avoid adverse effects of I deficiency or excess, particularly in susceptible populations such as pregnant or lactating women and infants.

Sufficient iodine intake by pregnant and lactating women is crucial to their offspring's cognitive development. The aim of the present study was to explore the impact of iodised salt intake on the iodine status of pregnant and lactating women. Thirty towns were selected from 211 towns in the rural areas of Shijiazhuang city using probability proportionate to size sampling in this cross-sectional survey. In each selected town, forty pregnant women and forty lactating women were randomly selected to contribute urine samples to determine iodine content. The median urinary iodine content (UIC) of 1200 pregnant women in all was 146 (interquartile range (IQR) 88–239) μg/l. The median UIC in the first, second and third trimesters were 166 (IQR 92–276) μg/l, 145 (IQR 83–248) μg/l and 134 (IQR 79–221) μg/l, respectively. The median UIC in the first trimester was significantly higher than that in the third trimester (P= 0·04). The median UIC of 1200 lactating women in all was 120 (IQR 66–195) μg/l. Their median UIC in every 4-week block was higher than the WHO criteria except in weeks 25–28 and weeks 33–36 of lactation. Pregnant women's median UIC did not correlate with median salt iodine (MSI) (P= 0·402); however, there was a linear correlation between MSI and the lactating women's median UIC (P= 0·007). Iodised salt failed to provide adequate iodine to pregnant women possibly due to limited intake of iodised salt during pregnancy, though it was found to provide adequate iodine to lactating women in the rural areas of Shijiazhuang city.

It is known that iodine deficiency during pregnancy can interfere with normal fetal growth and development. However, iodine levels of pregnant women in Shanghai, China, and factors that could influence its levels remain unclear. A total of 916 pregnant women were selected from the Maternal and Child Care Service Centre of Minhang District in Shanghai. Morning urinary iodine (UI) and iodine content of salt from the participants' home were measured, and UI concentration was adjusted by creatinine concentrations. Serum tri-iodothyronine, thyroxin, free tri-iodothyronine, free thyroxine and thyroid-stimulating hormone were tested in the second trimester of pregnancy by time-resolved fluoroimmunoassay. The median levels of UI in pregnant women were 156·3, 176·9 and 175·1 μg/g creatinine in the first, second and third trimesters of pregnancy, respectively. The prevalence of UI deficiency (UI < 150 μg/g creatinine) was 48·3, 34·2 and 36·2 % in the three trimesters of pregnancy, respectively. Factors that significantly influenced the UI levels include the following: iodine content of household salt; age; occupation; multivitamin supplement with iodine; seaweed intakes. Furthermore, UI and iodine content of salt were moderately correlated (r 0·406, P< 0·001). In addition, there was no significant association between UI and thyroid hormone levels. The present study showed a high prevalence of UI deficiency in pregnant women in Shanghai, especially during the first trimester of pregnancy. Both iodine content of household salt and multivitamin supplement with iodine are the main determinants of UI levels in Shanghai.

Little information is available as to whether doses of iodide similar to those recommended in clinical practice for the prevention of iodine deficiency in pregnant women affect thyroid function. The aim of the present study was to analyse whether doses of iodide can affect thyroid function in adults, and evaluate its effect on plasma markers of oxidative stress, inflammation and acute-phase proteins. A total of thirty healthy volunteers (ten men and twenty women) with normal thyroid function were randomly assigned to three groups (n 10). Each group received a daily dose of 100, 200 or 300 μg of iodide in the form of KI for 6 months. Free tetraiodothyronine (FT4) levels at day 60 of the study were higher in the groups treated with 200 and 300 μg (P = 0·01), and correlated with the increase in urinary iodine (r 0·50, P = 0·007). This correlation lost its significance after adjustment for the baseline FT4. The baseline urinary iodine and FT4 correlated positively with the baseline glutathione peroxidase. On day 60, urinary iodine correlated with C-reactive protein (r 0·461, P = 0·018), and free triiodothyronine correlated with IL-6 (r − 0·429, P = 0·025). On day 60, the changes produced in urinary iodine correlated significantly with the changes produced in α1-antitrypsin (r 0·475, P = 0·014) and ceruloplasmin (r 0·599, P = 0·001). The changes in thyroid-stimulating hormone correlated significantly with the changes in α1-antitrypsin (r − 0·521, P = 0·005) and ceruloplasmin (r − 0·459, P = 0·016). In conclusion, the administration of an iodide supplement between 100 and 300 μg/d did not modify thyroid function in a population with adequate iodine intake. The results also showed a slight anti-inflammatory and antioxidative action of iodide.