Hypothyroidism due to iodine deficiency can impair physical development, most visibly in the marked stunting of myxedematous cretinism caused by severe in utero iodine deficiency. Whether iodine repletion improves growth in noncretinous children is uncertain. Therefore, the aim of our systematic review was to assess the effects of iodine fortification or supplementation on prenatal and postnatal growth outcomes in noncretinous children. Following Cochrane methods and PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) reporting guidelines, we searched 10 databases including 2 Chinese databases (latest search February 2017). We included randomized and nonrandomized controlled trials (RCTs; non-RCTs), controlled before-after (CBA) studies, and interrupted time-series studies in pregnant women and children (≤18 y), which compared the effects of iodine (any form, dose, regimen) to placebo, noniodized salt, or no intervention on prenatal and postnatal growth outcomes. We calculated mean differences with 95% CIs, performed random-effects meta-analyses, and assessed the quality of evidence with the use of GRADE (Grading of Recommendations Assessment, Development and Evaluation). We included 18 studies (13 RCTs, 4 non-RCTs, 1 CBA) (n = 5729). Iodine supplementation of severely iodine-deficient pregnant women increased mean birthweight [mean difference (MD): 200 g; 95% CI: 183, 217 g; n = 635; 2 non-RCTs] compared to controls, but the quality of this evidence was assessed as very low. Iodine repletion across the other groups showed no effects on primary growth outcomes (quality of evidence mostly low and very low). Meta-analyses showed a positive effect in moderate-to-mildly iodine-deficient schoolchildren on insulin-like growth factor-1 (MD: 38.48 ng/mL; 95% CI: 6.19, 70.76 ng/mL; n = 498; 2 RCTs, low-quality evidence) and insulin-like growth factor binding protein-3 (MD: 0.46 μg/mL; 95% CI: 0.25, 0.66 μg/mL; n = 498; 2 RCTs, low-quality evidence). In conclusion, we identified few well-designed trials examining the effects of iodine repletion on growth. We are uncertain whether prenatal iodine repletion increases infant growth. Postnatal iodine repletion may improve growth factors but has no clear effects on somatic growth. Our systematic review was registered with PROSPERO as CRD42014012940.

Objectives: The aim of the study was to assess the iodine status of pregnant women and children age 6 to 12 years feeding from the same food basket in Mopani District. Design: A cross-sectional study was conducted. Setting: The setting was primary health care clinics and households from five municipalities of Mopani District in Limpopo province. Subjects: A total of 565 conveniently selected pregnant women and 116 children aged 6 to 12 years were recruited, of which 116 were mother–child pairs. Methods: The demographic information, iodine nutrition knowledge and salt consumption patterns were obtained using a validated questionnaire. Spot urine, household drinking water and salt samples were collected and analysed for iodine using standard procedures. A professional nurse, using filter paper to determine thyroid stimulating hormone (TSH) levels, collected spot finger-stick blood samples from pregnant women. Results: The findings showed that only 52.5% of household salt had an iodine concentration level of more than and equal to 15 ppm. The median iodine concentration of household drinking water was 46.2 μg/l (interquartile range [IQR] 10.8–73.4 μg/l). The TSH levels of the majority of pregnant women were normal and the maternal overall median urinary iodine concentration (UIC) was 164 μg/l (IQR 92–291 μg/l), indicating maternal iodine sufficiency. However, median UIC in the first and third trimesters was below 150 μg/l, indicating iodine insufficiency. The UIC level of children in the study was 386 μg/l (IQR 200–525 μg/l), signifying iodine excess. Conclusion: Iodine status of pregnant women in this study was sufficient, with UIC for children excessively high, more than two times higher than the iodine status of pregnant women. The reasons for the excessive UIC in school-age children need to be elucidated.

IntroductionIodine is an essential micronutrient and component of the thyroid hormones. Sufficient ingestion of iodine is necessary for normal growth and development. If iodine requirements are not met, growth can be impaired. Salt iodisation and supplementation with iodine can prevent iodine deficiency disorders and stunted growth. No systematic review has yet collated the evidence linking iodine to growth. With an increased emphasis on stunting within the WHO Global Nutrition Targets for 2025, we propose a systematic review to address this question.Methods and analysisWe will undertake a systematic review, and if appropriate, meta-analyses, evaluating the effects of iodised salt or iodine supplements on prenatal and postnatal somatic growth, until age 18. We will search a number of databases, including MEDLINE, EMBASE, Web of Science, CINAHL, PsychINFO, the Cochrane Library, including the CENTRAL register of Controlled Trials and also the WHO library and ICTRP (International Clinical Trials Registry Platform), which includes the Clinicaltrials.gov repository. We will also search Wanfang Data and the China Knowledge Resource Integrated Database. Included studies must have compared exposure to iodised salt, iodine supplements or iodised oil, to placebo, non-iodised salt or no intervention. Primary outcomes will be continuous and categorical markers of prenatal and postnatal somatic growth. Secondary outcomes will cover further measures of growth, including growth rates and indirect markers of growth such as insulin-like growth factor-1 (IGF-1).Ethics and disseminationThe systematic review will be published in a peer-reviewed journal, and will be sent directly to the WHO, United Nations Children's Fund, International Council for the Control of Iodine Deficiency Disorders and other stakeholders. The results generated from this systematic review will provide evidence to support future programme recommendations regarding iodine fortification or supplementation and child growth.Trial registration numberPROSPERO CRD42014012940.

Objectives: The mandate of this working group was to assess the importance of salt iodine quality in successful IDD prevention and control. Examine the role of salt iodine content in quality assurance, inspection, surveillance, and coalition oversight of IDD programs. Methods: Scientific literature, technical reports and a range of data and information sources were reviewed to determine whether accurate salt iodization was making a critical contribution toward safe and successful IDD programs. Results: Evidence and examples were collected on salt iodine data in quality assurance of iodization by salt industry, assessments of iodized salt quality by inspectors in factories and markets, surveillance of USI strategies and dietary iodine supplies by program managers, and in provision of coalition oversight by high-level officials. Conclusions: Because salt iodization is a supply-based strategy, reliable accuracy at the source is most critical. It is therefore vital that each salt factory should adopt a quality management system, with standard operating procedures at least for the manufacturing and packaging of iodized salt. Titration is preferred but other quantitative methods with e.g. the WYD Checker, i-Reader or Bioanalyt can also yield accurate data. Improved accuracy down the supply chain is desirable, especially in surveillance, but commonly points to the need for ensured accuracy at the source when quality failures are discovered. The need remains for an agreed approach to obtain reliable data of the use of iodized salt in the food manufacturing industry.

Iodine is essential for the synthesis of thyroid hormone. Iodine deficiency develops due to imbalance between dietary iodine intake and thyroid requirements. Iodine deficiency disorders (IDD) includes a wide spectrum of abnormalities in the physical and cognitive development of human.

BACKGROUND:Hypothyroidism is a known side effect of treatment for multidrug-resistant tuberculosis (MDR-TB), but it is considered to be rare. Hypothyroidism has vague and non-specific symptoms, and can be easily missed by clinicians.OBJECTIVE:To report the high rate of hypothyroidism in a cohort of MDR-TB patients in Lesotho and to describe our approach to diagnosis and management.DESIGN:A retrospective study of 212 patients who initiated treatment for MDR-TB in Lesotho between 27 July 2007 and 24 March 2009 was performed.RESULTS:Among 186 patients screened, 129 (69%) had hypothyroidism, defined as at least one documented thyroid-stimulating hormone (TSH) result > 10.0 mIU/l; 100 (54%) patients had a maximum TSH > 20.0 mIU/l. At 93 days after starting MDR-TB treatment, half of the patients had developed hypothyroidism.CONCLUSION:Hypothyroidism may be more common during MDR-TB treatment than previously recognized. Screening all patients, even those without symptoms, for hypothyroidism within 2-3 months of starting MDR-TB treatment should be considered until prospective studies can inform screening guidelines.

Objective: Universal salt iodization is an effective strategy to optimize population-level iodine. At the same time as salt-lowering initiatives are encouraged globally, there is concern about compromised iodine intakes. This study investigated whether salt intakes at recommended levels resulted in a suboptimal iodine status in a country where salt is the vehicle for iodine fortification. Methods: Three 24-h urine samples were collected for the assessment of urinary sodium and one sample was taken for urinary iodine concentrations (UICs) in a convenience sample of 262 adult men and women in Cape Town, South Africa. Median UIC was compared across categories of sodium excretion equivalent to salt intakes lower than 5, 5 to 9, and greater than or equal to 9 g/d. Results: The median UIC was 120 mg/L (interquartile range 75.3–196.3), indicating iodine sufficiency. Less one-fourth (23.2%) of subjects had urinary sodium excretion values within the desirable range (salt <5 g/d), 50.7% had high values (5–9 g/d), and 22.8% had very high values (� 9 g/d). No association between urinary iodine and mean 3 � 24-h urinary sodium concentration was found (r ¼ 0.087, P ¼ 0.198) and UIC status did not differ according to urinary sodium categories (P ¼ 0.804). Conclusion: In a country with mandatory universal salt iodization, consumers with salt intakes within the recommended range (<5 g/d) are iodine replete, and median UIC does not differ across categories of salt intake. This indicates that much of the dietary salt is provided from non-iodinated sources, presumably added to processed foods.

Iodine deficiency is a global problem of immense magnitude afflicting 2 billion of the world's population. The adverse effects of iodine deficiency in humans, collectively termed iodine deficiency disorders, result from decreased thyroid hormone production and action, and vary in severity from thyroid enlargement (goiter) to severe, irreversible brain damage, termed endemic cretinism. Thyroid hormone is essential throughout life, but it is critical for normal brain development in the fetus and throughout childhood. During pregnancy, maternal thyroid hormone production must increase by 25-50% to meet maternal-fetal requirements. The principal sources of iodine in the diet include milk and dairy products, seafoods and foods with added iodized salt. Vegetables, fruits and cereals are generally poor sources of iodine because most of our soils and water supplies are deficient in iodine. The accepted solution to the problem is Universal Salt Iodization where all salt for human and animal consumption is iodized at a level of 20-40 µg/g. In principle, mandatory fortification represents the most effective public health strategy where safety and efficacy can be assured and there is a demonstrated need for the nutrient in the population. Voluntary fortification of salt and other foods has many limitations and few benefits. Iodine supplementation is a useful, but expensive, inefficient and unsustainable strategy for preventing iodine deficiency. The current worldwide push to decrease salt intake to prevent cardiovascular disease presents an entirely new challenge in addressing iodine deficiency in both developing and developed countries.

Good quality data on iodine concentrations in urine and salt samples are indispensable for the efficient management of national salt iodisation programmes and for evaluating iodine interventions. Most of the analytical methods for urinary iodine concentration are based on the manual spectrophotometric measurement of Sandell-Kolthoff reduction reaction catalysed by iodine using different oxidising reagents in the initial digestion step. Other analytical methods include semi-quantitative methods, a microplate method, automated methods; and the technologically advanced methods include the inductively coupled plasma mass-spectrometer method. Iodine in salt is determined quantitatively by the titration method, colorimetrically by the WYD iodine checker or by a technologically advanced potentiometric method. Worldwide, titration is the method of choice because of its accuracy, ease of operation and low cost. Rapid test kits are suitable for qualitative use in situations where iodised salt need to be distinguished from non-iodised salt, preferably with titration back-up.

Knowledge of iodine nutrition among the various role players involved in a national salt iodization program could be considered as one of the important, but often neglected, components of such programs. Moreover, the scant information published on this topic shows variable levels of knowledge of iodine in different countries. Knowledge of iodine nutrition is considered one of the process factors operating either on its own, or via one of the other process indicators, which has an impact on the iodine status of people, and most likely plays a crucial role in the sustainability of salt iodization programs. Because of its importance, various groups or role players in any country, such as politicians and health ministerial staff, salt producers, wholesalers and retailers, consumers, producers of processed foods, and medical and health professionals, should be knowledgeable about iodine nutrition. The level of knowledge regarding iodine nutrition can be assessed in these groups using appropriately designed questionnaires.

BACKGROUND:Chronic iodine deficiency (ID) increases thyrotropin (TSH) concentrations and produces a thyroid hormone pattern consistent with subclinical hypothyroidism (ScH). ScH may be associated with cardiovascular disease risk factors. Thus, the study aim was to determine if iodine treatment of children with elevated TSH concentrations due to ID would affect their lipid profile, insulin (C-peptide) levels, and/or subclinical inflammation.METHODS:In controlled intervention trials of oral iodized oil or iodized salt, 5-14-year-old children from Morocco, Albania, and South Africa with TSH concentrations > or = 2.5 mU/L (n = 262) received 400 mg iodine as oral iodized oil or household distribution of iodized salt containing 25 microg iodine/g salt. At baseline and after 5 or 6 months, urinary iodine (UI) and blood concentrations of total thyroxine, TSH, C-reactive protein (CRP), C-peptide, and lipids were measured.RESULTS:Median (range) UI at baseline was 46 (2-601) microg/L. Compared to the control group, iodine treatment significantly increased UI and total thyroxine and decreased TSH, C-peptide, and total and low-density lipoprotein cholesterol. The mean low-density lipoprotein/high-density lipoprotein cholesterol ratio fell from 3.3 to 2.4 after iodine treatment (p < 0.001). Iodine treatment had no significant effect on concentrations of high-density lipoprotein cholesterol, triglycerides, or C-reactive protein.CONCLUSIONS:Correction of ID-associated ScH improves the insulin and lipid profile and may thereby reduce risk for cardiovascular disease. This previously unrecognized benefit of iodine prophylaxis may be important because ID remains common in rapidly developing countries with increasing rates of obesity and cardiovascular disease.

Objectives: To gather baseline information on the knowledge, attitudes and practices regarding iodine and iodised salt among patients with hyperthyroidism in the Free State.Subjects and Setting: The study was part of a large cohort study that included the first 96 patients aged 13 years or older diagnosed with hyperthyroidism and referred to Universitas Academic Hospital in Bloemfontein, South Africa during 2005.Methods: The patients were interviewed in their language using a structured validated questionnaire. Descriptive statistics were used for data analysis.Results: The majority of the patients (86.9%) did not know what iodine was. Similarly, a higher percentage of patients (76.7%) were unaware of the most important or main source of iodine in the food of South Africans. Regarding knowledge of the most important harmful effect on the health of children if they did not get enough iodine, almost all of the patients (89.1%) did not know what it was. Ninety-five per cent of salt was obtained from the local shops, and only 36.1% of the patients read the labelling on the package during purchase. A very small proportion of patients (1.6%) stored salt in closed containers and away from sunlight, while about half of them (49.2%) stored salt in open containers without lids, 36.1% stored it in rigid plastic containers with holes at the top, and 13.1% stored it in the open plastic bags in which the salt was bought.Conclusions: Patients with hyperthyroidism lacked knowledge of iodine, as well as of the storage of iodised salt, and this could have contributed to the persisting endemic goitre reported in previous studies. An aggressive awareness programme, targeting policy makers and the public, is recommended to ensure sustainable elimination of iodine deficiency disorders in South Africa.

Before the introduction of salt iodisation in 1954, South Africa was one of the many countries of the world with a lack of iodine in most of its territory and hence there was a need for a salt iodisation programme. The understanding of the iodine situation in South Africa, the basics of iodine nutrition and progress toward eliminating iodine deficiency internationally and in South Africa are reviewed in this paper. Voluntary salt iodisation in the country at 10-20 ppm introduced in 1954 failed to eliminate endemic goitre and iodine deficiency. In contrast, considerable progress has been achieved in South Africa in eliminating iodine deficiency by introducing mandatory iodisation of table salt at 40-60 ppm in 1995. A 1998 survey showed that optimal iodine nutrition was achieved nationally and in seven of the nine provinces, with more than adequate iodine intake in two provinces. At that time, 86.4% of households used iodised salt and 62.4% used adequately iodised salt that contained more than 15 ppm of iodine, with low coverage rates (< 50%) in the three northern provinces (Limpopo, Mpumalanga and North West). Closer collaboration between the South African Iodine Deficiency Disorders Network and the salt industry resulted in improved accuracy of salt iodisation. Knowledge of iodine nutrition amongst adults is low, particularly in low socioeconomic households, leading to the vulnerability of these groups to obtain non-iodised salt for cooking via unconventional sources. In South Africa a sound scientific data base should be used to maintain the strengths of the national salt iodisation programme and improve on any aspects of the programme in need of attention.

2 billion individuals worldwide have insufficient iodine intake, with those in south Asia and sub-Saharan Africa particularly affected. Iodine deficiency has many adverse effects on growth and development. These effects are due to inadequate production of thyroid hormone and are termed iodine-deficiency disorders. Iodine deficiency is the most common cause of preventable mental impairment worldwide. Assessment methods include urinary iodine concentration, goitre, newborn thyroid-stimulating hormone, and blood thyroglobulin. In nearly all countries, the best strategy to control iodine deficiency is iodisation of salt, which is one of the most cost-effective ways to contribute to economic and social development. When iodisation of salt is not possible, iodine supplements can be given to susceptible groups. Introduction of iodised salt to regions of chronic iodine-deficiency disorders might transiently increase the proportion of thyroid disorders, but overall the small risks of iodine excess are far outweighed by the substantial risks of iodine deficiency. International efforts to control iodine-deficiency disorders are slowing, and reaching the third of the worldwide population that remains deficient poses major challenges.

Background — Both inadequate and high intakes of iodine are associated with thyroid disease and associated abnormalities. Consumption of foods deficient in iodine induces hypothyroidism. Conversely, excessive intake of the nutrient precipitates hyperthyroidism. Iodine deficiency causes impairment of thyroid hormonogenesis resulting in goiter (struma), cretinism which is associated with increased prenatal and infant mortality, deafness, motor disabilities and mental retardation due to damage during fetal and neonatal brain development. We have assessed the iodine status of school children from the locality of Port Sudan, Red Sea State of Eastern Sudan. The primary sources of iodine of the children are mainly iodized salt and rations supplied by local donors and various aid agencies operating in the Sudan. Methods — Male and female children (n=141), aged 6 to 12 years (median age 9.8 years), were selected for the survey using a multistage random sampling technique, between May 22 and August 25, 2006. All the children were assessed for urinary iodine and visible goiter. In addition, the iodine content of twenty salt samples was determined using the Iodometric titration method and spot test kits. The components of other foods that are routinely consumed by the children and households were noted using a questionnaire form. Findings — Urinary iodine concentration exceeded 300µg/l and 1000µg/l in 65% and 9.9% of the children, respectively. The highest urinary iodine level was 1470µg/l. The prevalence of visible goiter was 17%. All the salt samples collected from the schools had more than 150mg potassium iodate per kg of salt. Conclusions — The results of this pilot survey reveal that excessive intake of iodine in children exists in Port Sudan. Inappropriate and unregulated local fortification of salt and lack of monitoring of the imported and donated salt is the primary reason for the excessive intake. There is an urgent need for a regulatory mechanism during the process of iodine fortification and at the point of entry of imported and donated iodized salt as well as the mode of delivery in order to avoid hyperthyroidism and associated disorders. In addition, independent professionals should critically evaluate the health impact of excessive consumption of the nutrient.