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Michael B Zimmermann - One of the best experts on this subject based on the ideXlab platform.
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decision analytic modeling studies in prevention and treatment of Iodine Deficiency and thyroid disorders a systematic overview
Thyroid, 2020Co-Authors: U Rochau, Vjollca Qerimi Rushaj, M Schaffner, Marie Schonhensch, I Stojkov, Beate Jahn, Alicija Hubalewskadydejczyk, Iris Erlund, Betina H Thuesen, Michael B ZimmermannAbstract:Background: Prevention and treatment of Iodine Deficiency-related diseases remain an important public health challenge. Iodine Deficiency can have severe health consequences, such as cretinism, goi...
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Iodine Deficiency and thyroid disorders
The Lancet Diabetes & Endocrinology, 2015Co-Authors: Michael B Zimmermann, Kristien BoelaertAbstract:Iodine Deficiency early in life impairs cognition and growth, but Iodine status is also a key determinant of thyroid disorders in adults. Severe Iodine Deficiency causes goitre and hypothyroidism because, despite an increase in thyroid activity to maximise Iodine uptake and recycling in this setting, Iodine concentrations are still too low to enable production of thyroid hormone. In mild-to-moderate Iodine Deficiency, increased thyroid activity can compensate for low Iodine intake and maintain euthyroidism in most individuals, but at a price: chronic thyroid stimulation results in an increase in the prevalence of toxic nodular goitre and hyperthyroidism in populations. This high prevalence of nodular autonomy usually results in a further increase in the prevalence of hyperthyroidism if Iodine intake is subsequently increased by salt iodisation. However, this increase is transient because Iodine sufficiency normalises thyroid activity which, in the long term, reduces nodular autonomy. Increased Iodine intake in an Iodine-deficient population is associated with a small increase in the prevalence of subclinical hypothyroidism and thyroid autoimmunity; whether these increases are also transient is unclear. Variations in population Iodine intake do not affect risk for Graves' disease or thyroid cancer, but correction of Iodine Deficiency might shift thyroid cancer subtypes toward less malignant forms. Thus, optimisation of population Iodine intake is an important component of preventive health care to reduce the prevalence of thyroid disorders.
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Iodine Deficiency disorders and their correction using iodized salt and or Iodine supplements
Iodine Chemistry and Applications, 2014Co-Authors: Michael B ZimmermannAbstract:Iodine is an essential component of hormones produced by the thyroid gland. Thyroid hormones, and therefore Iodine, are essential for mammalian life. Optimal dietary Iodine intake for healthy adults is 150–250 μg day-1. In regions where Iodine in soils and drinking water is low, humans and animals may become Iodine deficient. Iodine Deficiency has multiple adverse effects in humans due to inadequate thyroid hormone production that are termed the Iodine Deficiency disorders (IDD). Iodine Deficiency during pregnancy and infancy may impair growth and neurodevelopment of the offspring and increase infant mortality. Deficiency during childhood reduces somatic growth and cognitive and motor function. Assessment methods include urinary Iodine concentration (UIC), goiter, newborn thyrotropin (TSH), and blood thyroglobulin. In most countries, the best strategy to control Iodine Deficiency in populations is iodization of salt, one of the most cost-effective ways to contribute to economic and social development.
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the effects of Iodine Deficiency in pregnancy and infancy
Paediatric and Perinatal Epidemiology, 2012Co-Authors: Michael B ZimmermannAbstract:Iodine requirements are increased ≥ 50% during pregnancy. Iodine Deficiency during pregnancy can cause maternal and fetal hypothyroidism and impair neurological development of the fetus. The consequences depend upon the timing and severity of the hypothyroidism; the most severe manifestation is cretinism. In moderate-to-severely Iodine-deficient areas, controlled studies have demonstrated that Iodine supplementation before or during early pregnancy eliminates new cases of cretinism, increases birthweight, reduces rates of perinatal and infant mortality and generally increases developmental scores in young children by 10-20%. Mild maternal Iodine Deficiency can cause thyroid dysfunction but whether it impairs cognitive and/or neurologic function in the offspring remains uncertain. Two meta-analyses have estimated that Iodine-deficient populations experience a mean reduction in IQ of 12-13.5 points. In nearly all regions affected by Iodine Deficiency, salt iodisation is the most cost-effective way of delivering Iodine and improving maternal and infant health.
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Iodine Deficiency in pregnancy and the effects of maternal Iodine supplementation on the offspring a review
The American Journal of Clinical Nutrition, 2009Co-Authors: Michael B ZimmermannAbstract:The World Health Organization (WHO) recently increased their recommended Iodine intake during pregnancy from 200 to 250 microg/d and suggested that a median urinary Iodine (UI) concentration of 150-249 microg/L indicates adequate Iodine intake in pregnant women. Thyrotropin concentrations in blood collected from newborns 3-4 d after birth may be a sensitive indicator of even mild Iodine Deficiency during late pregnancy; a 5 mU/L indicates Iodine sufficiency. New reference data and a simple collection system may facilitate use of the median UI concentration as an indicator of Iodine status in newborns. In areas of severe Iodine Deficiency, maternal and fetal hypothyroxinemia can cause cretinism and adversely affect cognitive development in children; to prevent fetal damage, Iodine should be given before or early in pregnancy. Whether mild-to-moderate maternal Iodine Deficiency produces more subtle changes in cognitive function in offspring is unclear; no controlled intervention studies have measured long-term clinical outcomes. Cross-sectional studies have, with few exceptions, reported impaired intellectual function and motor skills in children from Iodine-deficient areas, but many of these studies were likely confounded by other factors that affect child development. In countries or regions where <90% of households are using iodized salt and the median UI concentration in school-age children is <100 microg/L, the WHO recommends Iodine supplementation in pregnancy and infancy.
Francois Delange - One of the best experts on this subject based on the ideXlab platform.
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neonatal thyroid screening as a monitoring tool for the control of Iodine Deficiency
Acta Paediatrica, 2007Co-Authors: Francois DelangeAbstract:In conditions of Iodine Deficiency, the frequency distribution of neonatal thyroid-stimulating hormone (TSH) is shifted towards elevated values. Elevated serum TSH in the neonate indicates insufficient supply of thyroid hormones to the developing brain, and therefore constitutes the only indicator that allows prediction of brain damage, which is the main complication of Iodine Deficiency. This paper reviews studies on neonatal thyroid function in Iodine Deficiency and confirms the former statement by WHO/UNICEF/ICCIDD that the frequency of neonatal TSH above 5 mU/L blood is below 3% in conditions of normal Iodine supply, that a frequency of 3-19.9% indicates mild Iodine Deficiency and that frequencies of 20-39.9% and above 40% indicate moderate to severe Iodine Deficiency, respectively. Neonatal thyroid screening appears as a particularly sensitive index in the monitoring of Iodine supply at a population level.
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world status of monitoring of Iodine Deficiency disorders control programs
Thyroid, 2002Co-Authors: Francois Delange, Hans Burgi, Zu Pei Chen, John T DunnAbstract:Monitoring and evaluation are the last phases of a national Iodine Deficiency disorders (IDD) control program but among the most important. This paper summarizes the latest recommendations by the World Health Organization (WHO), the United Nations Children's Fund (UNICEF), and the International Council for Control of Iodine Deficiency Disorders (ICCIDD) about indicators and their normative values for monitoring the progress of IDD elimination and illustrates the successful monitoring programs in Switzerland and in China. Salt is the usual vehicle for Iodine supplementation and quality control for Iodine content can be assessed quantitatively by titration and qualitatively by simple test kits that can be used in the field. The most useful indicator of Iodine nutrition is the median urinary Iodine concentration. Thyroid size, especially by ultrasound, and neonatal thyrotropin (TSH) are also valuable. In Switzerland, access to iodized salt on a voluntary basis started in 1922. The initial level of iodization, 1.9-3.75 ppm Iodine as potassium iodide (KI), was slowly increased to 15 ppm, and recently to 20 ppm, after careful epidemiologic and biologic monitoring. Elimination of IDD has been highly successful. The program costs US dollars 0.07 per year per person. In China, a national program of iodized salt (10-30 ppm) started in 1960 under the authority of the central government and rapidly expanded. National monitoring surveys have taken place every 2 years since 1993. Median urinary Iodine, initially low, increased to 165 microg/L in 1995 and to 306 microg/L in 1999, prompting a decrease in the amount of Iodine added to salt. The total goiter rate decreased to 20.4% in 1995 and to 8.8% in 1999. IDD can presently be considered as eliminated in China. Review of monitoring in the 128 other major countries affected by IDD shows extremely variable achievements, with evidence of IDD elimination in at least 18 additional countries. Some countries that were severely Iodine deficient in the past are now exposed to Iodine excess and risk its effects. Sustainable elimination of IDD is within reach and would constitute an unprecedented global success story in the field of noncommunicable diseases, but continuing vigorous action is required to attain this goal.
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Iodine Deficiency as a cause of brain damage
Postgraduate Medical Journal, 2001Co-Authors: Francois DelangeAbstract:This editorial reviews the impact of Iodine Deficiency (1) on thyroid function in pregnant women and neonates and (2) on the neurointellectual development of infants and children. All degrees of Iodine Deficiency (mild: Iodine intake of 50–99 μg/day, moderate: 20–49 μg/day, and severe: Iodine Deficiency results in a global loss of 10–15 IQ points at a population level and constitutes the world9s greatest single cause of preventable brain damage and mental retardation.
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screening for congenital hypothyroidism used as an indicator of the degree of Iodine Deficiency and of its control
Thyroid, 1998Co-Authors: Francois DelangeAbstract:Neonatal thyroid screening using serum thyrotropin (TSH) as the primary screening test detects not only permanent sporadic congenital hypothyroidism, whose incidence is about 1 per 4000 births, but also compensated or transient primary hypothyroidism, whose incidence can be as high as 1 in 10 neonates and whose main cause is Iodine Deficiency. Elevated serum TSH in the neonate indicates insufficient supply of thyroid hormones to the developing brain, and therefore, constitutes the only indicator that allows prediction of possible impairment of mental development at a population level, which is the main consequence of Iodine Deficiency. Therefore, the World Health Organization (WHO), United Nations International Children's Emergency Fund (UNICEF), and the International Council for Control of Iodine Deficiency Disorders (ICCIDD) included neonatal TSH as one of the indicators for assessing Iodine Deficiency disorders (IDD) and their control. In the absence of Iodine Deficiency, the frequency of neonatal TSH above 5 mU/L whole blood (or 10 mU/L serum) is less than 3%. A frequency of 3%-19.9% indicates mild IDD. Frequencies of 20%-39.9% and above 40% indicate moderate and severe IDD, respectively. Neonates exhibit elevated serum TSH more frequently than adults for a similar degree of Iodine Deficiency. Consequently, they appear hypersensitive to the effects of Iodine Deficiency. This characteristic is explained by a particularly low Iodine content of the thyroid of neonates and, consequently, by an accelerated turnover rate of their intrathyroidal Iodine reserves. This turnover rate is 1% in adults. It is 17% in the neonate in conditions of Iodine repletion, but is as high as 62% and 125% in conditions of moderate and severe Iodine Deficiency, respectively. Such an accelerated turnover rate requires thyroid hyperstimulation by TSH that is morphologically evidenced even in moderately Iodine deficient neonates. Neonatal screening using primary TSH is implemented in most countries with mild IDD where it detects the cases of sporadic, permanent congenital hypothyroidism and where it is also used as a monitoring tool for IDD evaluation and control. However, the implementation of such programs in countries affected by moderate or severe IDD is still insufficient because of lack of resources of the countries. This should be considered in the framework of the external support often provided to these countries for the implementation of programs of universal salt iodization. Monitoring of these programs in order to achieve the goal of sustainable elimination of IDD now constitutes an absolute priority.
Kristien Boelaert - One of the best experts on this subject based on the ideXlab platform.
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Iodine Deficiency and thyroid disorders
The Lancet Diabetes & Endocrinology, 2015Co-Authors: Michael B Zimmermann, Kristien BoelaertAbstract:Iodine Deficiency early in life impairs cognition and growth, but Iodine status is also a key determinant of thyroid disorders in adults. Severe Iodine Deficiency causes goitre and hypothyroidism because, despite an increase in thyroid activity to maximise Iodine uptake and recycling in this setting, Iodine concentrations are still too low to enable production of thyroid hormone. In mild-to-moderate Iodine Deficiency, increased thyroid activity can compensate for low Iodine intake and maintain euthyroidism in most individuals, but at a price: chronic thyroid stimulation results in an increase in the prevalence of toxic nodular goitre and hyperthyroidism in populations. This high prevalence of nodular autonomy usually results in a further increase in the prevalence of hyperthyroidism if Iodine intake is subsequently increased by salt iodisation. However, this increase is transient because Iodine sufficiency normalises thyroid activity which, in the long term, reduces nodular autonomy. Increased Iodine intake in an Iodine-deficient population is associated with a small increase in the prevalence of subclinical hypothyroidism and thyroid autoimmunity; whether these increases are also transient is unclear. Variations in population Iodine intake do not affect risk for Graves' disease or thyroid cancer, but correction of Iodine Deficiency might shift thyroid cancer subtypes toward less malignant forms. Thus, optimisation of population Iodine intake is an important component of preventive health care to reduce the prevalence of thyroid disorders.
Torben Jorgensen - One of the best experts on this subject based on the ideXlab platform.
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effect of a mandatory iodization program on thyroid gland volume based on individuals age gender and preceding severity of dietary Iodine Deficiency a prospective population based study
The Journal of Clinical Endocrinology and Metabolism, 2007Co-Authors: Pernille Vejbjerg, Nils Knudsen, Hans Perrild, Allan Carle, Peter Laurberg, Inge Bulow Pedersen, Lone Banke Rasmussen, Lars Ovesen, Torben JorgensenAbstract:Objective: We aimed to evaluate prospectively the effect of 4 yr of mandatory iodization of salt (13 ppm Iodine) on thyroid volume in two regional areas with respectively mild and moderate Iodine Deficiency. Methods: Two separate cross-sectional studies were performed before (n = 4649) and after (n = 3570) the iodization in year 2000 in two areas with mild and moderate Iodine Deficiency. Women aged 18–22, 25–30, 40–45, and 60–65 yr and men aged 60–65 yr were examined. Thyroid ultrasonography was performed. Results: A lower median thyroid volume was seen in all age groups after iodization. The largest relative decline was found among the younger females from the area with previous, moderate Iodine Deficiency. Only a minor decrease was seen among the youngest participants in the area with previous, mild Iodine Deficiency. After iodization, there were no regional differences in median thyroid volume in the age groups younger than 45 yr. When adjusted for confounders, a lower mean volume was seen among those ...
Paolo Vitti - One of the best experts on this subject based on the ideXlab platform.
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effect of iodized salt on thyroid volume of children living in an area previously characterized by moderate Iodine Deficiency
The Journal of Clinical Endocrinology and Metabolism, 1997Co-Authors: F Aghinilombardi, L Antonangeli, Teresa Rago, Aldo Pinchera, Francesco Leoli, Anna M Bartolomei, Paolo VittiAbstract:It is well established that an adequate Iodine intake prevents Iodine Deficiency disorders. Prophylaxis through iodized salt is able to correct urinary Iodine Deficiency and to prevent goiter endemia, but scanty data are available about its effect on decreasing the thyroid size in goitrous children born before prophylaxis. The prevalence of goiter was evaluated by ultrasound in the school-children population of an area of Eastern Tuscany (Tiberina Valley) characterized by moderate Iodine Deficiency in 1985. At present, after the implementation of voluntary iodized salt consumption, Iodine urinary excretion was borderline sufficient (median, 98 micrograms/L). Goiter prevalence was higher at ultrasound (17%) than by palpation (10%). The median thyroid volume ranged from 3.1 mL in 7-yr-old children to 9.2 mL in 14-yr-old children. In the 7-10 yr age class (i.e. in children born after Iodine prophylaxis), no statistical difference in thyroid volume was found with respect to controls. In older children (11-14 yr) born before the institution of Iodine prophylaxis, the median thyroid volume was significantly higher than that in age-matched controls. Moreover, in this cluster of subjects, the median thyroid volume in nongoitrous children was higher than that in controls. In conclusion, the data of the present study indicate that the iodized salt prophylaxis is able to prevent the development of goiter in children born after the implementation of iodized salt consumption and to further control thyroid enlargement in older children, but is less effective (or rapid) in reducing goiter size in children exposed to Iodine Deficiency in the first years of life.
