Talk:Abnormal Development - Iodine Deficiency

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Cite this page: Hill, M.A. (2019, August 18) Embryology Abnormal Development - Iodine Deficiency. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Abnormal_Development_-_Iodine_Deficiency

2016

Iodine Supplementation in Pregnancy - is it time?

Clin Endocrinol (Oxf). 2016 Mar 21. doi: 10.1111/cen.13065. [Epub ahead of print]

Taylor P1, Vaidya B1, Taylor P1, Vaidya B2.

Abstract

Iodine is essential for the synthesis of thyroid hormone and optimal fetal neurological development. Pregnant women living in borderline or moderate-severe iodine deficient areas are at particularly high risk of being iodine deficient, and this may have important clinical consequences, particularly for the neurocognitive development of the offspring. It is a substantial problem and many countries including the UK are mild-moderately iodine deficient. Although the detrimental effects of severe iodine deficiency are well recognised, the benefits of correcting mild-to-moderate iodine deficiency are unclear due to a lack of randomized controlled trials in this area. However, observational data increasingly indicate that there may be substantial health and economic benefits from correcting iodine deficiency in pregnancy. There is now a growing trend from learned societies that iodine supplementation should be utilized in pregnancy in countries with mild-to-moderate iodine deficiency. The dose of iodine supplement needs to reflect local iodine status and iodisation policies and will need careful monitoring at the population level to ensure doses to prevent under/excess dosing which would undermine the potential benefits. National tailored guidance is therefore essential. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved. KEYWORDS: IQ ; Iodine; Thyroid; deficiency; pregnancy; supplementation PMID 26998765

2015

Iodine deficiency during pregnancy: a national cross-sectional survey in Latvia

Public Health Nutr. 2015 Mar 3:1-8. [Epub ahead of print]

Konrade I1, Kalere I1, Strele I1, Makrecka-Kuka M1, Jekabsone A1, Tetere E1, Veisa V1, Gavars D2, Rezeberga D1, Pīrāgs V3, Lejnieks A1, Dambrova M1. Author information

OBJECTIVE: Low iodine intake during pregnancy may cause thyroid dysfunction, which results in inadequate fetal brain development. In the absence of a universal salt iodization programme, we conducted a nationwide survey of iodine deficiency in pregnant women in Latvia. DESIGN: A countrywide twenty-cluster survey, with at least twenty women per cluster. Participants completed a questionnaire on dietary habits concerning iodine intake (n 739). Thyroid function (thyroid-stimulating hormone, free thyroxine and thyroperoxidase antibodies) was measured (n 550). Urinary iodine was measured using the ammonium persulfate method (n 696). SETTING: The survey was performed in all regions of Latvia during the spring and autumn seasons in 2013. SUBJECTS: Pregnant women (n 829). RESULTS: The median creatinine (Cr)-standardized urinary iodine concentration (UIC) was 80·8 (interquartile range (IQR) 46·1-130·6) µg/g Cr or 69·4 (IQR 53·9-92·6) µg/l during pregnancy, and 81 % of pregnant women had UIC levels below the WHO recommended range of 150-250 µg/g Cr. The UIC was lowest during the first trimester of pregnancy, 56·0 (IQR 36·4-100·6) µg/g Cr, reaching higher concentrations of 87·5 (IQR 46·4-141·7) µg/g Cr and 86·9 (IQR 53·8-140·6) µg/g Cr in the second and third trimesters, respectively. Women taking supplements containing ≥150 µg iodine (6·8 % of respondents) had non-significantly higher UIC than did women without supplementation (96·2 v. 80·3 µg/g Cr, respectively, P=NS). Thyroperoxidase antibody concentration did not correlate significantly with UIC: Spearman's ρ=-0·012, P=0·78. CONCLUSIONS: The median UIC indicates iodine deficiency in pregnant women in Latvia. Iodine supplementation (150 µg daily) and regular UIC monitoring should be suggested to overcome iodine deficiency and to reach the recommended levels without inducing autoimmune processes. KEYWORDS: Iodine supplementation

PMID 25731595

2014

Iodine deficiency in children

Endocr Dev. 2014;26:130-8. doi: 10.1159/000363160. Epub 2014 Aug 29.

Pearce EN.

Abstract

Iodine is an essential trace mineral, required for the production of thyroid hormone. Iodine deficiency may result in goiter, hypothyroidism, miscarriage, stillbirth, congenital anomalies, infant and neonatal mortality, and impaired growth. Adequate thyroid hormone is critically important for normal growth and neurodevelopment in fetal life, infancy and childhood. The population iodine status is most commonly assessed using median urinary iodine concentration values, but goiter prevalence (determined by palpation or by ultrasound), serum thyroglobulin levels, and neonatal thyroid-stimulating hormone values can also be used. Universal salt iodization programs have been the mainstay of public health efforts to eliminate iodine deficiency worldwide. However, in some regions targeted fortification of foods such as bread has been used to combat iodine deficiency. Iodine supplementation may be required in areas where dietary fortification is not feasible or where it is not sufficient for vulnerable groups such as pregnant women. Although international public health efforts over the past several decades have been highly effective, nearly one third of children worldwide remain at risk for iodine deficiency, and iodine deficiency is considered the leading preventable cause of preventable intellectual deficits.

PMID 25231449

Maternal Urinary Iodine Concentration up to 1.0 mg/L Is Positively Associated with Birth Weight, Length, and Head Circumference of Male Offspring

J Nutr. 2014 Jul 16. pii: jn.114.193029. [Epub ahead of print]

Rydbeck F1, Rahman A2, Grandér M1, Ekström EC3, Vahter M1, Kippler M4.

Abstract

Adequate iodine status in early life is crucial for neurodevelopment. However, little is known about the effects of maternal iodine status during pregnancy on fetal growth. The present study investigated the potential impact of maternal iodine status during pregnancy on offspring birth size. This large prospective cohort study was nested in a Bangladeshi population-based randomized supplementation trial in pregnant women [MINIMat (Maternal and Infant Nutrition Interventions in Matlab)]. Urine samples obtained at 8 wk of gestation from 1617 women were analyzed for iodine and other elements, such as arsenic and cadmium, using inductively coupled plasma mass spectrometry. Anthropometric measurements at birth included weight, length, and head and chest circumference. Maternal urinary iodine concentrations (UICs) ranged from 0.020 to 10 mg/L, with a median of 0.30 mg/L. Below ∼1.0 mg/L, UIC was significantly positively associated with birth weight and length. Birth weight and length increased by 9.3 g (95% CI: 2.9, 16) and 0.042 cm (95% CI: 0.0066, 0.076), respectively, for each 0.1-mg/L increase in maternal UIC. No associations were observed between UIC and head or chest circumference. When we stratified the analyses by newborn sex, the positive associations between maternal UIC (<1 mg/L) and measurements of size at birth were restricted to boys, with no evidence in girls. Among boys, the mean weight, length, and head circumference increased by 70 g (P = 0.019), 0.41 cm (P = 0.013), and 0.28 cm (P = 0.031) for every 0.5-mg/L increase in maternal UIC. Maternal iodine status was positively associated with weight, length, and head circumference in boys up to ∼1 mg/L, which is well above the recommended maximum concentration of 0.5 mg/L. The associations leveled off at UIC ≥ 1 mg/L. Our findings support previous conclusions that the advantages of correcting potential iodine deficiency outweigh the risks of excess exposure. © 2014 American Society for Nutrition.

PMID 25031330

2012

Screening for thyroid disease and iodine deficiency

Pathology. 2012 Feb;44(2):153-9.

Eastman CJ. Source International Council for Control of Iodine Deficiency Disorders, and Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia. ceastman@med.usyd.edu.au

Abstract

The high global prevalence of iodine deficiency and autoimmune thyroid disorders and the mental and physical consequences of these disorders creates a huge human and economic burden that can be prevented, in large part, by early detection and appropriate preventative or therapeutic measures. The availability of sophisticated, sensitive and accurate laboratory testing procedures provides an efficient and effective platform for the application of screening for these disorders. Measurement of urine iodine concentration (UIC) in school children or pregnant women is the recommended indicator for screening populations for iodine deficiency. The severity of the iodine deficiency is classified according to the UIC. Measurement of serum thyrotropin (TSH) as an indicator for population iodine deficiency is used only in neonates and is supplementary to UIC screening. Other indicators such as goitre rates, thyroid function and serum thyroglobulin levels are useful adjunctive but not frontline process indicators. The human and economic benefits of screening for congenital hypothyroidism by measurement of heel-prick TSH have been well documented and justify its universal application. Using this measurement for monitoring population iodine intake is recommended by the World Health Organization but further validation is required before it can be universally recommended. Subclinical thyroid dysfunction is readily detected by current highly sensitive serum TSH assays and its prevalence appears to increase with age, varies with iodine intake and ethnicity and may occur in up to 20% of older age people. Subclinical hyperthyroidism is the less common disorder and screening cannot be justified because of its low prevalence and minimal or insignificant clinical effects. The argument for screening for subclinical hypothyroidism in middle-aged and older women is stronger but lacks evidence of benefit from randomised controlled trials or cost benefit analyses of therapeutic intervention, so it cannot currently be recommended. The publication of recent Clinical Practice Guidelines for management of thyroid disease in pregnancy from the American Endocrine Society and American Thyroid Association provide persuasive arguments for early detection and treatment of overt and subclinical hypothyroidism to prevent obstetric complications and potential neurocognitive disorders in the offspring. Given the indisputable benefits of therapy, the sooner thyroid dysfunction is detected, before or as early as possible in gestation, the more likely there will be a better outcome. Because of the limitations of targeted case detection in women at risk of subclinical hypothyroidism, there has been a gradual shift in opinion to universal TSH screening of all women as soon as practicable in pregnancy. While a positive association exists between the presence of anti-thyroid antibodies and increased pregnancy loss, universal screening of all pregnant women for underlying autoimmune thyroid disease is difficult to justify until there is evidence of beneficial outcomes from randomised controlled trials. Vigorous and liberal targeted case detection remains the recommended strategy to address this problem.

PMID 22297907

2011

Thyroidology over the ages

Indian J Endocrinol Metab. 2011 Jul;15(Suppl 2):S121-6.

Niazi AK, Kalra S, Irfan A, Islam A. Source Shifa College of Medicine, Islamabad, Pakistan.

Abstract

Thyroidolody, the study of the thyroid gland, is considered to be a relatively new field of endocrinology. However, references to the thyroid gland and its diseases can be seen in the literature of ancient Greek, Indian and Egyptian medicine. Goiter has always been a disease of immense interest of the general population due to its widespread prevalence. It is one of the most common medical problems portrayed in ancient paintings. Owing to the lack of awareness and poor nutritious habits of the people in that era, diseases such as iodine deficiency goiter were common. Physicians, healers and philosophers had been attempting time and again until the 19(th) century to come up with explanations of the thyroid gland and provide a reasonable basis of its diseases. Although the discovery of thyroid gland, its structure, function and diseases has been accredited to modern scientists who presented their work mostly in the 19(th) and 20(th) century, it is of significance to note that much of what we discovered in the 19(th) and 20(th) century had already been known centuries ago. This review attempts to explain the knowledge of thyroid gland, its function and diseases as held by the people in the previous centuries; and how this knowledge evolved over the years to become what it is today.

PMID 21966648

2010

Consuming iodine enriched eggs to solve the iodine deficiency endemic for remote areas in Thailand

Nutr J. 2010 Dec 20;9(1):68. [Epub ahead of print]

Charoensiriwatana W, Srijantr P, Teeyapant P, Wongvilairattana J.

Abstract ABSTRACT:

BACKGROUND: Evidence showed that the occurrence of iodine deficiency endemic areas has been found in every provinces of Thailand. Thus, a new pilot programme for elimination of iodine deficiency endemic areas at the community level was designed in 2008 by integrating the concept of Sufficient Economic life style with the iodine biofortification of nutrients for community consumption.

METHODS: A model of community hen egg farm was selected at an iodine deficiency endemic area in North Eastern part of Thailand. The process for the preparation of high content iodine enriched hen food was demonstrated to the farm owner with technical transfer in order to ensure the sustainability in the long term for the community. The iodine content of the produced iodine enriched hen eggs were determined and the iodine status of volunteers who consumed the iodine enriched hen eggs were monitored by using urine iodine excretion before and after the implement of iodine enrichment in the model farm.

RESULTS: The content of iodine in eggs from the model farm were 93.57 ug per egg for the weight of 55 - 60 g egg and 97.76 ug for the weight of 60 - 65 g egg. The biological active iodo-organic compounds in eggs were tested by determination of the base-line urine iodine of the volunteer villagers before and after consuming a hard boiled iodine enriched egg per volunteer at breakfast for five days continuous period in 59 volunteers of Ban Kew village, and 65 volunteers of Ban Nong Nok Kean village. The median base-line urine iodine level of the volunteers in these two villages before consuming eggs were 7.00 and 7.04 ug/dL respectively. After consuming iodine enriched eggs, the median urine iodine were raised to the optimal level at 20.76 ug/dL for Ban Kew and 13.95 ug/dL for Ban Nong Nok Kean.

CONCLUSIONS: The strategic programme for iodine enrichment in the food chain with biological iodo-organic compound from animal origins can be an alternative method to fortify iodine in the diet for Iodine Deficiency Endemic Areas at the community level in Thailand.

PMID: 21167081


Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion

J Clin Invest. 2010 Sep 1;120(9):3377-88. doi: 10.1172/JCI42113. Epub 2010 Aug 2.

Di Cosmo C, Liao XH, Dumitrescu AM, Philp NJ, Weiss RE, Refetoff S.

Department of Medicine, University of Chicago, Chicago, Illinois, USA.

The mechanism of thyroid hormone (TH) secretion from the thyroid gland into blood is unknown. Humans and mice deficient in monocarboxylate transporter 8 (MCT8) have low serum thyroxine (T4) levels that cannot be fully explained by increased deiodination. Here, we have shown that Mct8 is localized at the basolateral membrane of thyrocytes and that the serum TH concentration is reduced in Mct8-KO mice early after being taken off a treatment that almost completely depleted the thyroid gland of TH. Thyroid glands in Mct8-KO mice contained more non-thyroglobulin-associated T4 and triiodothyronine than did those in wild-type mice, independent of deiodination. In addition, depletion of thyroidal TH content was slower during iodine deficiency. After administration of 125I, the rate of both its secretion from the thyroid gland and its appearance in the serum as trichloroacetic acid-precipitable radioactivity was greatly reduced in Mct8-KO mice. Similarly, the secretion of T4 induced by injection of thyrotropin was reduced in Mct8-KO in which endogenous TSH and T4 were suppressed by administration of triiodothyronine. To our knowledge, this study is the first to demonstrate that Mct8 is involved in the secretion of TH from the thyroid gland and contributes, in part, to the low serum T4 level observed in MCT8-deficient patients.

PMID: 20679730

The measurement, definition, aetiology and clinical consequences of neonatal transient hypothyroxinaemia

Ann Clin Biochem. 2010 Oct 7.

Williams F, Hume R.

Clinical and Population Sciences and Education, Human Brain Development Group, Mackenzie Building, Ninewells Hospital and Medical School Campus, Kirsty Semple Way, Dundee DD2 4BF, UK. Abstract This review focuses on neonatal transient hypothyroxinaemia, a condition characterized by temporary postnatal reductions in concentrations of Total T4 or Free T4, with normal or low concentrations of thyroid stimulating hormone (TSH). There is neither an agreed quantitative definition, nor an agreed mode of measurement for the condition. Transient hypothyroxinaemia is not routinely monitored yet it is thought to affect about 50% of preterm infants; it was thought to be without long-term sequelae but observational studies indicate that neurodevelopment may be compromised. The aetiology of transient hypothyroxinaemia is complex. There are significant contributions from the withdrawal of maternal-placental thyroxine transfer, hypothalamic-pituitary-thyroid immaturity, developmental constraints on the synthesis and peripheral metabolism of iodothyronines and iodine deficiency. It is not possible to distinguish clinically, or from laboratory measurements, whether transient hypothyroxinaemia is an independent condition or simply a consequence of non-thyroidal illness and/or drug usage. An answer to this question is important because studies of thyroid hormone replacement have been instigated, with mixed results. Until the aetiology of transient hypothyroxinaemia is better understood it would seem prudent not to routinely supplement preterm infants with thyroid hormones. Iodine deficiency, non-thyroidal illness and drug usage are the most modifiable risk factors for transient hypothyroxinaemia and are the clear choices for attempts at reducing its incidence. We suggest that transient hypothyroxinaemia in preterm infants is defined as a normal or low TSH concentration in conjunction with a concentration of Total T4, that is ≤10th percentile of cord Total T4 of the equivalent gestational age had the infant remained in utero.

PMID: 20930033

A sprinkle of salt needed for Nepal's hidden hunger

Siva N. Lancet. 2010 Aug 28;376(9742):673-4. No abstract available. PMID: 20879078

Iodine deficiency in Australia: is iodine supplementation for pregnant and lactating women warranted? Comment

Anderson WP, Zhou SJ, Skeaff SA, Ryan P, Makrides M, Gallego G, Goodall S, Eastman CJ. Med J Aust. 2010 Sep 6;193(5):309; author reply 310-1. No abstract available.

In January 2010, the National Health and Medical Research Council (NHMRC) released a public statement, Iodine supplementation for pregnant and breastfeeding women.2

PMID: 20819054


Estimating the impact of mandatory fortification of bread with iodine on pregnant and post-partum women

J Epidemiol Community Health. 2010 Aug 13. [Epub ahead of print]

Mackerras D, Powers J, Boorman J, Loxton D, Giles GG.

Canberra, Australia. Abstract Background Iodine deficiency has re-emerged in Australia. Pregnant and breastfeeding women need higher iodine intakes (estimated average requirements: 160 mug/day and 190 mug/day) than non-pregnant women (100 mug/day) because iodine is critical for early infant development. The impact of iodine fortification of bread on women's iodine intake is evaluated by reproductive status using 2003 Australian Longitudinal Study on Women's Health (ALSWH) food frequency data and projected onto 1995 National Nutrition Survey (NNS) daily food consumption data for women of child-bearing age. Methods Recent iodine analyses of Australian foods were combined with reported intakes of key foods to estimate iodine intake before and after fortification for 665 pregnant, 432 zero to 6 months postpartum, 467 seven to 12 months postpartum and 7324 non-pregnant women. Differences in mean iodine intake between these groups were projected onto NNS estimates of total iodine intake for women of child-bearing age. Results Pregnant and postpartum women reported eating more bread than did non-pregnant women. Mean iodine intakes (mug/day before; and after fortification) from key foods were higher in pregnant (78; 124), 0-6 months postpartum (75; 123) and 7-12 months postpartum (71; 117) than in non-pregnant women (65; 103). Projecting ALSWH results onto the NNS yields total mean iodine intakes of 167, 167, 160 and 146 for the same groups. Conclusion Current iodine intakes are well below dietary recommendations. The impact of iodine fortification of bread would be greater for pregnant and postpartum women than has been previously estimated using general population intakes, but additional strategies to increase intakes by these groups are still needed.

PMID: 20709857


Iodine excess

Best Pract Res Clin Endocrinol Metab. 2010 Feb;24(1):107-15.

Bürgi H.

International Council for the Control of Iodine Deficiency Disorders (ICCIDD), CH-4500 Solothurn, Switzerland. hans.buergi@gmail.com Abstract Several mechanisms are involved in the maintenance of normal thyroid hormone secretion, even when iodine intake exceeds physiologic needs by a factor of 100. The sodium-iodide symporter system contributes most to this stability. Faced with an iodine excess, it throttles the transport of iodide into the thyroid cells, the rate-limiting step of hormone synthesis. Even before the iodine symporter reacts, a sudden iodine overload paradoxically blocks the second step of hormone synthesis, the organification of iodide. This so-called Wolff-Chaikoff effect requires a high (>or=10(-3) molar) intracellular concentration of iodide. The block does not last long, because after a while the sodium-iodide symporter shuts down; this allows intracellular iodide to drop below 10(-3) molar and the near-normal secretion to resume. In some susceptible individuals (e.g., after radio-iodine treatment of Graves' disease or in autoimmune thyroiditis), the sodium-iodide symporter fails to shut down, the intracellular concentration of iodide remains high and chronic hypothyroidism ensues. To complicate matters, iodine excess may also cause hyperthyroidism. The current explanation is that this happens in persons with goitres, for example, after long-standing iodine deficiency. These goitres may contain nodules carrying a somatic mutation that confers a 'constitutive' activation of the TSH receptor. Being no more under pituitary control, these nodules overproduce thyroid hormone and cause iodine-induced hyperthyroidism, when they are presented with sufficient iodine. These autonomous nodules gradually disappear from the population after iodine deficiency has been properly corrected. More recent studies suggest that chronic high iodine intake furthers classical thyroid autoimmunity (hypothyroidism and thyroiditis) and that iodine-induced hyperthyroidism may also have an autoimmune pathogenesis.

Copyright 2009 Elsevier Ltd. All rights reserved. PMID: 20172475


The impact of common micronutrient deficiencies on iodine and thyroid metabolism: the evidence from human studies

Best Pract Res Clin Endocrinol Metab. 2010 Feb;24(1):117-32.

Hess SY.

Program in International and Community Nutrition, Department of Nutrition, University of California, Davis, CA, USA. syhess@ucdavis.edu Abstract Deficiencies of micronutrients are highly prevalent in low-income countries. Inadequate intake of iodine impairs thyroid function and results in a spectrum of disorders. Other common deficiencies of micronutrients such as iron, selenium, vitamin A, and possibly zinc may interact with iodine nutrition and thyroid function. Randomised controlled intervention trials in iodine- and iron-deficient populations have shown that providing iron along with iodine results in greater improvements in thyroid function and volume than providing iodine alone. Vitamin A supplementation given alone or in combination with iodised salt can have a beneficial impact on thyroid function and thyroid size. Despite numerous studies of the effect of selenium on iodine and thyroid metabolism in animals, most published randomised controlled intervention trials in human populations failed to confirm an impact of selenium supplementation on thyroid metabolism. Little evidence is available on interactions between iodine and zinc metabolism.

Copyright 2009 Elsevier Ltd. All rights reserved. PMID: 20172476

2006

Urinary iodine concentration of pregnant women and female adolescents as an indicator of excessive iodine intake in Sri Lanka

Food Nutr Bull. 2006 Mar;27(1):12-8.

Silva KD, Munasinghe DL. Source Department of Applied Nutrition, Faculty of Livestock, Fisheries and Nutrition, Wayamba University of Sri Lanka, Makandura, Gonawila 60170, Sri Lanka. renuka_projects@yahoo.com Abstract BACKGROUND: Mild deficiencies and excesses of iodine have deleterious effects in both females and males. The iodine status of the population after implementation of the universal salt iodization program in Sri Lanka is not known. OBJECTIVE: This cross-sectional study was carried out to assess the iodine status of pregnant women and female adolescents, with urinary iodine concentration used as the measure of outcome. METHODS: The participants were 100 women in the first trimester of pregnancy and 99 female adolescents in Kuliyapitiya, Kurunegala District, North-Western Province, Sri Lanka. The urinary iodine concentration was measured in a casual urine sample from each subject. The iodate contents of salt samples collected from households of the adolescents participating in the study were also measured. RESULTS: The median urinary iodine concentration of 185.0 microg/L and the prevalence of values under 50 microg/L of only 1% among the pregnant women indicate adequate iodine intake and optimal iodine nutrition. The median urinary iodine concentration (213.1 microg/L) among female adolescents indicates a more than adequate iodine intake and a risk of iodine-induced hyperthyroidism. Approximately 8% and 4% of the adolescents and pregnant women, respectively, had urinary iodine concentrations in the range of mild iodine deficiency (51 to 100 microg/L). More than half of the adolescents (56%) and 39% of the pregnant women had urinary iodine concentrations higher than optimal. The median iodine content in salt samples was 12.7 ppm. Only 20.2% of the samples were adequately iodized, and 10.1% of the samples had very high iodine levels. CONCLUSIONS: Female adolescents and pregnant women had no iodine deficiency, but a considerable proportion of them, especially female adolescents, were at risk for iodine-induced hyperthyroidism. There is thus a need for proper monitoring of the salt iodization program to achieve acceptable iodine status.

PMID: 16572714 http://www.ncbi.nlm.nih.gov/pubmed/16572714