scholarly journals The Role of Iodine for Thyroid Function in Lactating Women and Infants

2021 ◽  
Author(s):  
Maria Andersson ◽  
Christian P Braegger

Abstract Iodine is a micronutrient needed for the production of thyroid hormones, which regulate metabolism, growth, and development. Iodine deficiency or excess may alter the thyroid hormone synthesis. The potential effects on infant development depend on the degree, timing, and duration of exposure. The iodine requirement is particularly high during infancy because of elevated thyroid hormone turnover. Breastfed infants rely on iodine provided by human milk, but the iodine concentration in breast milk is determined by the maternal iodine intake. Diets in many countries cannot provide sufficient iodine, and deficiency is prevented by iodine fortification of salt. However, the coverage of iodized salt varies between countries. Epidemiological data suggest large differences in the iodine intake in lactating women, infants, and toddlers worldwide, ranging from deficient to excessive intake. In this review, we provide an overview of the current knowledge and recent advances in the understanding of iodine nutrition and its association with thyroid function in lactating women, infants, and toddlers. We discuss risk factors for iodine malnutrition and the impact of targeted intervention strategies on these vulnerable population groups. We highlight the importance of appropriate definitions of optimal iodine nutrition and the need for more data assessing the risk of mild iodine deficiency for thyroid disorders during the first 2 years in life.

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Izuki Amano ◽  
Yusuke Takatsuru ◽  
Asahi Haijima ◽  
Shogo Haraguchi ◽  
Noriyuki Koibuchi

Abstract Iodine is one of the essential micronutrient which is required for the synthesis of thyroid hormones. Thus, iodine deficiency may result in the hypothyroidism. Iodine deficiency is one of the most common causes of preventable mental retardation and brain damage in the world. On the other hand, Japanese iodine intake exceeds that of most other countries, due to the significant seaweed consumption such as kelp. The Japanese Ministry of Health, Labour and Welfare estimates average iodine consumption at 1.2mg/day in Japan. In contrast, the recommended tolerable upper intake levels for adult is 1.1 mg / day in the United States. Generally, Japanese takes twenty times higher amount of iodine than Americans. Iodine tolerance among individual humans varies greatly, and the excess iodine can cause both hyper- and hypo- thyroidism. Furthermore, the effect of thyroid dysfunction due to iodine excess on brain function has not been clarified. In this study, we generated a mouse models for chronic iodine excess and evaluated its effect on brain development. C57BL/6 dams and their pups mice were treated with KIO3 37.4mg/l through drinking water. Behavioral experiments (novel object recognition test, novel object in location test, visual discrimination test, and three-room social behavior test) were conducted at 10-weeks-old. After the behavioral analysis, mice were sacrificed to collect trunk blood and tissues. Excess iodine intake caused hypertrophy of thyroid follicles regardless of the administered dose. However, there were no differences in thyroid hormone status among groups. Thyroid hormone responsive genes in the hippocampus were also not affected in experiment group. In the behavioral analysis, female mice showed an increase in learning ability. In summary, although the chronic overdose of iodine does not affect thyroid hormone levels, it may affect cognitive learning function. The gender difference in the consequence was also observed. These results indicate that the chronic iodine excess may cause various changes, although the body is tolerable with excess iodine.


2016 ◽  
Vol 19 (15) ◽  
pp. 2808-2817 ◽  
Author(s):  
Yaniv S Ovadia ◽  
Dov Gefel ◽  
Dorit Aharoni ◽  
Svetlana Turkot ◽  
Shlomo Fytlovich ◽  
...  

AbstractObjectiveOver 300 million people rely on desalinated seawater and the numbers are growing. Desalination removes iodine from water and could increase the risk of iodine-deficiency disorders (IDD). The present study assessed the relationship between iodine intake and thyroid function in an area reliant on desalination.DesignA case–control study was performed between March 2012 and March 2014. Thyroid function was rigorously assessed by clinical examination, ultrasound and blood tests, including serum thyroglobulin (Tg) and autoimmune antibodies. Iodine intake and the contribution made by unfiltered tap water were estimated by FFQ. The contribution of drinking-water to iodine intake was modelled using three iodine concentrations: likely, worst-case and best-case scenario.SettingThe setting for the study was a hospital located on the southern Israeli Mediterranean coast.SubjectsAdult volunteers (n102), 21–80 years old, prospectively recruited.ResultsAfter screening, seventy-four participants met the inclusion criteria. Thirty-seven were euthyroid controls. Among those with thyroid dysfunction, twenty-nine were classified with non-autoimmune thyroid disease (NATD) after excluding eight cases with autoimmunity. Seventy per cent of all participants had iodine intake below the Estimated Average Requirement (EAR) of 95 µg/d. Participants with NATD were significantly more likely to have probable IDD with intake below the EAR (OR=5·2; 95 % CI 1·8, 15·2) and abnormal serum Tg>40 ng/ml (OR=5·8; 95 % CI 1·6, 20·8).ConclusionsEvidence of prevalent probable IDD in a population reliant on desalinated seawater supports the urgent need to probe the impact of desalinated water on thyroid health in Israel and elsewhere.


1967 ◽  
Vol 55 (2) ◽  
pp. 361-368 ◽  
Author(s):  
R. McG. Harden ◽  
W. D. Alexander ◽  
S. Papadopoulos ◽  
M. T. Harrison ◽  
S. Macfarlane

ABSTRACT Iodine metabolism and thyroid function were studied in a patient with hypothyroidism and goitre due to dehalogenase deficiency. Initially the plasma inorganic iodine (PII) level was within the normal range but circulating levels of hormone were low and the thyroid clearance and absolute uptake of iodine (AIU) by the thyroid were high. Administration of iodide supplements resulted in a rapid rise in the plasma thyroxine concentration and restoration of the euthyroid state. Thyroid hormone synthesis appeared to proceed normally when the PII exceeded 1.0 μg/100 ml. This was achieved by increasing the intake of iodide by 612 μg per day. At PII levels around 10 μg/100 ml there was evidence of increased levels of circulating thyroid hormone.


2013 ◽  
Vol 3 (2) ◽  
Author(s):  
Starry H. Rampengan

Abstract: Amiodarone is a highly effective anti-arrhythmic agent used in certain arrhythmias from supraventricular tachycardia to life-threatening ventricular tachycardia. Its use is associated with numerous side-effects that could deteriorate a patient’s condition. Consequently, a clinician should consider the risks and benefits of amiodarone before initiating the treatment.The thyroid gland is one of the organs affected by amiodarone. Amiodarone and its metabolite desethyl amiodaron induce alterations in thyroid hormone metabolism in the thyroid gland, peripheral tissues, and probably also in the pituitary gland. These actions result in elevations of serum T4 and rT3 concentrations, transient increases in TSH concentrations, and decreases in T3 concentrations. Both hypothyroidism and hyperthyroidism are prone to occur in patients receiving amiodarone. Amiodarone-induced hypothyroidism (AIH) results from the inability of the thyroid to escape from the Wolff-Chaikoff effect and is readily managed by either discontinuation of amiodarone or thyroid hormone replacement. Amiodarone-induced thyrotoxicosis (AIT) may arise from either iodine-induced excessive thyroid hormone synthesis (type I, usually with underlying thyroid abnormality), or destructive thyroiditis with release of preformed hormones (type II, commonly with apparently normal thyroid glands). Therefore, monitoring of thyroid function should be performed in all amiodarone-treated patients to facilitate early diagnosis and treatment of amiodarone-induced thyroid dysfunction. Key words: Amiodarone, thyroid function, side effect, management, monitoring.     Abstrak: Amiodaron adalah obat antiaritmia yang cukup efektif dalam menangani beberapa keadaaan aritmia mulai dari supraventrikuler takikardia sampai takikardia ventrikuler yang mengancam kehidupan. Namun penggunaan obat ini ternyata menimbulkan efek samping pada organ lain yang dapat menimbulkan perburukan keadaan pasien. Sehingga, dalam penggunaan amiodaron, klinisi juga harus menimbang keuntungan dan kerugian yang ditimbulkan oleh obat ini. Salah satu organ yang dipengaruhi oleh amiodaron adalah kelenjar tiroid. Amiodaron dan metabolitnya desetil amiodaron memengaruhi hormon tiroid pada kelenjar tiroid, jaringan perifer, dan mungkin pada pituitari. Aksi amiodaron ini menyebabkan peningkatan T4, rT3 dan TSH, namun menurunkan kadar T3. Hipotiroidisme dan tirotoksikosis dapat terjadi pada pasien yang diberi amiodaron. Amiodarone-induced hypothyroidism (AIH) terjadi karena ketidakmampuan tiroid melepaskan diri dari efek Wolff Chaikof, dan dapat ditangani dengan pemberian  hormon substitusi T4 atau penghentian amiodaron. Amiodarone-induced thyrotoxicosis (AIT) terjadi karena sintesis hormon tiroid yang berlebihan yang diinduksi oleh iodium (tipe I, biasanya sudah mempunyai kelainan tiroid sebelumnya) atau karena tiroiditis destruktif yang disertai pelepasan hormon tiroid yang telah terbentuk (tipe II, biasanya dengan kelenjar yang normal). Pemantauan fungsi tiroid seharusnya dilakukan pada semua pasien yang diberi amiodaron untuk memfasilitasi diagnosis dan terapi yang dini terjadinya  disfungsi tiroid yang diinduksi amiodaron. Kata Kunci: Amiodaron, fungsi tiroid, efek samping, penanganan, pemantauan.


Iodine (I2) is essential in the synthesis of thyroid hormones T4 and T3 and functioning of the thyroid gland. Both T3 and T4 are metabolically active, but T3 is four times more potent than T4. Our body contains 20-30 mg of I2, which is mainly stored in the thyroid gland. Iodine is naturally present in some foods, added to others, and available as a dietary supplement. Serum thyroid stimulating hormone (TSH) level is a sensitive marker of thyroid function. Serum TSH is increased in hypothyroidism as in Hashimoto's thyroiditis. In addition to regulation of thyroid function, TSH promotes thyroid growth. If thyroid hormone synthesis is chronically impaired, TSH stimulation eventually may lead to the development of a goiter. This chapter explores the iodide metabolism and effects of Hashimoto's disease.


Mediscope ◽  
2018 ◽  
Vol 5 (2) ◽  
pp. 30-35
Author(s):  
GM Molla

Iodine is a micronutrient, which is essential for the synthesis of thyroid hormones. Thyroid hormones play a major role in the development of different functional components in different stages of life. The relationship between iodine intake level of a population and occurrences of thyroid disorders U-shaped with an increase from both low and high iodine intake. Iodine deficiency disorders (IDDs) are a major health problem worldwide in all age groups, but infants, school children, and pregnant and lactating women are vulnerable. During pregnancy and lactation, the fetus and infants are sensitive to maternal iodine intake. Even mild iodine deficiency may lead to irreversible brain damage during this period. A main cause of IDDs of neonates and infants is maternal iodine deficiency. Universal salt iodization strategy has been initiated by the World Health Organization and United Nation International Children Emergency Fund by the year 1993 for correction and prevention of iodine deficiency. Excessive iodine causes hypothyroidism, iodine-induced hyperthyroidism and autoimmune thyroid diseases. Iodine deficiency and excessive iodine, both cause goiter. There are many indicators for assessing the IDDs, such as measurement of thyroid size by palpation or ultrasonography, serum thyroid stimulating hormone, and thyroglobulin but these are less sensitive, costly and sometimes interpretation is difficult. Urinary iodine concentration (UIC) is a well-accepted, cost-efficient, and easily obtainable indicator of iodine status. Since the majority of iodine absorbed by the body is excreted in the urine, it is considered a sensitive marker of current iodine intake and can reflect recent changes in iodine status. Iodine requirements are greatly increased during pregnancy and lactation, owing to metabolic changes. During intrauterine life, maternal iodine is the only source of iodine for a fetus. UIC determines the iodine status of pregnant and lactating women. Breast milk is the only source of iodine for exclusively breastfed neonates and infants. Breast milk iodine concentration can be determined by UIC. UIC predicts the adverse health consequences of excessive iodine intake such as goiter, hypothyroidism, and hyperthyroidism. This review presents that iodine status in different groups of a population can be determined by UIC which will be helpful in assessing the iodine status in a community, finding out the cause of thyroid disorders, to predict the risk of adverse health effects of iodine deficiency and excessive iodine, and in making plan for iodine supplementation.Mediscope Vol. 5, No. 2: Jul 2018, Page 30-35


2016 ◽  
Vol 50 (1) ◽  
pp. 3-9 ◽  
Author(s):  
J Podoba ◽  
K Racova ◽  
H Urbankova ◽  
M Srbecky

AbstractObjective. Prophylaxis of iodine deficiency-related disorders with iodized salt in Slovakia was introduced in 1951. This prophylactic measure yielded remarkably good results. Endemic goiter and endemic cretinism disappeared. Sufficient iodine intake, mainly in children and adolescents, was confirmed in several local and international studies carried out in the period 1991–95. Unfortunately, since seventies, there has been no institution which would have dealt with iodine prophylaxis in such an extent as this important measure of Slovak preventive medicine would require. Neither systematic monitoring of iodine intake nor systematic population epidemiological studies have been carried out. We do not have any data on the iodine intake in pregnant women, the most vulnerable population group in relation to the iodine deficiency. During the period June 2014 – October 2015, we examined iodine excretion in 426 probands from three regions of Slovakia with an emphasis on the pregnant women.Results. Iodine intake was found to be sufficient, even more than adequate, in all age groups of Slovak population. The only population group with iodine intake borderline or very mild iodine deficiency are pregnant women.Conclusions: 1/ Iodine nutrition in Slovakia is generally sufficient, even oversteps the requirement, with the exception of pregnant women. Iodine intake in pregnant women should be fortified by iodine containing multivitamin preparations. 2/ We recommend to include the examination of urinary iodine into the screening of thyropathies in early pregnancy. 3/ It is not enough to implement the iodine deficiency-related disorders prevention programs, it is also necessary to stabilize such programs over time and balance the benefits with possible side effects of this program.


2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Christina Yarrington ◽  
Elizabeth N. Pearce

Iodine is a necessary element for the production of thyroid hormone. We will review the impact of dietary iodine status on thyroid function in pregnancy. We will discuss iodine metabolism, homeostasis, and nutritional recommendations for pregnancy. We will also discuss the possible effects of environmental contaminants on iodine utilization in pregnant women.


2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Norman Blumenthal ◽  
Karen Byth ◽  
Creswell J. Eastman

Aim. The primary objective of the study was to assess the iodine nutritional status, and its effect on thyroid function, of pregnant women in a private obstetrical practice in Sydney.Methods. It was a cross-sectional study undertaken between November 2007 and March 2009. Blood samples were taken from 367 women at their first antenatal visit between 7 and 11 weeks gestation for measurement of thyroid stimulating hormone (TSH) and free thyroxine (FT4) levels and spot urine samples for urinary iodine excretion were taken at the same time as blood collection.Results. The median urinary iodine concentration (UIC) for all women was 81 μg/l (interquartile range 41–169 μg/l). 71.9% of the women exhibited a UIC of <150 μg/l. 26% of the women had a UIC <50 μg/l, and 12% had a UIC <20 μg/l. The only detectable influences on UIC were daily milk intake and pregnancy supplements. There was no statistically significant association between UIC and thyroid function and no evidence for an effect of iodine intake on thyroid function.Conclusions. There is a high prevalence of mild to moderate iodine deficiency in women in Western Sydney but no evidence for a significant adverse effect on thyroid function. The 6.5% prevalence of subclinical hypothyroidism is unlikely to be due to iodine deficiency.


1998 ◽  
pp. 23-28 ◽  
Author(s):  
W Reinhardt ◽  
M Luster ◽  
KH Rudorff ◽  
C Heckmann ◽  
S Petrasch ◽  
...  

OBJECTIVE: Several studies have suggested that iodine may influence thyroid hormone status, and perhaps antibody production, in patients with autoimmune thyroid disease. To date, studies have been carried out using large amounts of iodine. Therefore, we evaluated the effect of small doses of iodine on thyroid function and thyroid antibody levels in euthyroid patients with Hashimoto's thyroiditis who were living in an area of mild dietary iodine deficiency. METHODS: Forty patients who tested positive for anti-thyroid (TPO) antibodies or with a moderate to severe hypoechogenic pattern on ultrasound received 250 microg potassium iodide daily for 4 months (range 2-13 months). An additional 43 patients positive for TPO antibodies or with hypoechogenicity on ultrasound served as a control group. All patients were TBII negative. RESULTS: Seven patients in the iodine-treated group developed subclinical hypothyroidism and one patient became hypothyroid. Three of the seven who were subclinically hypothyroid became euthyroid again when iodine treatment was stopped. One patient developed hyperthyroidism with a concomitant increase in TBII titre to 17 U/l, but after iodine withdrawal this patient became euthyroid again. Only one patient in the control group developed subclinical hypothyroidism during the same time period. All nine patients who developed thyroid dysfunction had reduced echogenicity on ultrasound. Four of the eight patients who developed subclinical hypothyroidism had TSH concentrations greater than 3 mU/l. In 32 patients in the iodine-treated group and 42 in the control group, no significant changes in thyroid function, antibody titres or thyroid volume were observed. CONCLUSIONS: Small amounts of supplementary iodine (250 microg) cause slight but significant changes in thyroid hormone function in predisposed individuals.


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