Environmental Iodine Deficiency Research Articles

A CLUSTER OF CASES OF THYROID HYPERPLASIA IN AQUARIUM-HOUSED TROPICAL MARINE TELEOSTS FOLLOWING A CHANGE OF SALT MIX BRAND

Follicular thyroid hyperplasia was diagnosed in nine out of 32 (28%) marine tropical teleosts housed in a public aquarium over a 9.5-mo period. These proliferative lesions were considered to be the cause of death in five of these fish. Iodine concentration was undetectable in nonozonized water (<0.005 mg/L), suggesting that an environmental iodine deficiency was the cause of these hyperplastic thyroid lesions. The only significant modification in the husbandry was a change, 18 mo before the first case, of the commercial salt mix brand used to make artificial seawater. The iodine content in this replacement salt mix was five times lower than that of the salt mix used before. This case series suggests that the iodine concentration in this new salt mix was insufficient to maintain thyroid homeostasis in reef teleosts under the husbandry provided in this institution.

The relationships between thyroid-stimulating hormone and/or dopamine levels in peripheral blood and IQ in children with different urinary iodine concentrations

Environmental iodine deficiency or excess can lead to inappropriate iodine nutrition in the population. Little research has been performed to determine whether changes in thyroid-stimulating hormone (TSH) and/or dopamine (DA) concentrations in peripheral blood are involved in intellectual impairment caused by inappropriate iodine nutrition. 498 children aged 7-12 from areas with different water iodine concentrations were included in the study. Children's intelligence and levels of urinary iodine and fluoride, TSH, free triiodothyronine (FT3), free thyroxine (FT4), and DA were evaluated. The relationship between TSH and/or DA levels and intelligence quotient (IQ) in all participants and in the population with different urinary iodine concentrations (UIC) was evaluated by multivariate regression analysis. The proportion of people with low average and lower intelligence in UIC ≥ 300 μg/L group was significantly higher than that in control group but only a positive correlation was found between DA and IQ in the population with UIC < 100 μg/L (bootstrapped estimation P = 0.032). TSH and/or DA in peripheral blood may be not involved in the progressive decline in intelligence caused by iodine excess but DA had positive correlation with intelligence in iodine deficiency group, and no relationship between TSH concentration and IQ was found in the general population or in different UIC groups.

Iodine deficiency diseases in children and adolescents (plenary lecture)

The main consequence of iodine deficiency in the environment is the development of goiter in people living in iodine-deficient regions (endemic goiter). In this regard, for a long time it was considered that goiter is the only manifestation of this condition. It has now been proven that, in addition to goiter, iodine deficiency also has other adverse effects on human health. In 1983, the term "endemic goiter" was replaced by the term "iodine deficiency diseases" (IDD). These diseases are caused by a decrease in the functional activity of the thyroid gland in response to iodine deficiency.

Hypothyroidism in Context: Where We've Been and Where We're Going.

Hypothyroidism affects up to 5% of the general population, with a further estimated 5% being undiagnosed. Over 99% of affected patients suffer from primary hypothyroidism. Worldwide, environmental iodine deficiency is the most common cause of all thyroid disorders, including hypothyroidism, but in areas of iodine sufficiency, Hashimoto’s disease (chronic autoimmune thyroiditis) is the most common cause of thyroid failure. Hypothyroidism is diagnosed biochemically, being overt primary hypothyroidism defined as serum thyroid-stimulating hormone (TSH) concentrations above and thyroxine concentrations below the normal reference range. Symptoms of hypothyroidism are non-specific and include mild to moderate weight gain, fatigue, poor concentration, depression, and menstrual irregularities, while the consequences of untreated or under-treated hypothyroidism include cardiovascular disease and increased mortality. Levothyroxine has long been the main tool for treating hypothyroidism and is one of the world’s most widely prescribed medicines. In adults with overt hypothyroidism, levothyroxine is usually prescribed at a starting dose of 1.6 µg/kg/day, which is then titrated to achieve optimal TSH levels (0.4–4.0 mIU/L), according to the therapeutic target. We here summarise the history of levothyroxine and discuss future issues regarding the optimal treatment of hypothyroidism. Because nearly one-third of patients with treated hypothyroidism still exhibit symptoms, it is important that levothyroxine is used more appropriately to achieve maximum benefit for patients. In order to ensure this, further research should include more accurate assessments of the true prevalence of hypothyroidism in the community, optimisation of the levothyroxine substitution dose, proper duration of treatment, and identification of patients who may benefit from combination therapy with levothyroxine plus levotriiodothyronine.Funding: Merck.Plain Language Summary: Plain language summary available for this article.

Influence of cooking on the iodine content in potatoes, pasta and rice using iodized salt

To counteract iodine deficiency in the population in areas of environmental iodine deficiency table salt is often fortified with potassium iodide or iodate. However, most estimations of iodine contribution from the diet rely on calculations based on the added iodized salt and very limited experimental data about the stability of potassium iodate (KIO3) or iodine uptake during food processing is available. Therefore, the influence of cooking on the iodine content of potatoes, pasta, and rice having different size, varieties or composition was investigated. Commonly used cooking procedures were applied, using KIO3-enriched table salt in the cooking water. After iodine extraction with 0.5% NH3 iodine content was measured by ICP-MS. All products showed an increase in iodine content. Waxy potatoes, especially cut in small pieces, and egg pasta showed the highest iodine uptake. Based on the results, the use of KIO3-enriched salt for cooking is recommended to enhance iodine supply.

Survey of iodine nutritional status in 2011, Zhejiang, China.

Universal salt iodization (USI) was introduced in China in 1995, but whether the iodine status is optimal is questionable. This study was conducted to assess the iodine nutrition among Zhejiang population in coastal regions in China. A cross-sectional survey for iodine nutritional status was conducted with general population (n=10,350), including pregnant and lactating women (n=450 each) selected by stratified multistage sampling. Iodine content in drinking water, table salt and urine, were determined using arsenic-cerium catalytic spectrophotometry, the direct titration and the arsenic-cerium catalytic spectrophotometry, respectively, and daily iodine intake was estimated by 3 days of 24-hour recall method. The median iodine content in drinking water was 2.46 μg/L, Zhejiang belonged to the region of iodine deficiency in outer environment according to China standard. The median iodine content in table salt was 27.9 mg/kg, conforming to the standard requirements; the household coverage rate of qualified iodized salt reached 76.8%, which does not reach the standard requirement of WHO >90%. The dietary iodine intake of a reference individual averaged 379 μg/d, which indicated that the current iodine intake in diet was appropriate. In addition, the median urinary iodine concentration (UIC) was 162 μg/L in general population, and 130 μg/L in pregnant women, which didn't reach the standard requirements. The current dietary iodine intake in Zhejiang was generally sufficient and safe, but there is a risk of iodine deficiency among pregnant women and the population who do not consume iodized salt.

Is Gippsland environmentally iodine deficient? Water iodine concentrations in the Gippsland region of Victoria, Australia

This paper provides evidence of environmental iodine deficiency in the Gippsland region. Quantitative study; water samples were collected from 18 water treatment plants and four rain water tanks across Gippsland and water iodine concentrations were measured. Gippsland region of Victoria, Australia. This paper reports on the iodine concentration of drinking water from sources across Gippsland and examines the contribution of iodine from water to the Gippsland diet. This study also briefly examines the relationship between the concentration of iodine in water and distance from the sea. The cut-off value for water iodine concentrations considered to be indicative of environmental iodine deficiency is <2 µg L(-1) . The mean iodine concentration of water from 18 Gippsland water treatment plants was 0.38 µg L(-1) and would therefore make negligible difference to the dietary intake of iodine. This finding also falls well below the suggested dietary intake of iodine from water estimated by the 22nd Australian Total Diet Study. Our study found no linear relationship between the water iodine concentration and distance from the sea. As Gippsland has environmental iodine deficiency there is a greater probability that people living in this region are at higher risk of dietary iodine deficiency than those living in environmentally iodine sufficient regions. Populations living in areas known to have environmental iodine deficiency should be monitored regularly to ensure that problems of iodine deficiency, especially amongst the most vulnerable, are addressed promptly.

The triad-iodine deficiency, hyperlipidaemia, high coronary risk- in a 'maternal-neonate' population of rural Africa.

In order to see the pattern of changes in differential serum lipid and lipoprotein fractions as a risk marker of coronary complication in paired 'maternal-neonate' blood samples in an iodine deficient zone, 26 pregnant women and their corresponding new born infants at term delivery from the iodine deficient Bassa region of Plateau state, Nigeria were assessed and the results were compared with those seen in a similar 44 group of women and their newborns assessed in non lodine deficient region of Jos. The serum thyroid function and lipid and lipoprotein profiles were determined by 'ELISA' and 'enzymatic' methods respectively. Urinary iodide excretion level was also measured in 14 pregnant women in Bassa, 23 pregnant women in Jos and 16 non pregnant control from Jos. Results indicate that the pregnant women assessed in Bassa were iodine deficient (P<0.01) and their thyroid status was strikingly reduced as reflected by a drop in serum level of T4/TBG ratio (P<0.01) and a rise in TSH (P<0.005) in comparison to that seen in Jos. There was marked hypertriglyceridaemia and total hypercholesterolaemia (P<0.005), with differential significant rise in LDL cholestotol fraction (P<0.005) in the women assessed in Bassa as compared to Jos. The HDL cholesterol however dropped less significantly in the group (P<0.05) with a concurrent marked rise (P<0.001) in the serum ratio of LDL cholesterol/HDL cholesterol, total cholesterol/HDL cholesterol and triglycerides/HDL cholesterol in the lodine deficient group. A similar pattern of changes were seen in the corresponding neonates in the Bassa group as compared to Jos group. It is concluded that the pregnant women and their newborn offsprings living in a longstanding environmental iodine deficiency run a higher risk of developing coronary complications than those living in non endemic region. It is striking that such newborns surrounded by a continued state of lodine deficient may at a later adult-period of life develop marked risk of coronary complication and other features of hyperlipidaemias associated with varying thyroid insufficiency and accompanied iodine deficiency disorders. Prophylaxis measures as intervention has been highlighted.

Iodide excess exerts oxidative stress in some target tissues of the thyroid hormones

Environmental iodine deficiency continues to be a significant public health problem worldwide. On the other hand, iodide excess results principally from the use of iodine-containing medicinal preparations or radiographic contrast media. For this reason we intended to explore iodide excess impairment on prooxidant/antioxidant balance of the thyroid gland, hepatic tissue and in blood and the effect of selenium administration on oxidative stress markers under the same circumstances. Experiments were performed for 10 days with white, male, Wistar rats, as follows: group 1: control-normal iodine supply group; 2: high iodine diet, group; 3: high iodine diet and selenium; group 4: high iodine diet and Carbimasole. Oxidative stress markers such as lipid peroxides were determined in thyroid gland, hepatic tissue and in blood. Measuring H+ donor ability of the sera and catalase activity in thyroid gland and in hepatic tissue assessed antioxidant defense. Iodide excess had prooxidant effects, leading to an increased lipid peroxides level and catalase activity in target tissues and in blood and to a decreased H+ donor ability of the sera. Selenium supplementation had opposite effects. Present data allow us to conclude that the alterations due to iodide excess in thyroid gland, hepatic tissue and in blood are mediated through oxidative stress.

Goitre and environmental iodine deficiency in the UK ? Derbyshire: A review

Endemic goitre was prevalent in the population of Derbyshire in the UK for many centuries until it declined from the 1930s. A contemporary medical survey showed that endemicity of goitre was particularly higher in the Carboniferous limestone areas of the Derbyshire-Peak District. Unlike classical goitrous areas of the world, where the distribution of goitre has been found to be related to the iodine content in the environment, there is no such relationship reported for the Derbyshire-Peak District area. The present study reviews the presence of endemic goitre in this area with reference to iodine in different environmental media using past and present data. In comparison with the world average values, the iodine contents in the soil and sediment in the Peak District are not deficient, but compared to England, Wales and Scotland averages, these levels are low. As no information on the mobility and bioavailability of iodine of this area is available, a cautious approach is necessary before any assumption is made on the aetiology of endemic goitre. The study also discusses some hypotheses relating to the possible cause of endemic goitre in the limestone areas. Further research needs are suggested depending on the land use and geochemistry of the Peak District to determine the underlying causes of the former endemic goitre in this area.

Genetic factors in the pathogenesis of iodine deficiency goiter

Iodine deficiency diseases (IDD) are the most common non-infectious human pathology. In general, 1.5 billion people live on the Earth in regions of iodine deficiency in the environment, 600 million of them have an increase in the thyroid gland, and 40 million have severe mental retardation as a result of iodine deficiency

Environmental Iodine Deficiency and Goiter Prevalence in A Block Area of The North Eastern Region: A Retrospective Analysis

Endemic Goiter the best known and easily recognizable form of iodine deficiency have been recognized for centuries. India is one of the major Endemia of goiter in the world. Reports published in 1996 stated that about 167 million persons were at risk of IDD in India including the 54 million with goiter 2.2 million with cretinism and 6.6 million with mild neurological deficits. No state in the country was believed to be free from Iodine Deficiency Disorders Though considerable progress has been achieved in minimising the ravage caused by Iodine Deficiency Disorders through implementation of National IDD Control Programme yet Goiter remains as an enigma to the Public Health Scientist. The Northeastern region of India is famous for its diverse ecology and distinct culture and lifestyle specific to different ethnic groups. Newly emergent foci of iodine deficiency disorders was encountered in different places reported from increasing number of outpatient attending cases of goiter in various Primary Health Centres of this region specifically in Assam. But no systematic study was undertaken to explore the iodine deficiency disorder status of this region. It was therefore decided to carry out a survey in a selected area to determine the magnitude of the problem of endemic goiter and other associated forms of IDD together with some aetiological factors potentially responsible for the goiter in this region. (excerpt)

The illusion of environmental iodine deficiency.

The distribution of endemic goitre in England and Wales was compared with the distribution of environmental iodine (atmospheric deposition, soil, surface water). Despite a very clear goitre belt through the west of England and Wales there was no patterning in the environmental iodine distribution. A clear seasonal variation in depositional iodine exists, with an unusually high concentration of iodine in March 1997. The temporal variation in iodine concentration is determined at the monthly and not the annual level. The presence of endemic goitre is no indicator of how iodine is distributed in the environment or vice versa!

Environmental Iodine Deficiency: A Challenge to the Evolution of Terrestrial Life?

Environmental Iodine Deficiency: A Challenge to the Evolution of Terrestrial Life?

Iodine content of commonly consumed foods and water from the goitre-endemic northeast region of India

Iodine content of commonly consumed foods and water from goitre-endemic northeast India is reported. The iodine content of water ranged between 3.0 and 31.5 μg litre −1 with 82% of the samples containing 5–10 μg litre −1. Pooled mean water iodine content from northeast India (7.38±2.7 μg litre −1) was very low compared with non-endemic areas like Hyderabad (36.5±4.8 μg litre −1. Similarly, foods from northeast India had low iodine with all the samples analysed exhibiting iodine contents below 30 μg per 100 g sample. Commonly consumed foods like cereals, legumes, spices, roots and tubers were 30–76% lower than values encountered from non-endemic areas like Hyderabad. The low iodine in foods and water from goitre-endemic northeast India reflects the environmental iodine deficiency in the region.

Major human cancers are preventable

It is proposed that the prerequisites for a low-risk to major cancers-breast, colon, lung, prostate, melanoma (as, for example in Africans, Chinese and Japanese) - include upregulated hypothalamic dopaminergic activity compared to depressed noradrenergic/thyrogenic function and raised vagal tone, and a neuroendocrine constellation that promotes improved immune efficiency and its inimical to the onset of aversive cell responses. Since the integrity of these tissues is regulated by hypothalamic-hypophyseal hormones, under tonic dopaminergic inhibition, cancers are potentially preventable as long as dopaminergic integrity is maintained, or the decline in ageing in slowed. Evidence for the impact of upregulated dopamine on tumour prevention includes: (1) a reduced (40%) rate of colonic cancer in exercised-trained ageing subjects; (2) reduced expected rates of lung/colon cancers, and skin tumours in prolonged post-menopausal oestrogen replacement; (3) the virtual suppression of all cancers during pregnancy (when dopamine synthesis increases); (4) the low rate of bronchogenic carcinoma correlates with reduced enzymatic conversion of dopamine to noradrenaline; and (5) neuroblastoma (specifically dopamine dysregulated tumour) regresses spontaneously on dopamine normalization. Similar tumour reduction is anticipated by controlling the intake of calories. The subtlety of the switch to upregulated dopamine, the speed of translation at the cellular level and the sustainability of responses as long as the initiating stimulus persists (as exposed by pregnancy), underline the plasticity of the neuroendocrine mechanism and ease of manipulation. Long exposure to environmental iodine deficiency, as seen for example in Africans and Chinese, reveals a crucial dopamine-thyroid action that slows cell timing mechanisms. The common neurohormonal basis identified for the prevention of human cancers has practical application, with reasonably assured positive results.

Clinical and epidemiological correlates of iodine deficiency disorders

Abstract The iodine deficiency disorders, endemic goitre, stillbirths, abortions, congenital abnormalities, endemic cretinism, and impaired mental function, are found worldwide. Known for millenia, they currently put 29% of the world’s population at risk. The most important is cretinism, found in two forms. Neurological cretinism possibly develops due to an insult in early pregnancy, hypothyroid cretinism to an insult late in pregnancy or in early life. The classical medical causes of environmental iodine deficiency, glaciation and leaching, do not adequately explain the prevalence and distribution of iodine deficiency disorders, nor have the new insights into the environmental chemistry of iodine been assimilated properly with medical knowledge. Joint studies would be of help. The presence of various factors other than iodine deficiency in the causation of the disorders is recognized. These are often thought to be geologically related. Recent work suggests plate tectonics as the unifying factor, since iodine deficiency disorders are found along many plate collision zones. Concentration of major and trace elements as a result of plate subduction provides a possible source of goitrogens. A systematic search is needed. The iodine goitrogen ratio could provide the link between environmental iodine and differing intensities of the iodine deficiency disorders found in affected communities.

The "feto-maternal" thyroid function interrelationships in an iodine-deficient region in Africa—the role of T3 in possible fetal defence

The thyroid status was investigated in 26 pregnant African women at term delivery in an iodine-deficient region (Jengere) of Nigeria, West Africa including the measurement of serum T4, T3, TSH, thyroxine binding capacity, TBG, free thyroxine index (FT4I) and the results were matched with those obtained in a corresponding group of 46 women at delivery in Jos, the non-iodine-deficient region which was used as a control. Corresponding cord-blood samples were obtained from all the neonates of the two groups. Twenty-three urinary samples in the former and 14 in the latter group were analysed for iodide levels to ascertain the degree of iodine deficiency. The results demonstrate that compared to the values seen in the Jos group the maternal serum T4, T3 and FT4I levels were significantly reduced in the iodine-deficient group, while TSH, TBG and thyroxine binding capacity were elevated. Cord serum samples showed a corresponding fall in T4 and FT4I levels in the group from the iodine-deficient region, while the T3 levels were significantly elevated with a concurrent significant rise in TSH and TBG levels. Significant correlations were found between the maternal and cord serum T4, TSH, TBG, thyroxine binding capacity and FT4I levels, but not T3. From these findings we suggest that fetal T3 plays an important defensive role against the danger of long-standing environmental iodine deficiency.

Iodine and Thyroid Disease

Iodine is a requisite substrate for the synthesis of the thyroid hormones, the minimum daily requirement being about 50 micrograms. An autoregulatory mechanism within the thyroid serves as the first line of defense against fluctuations in the supply of iodine and also permits escape from the inhibition of hormone synthesis that a very large quantity of iodine induces (Wolff-Chaikoff effect and escape therefrom). Environmental iodine deficiency continues to be a significant public health problem worldwide, compounded in some geographic regions by the presence of other goitrogens in some staple foods. The pathologic consequences of severe iodine deficiency include endemic goiter, endemic cretinism, increased fetal and infant mortality, and an increased prevalence in the community of cognitive and neuromotor disabilities. The implementation of an iodization program prevents endemic cretinism and reduces the frequency of the other pathologic consequences of iodine deficiency. Iodine excess results principally from the use of iodine-containing medicinal preparations or radiographic contrast media. The pathologic consequences of iodine excess will ensue only when thyroid autoregulation is defective, in that escape from the Wolff-Chaikoff effect cannot occur, or when autoregulation is absent. Defective autoregulation characterizes the fetal and neonatal thyroid, Hashimoto's thyroiditis, radioiodine or surgically treated Graves' hyperthyroidism, the thyroid of patients with cystic fibrosis, and the thyroid that has been exposed to weak inhibitors of the organic binding of iodine. In these circumstances, the provision of excess iodine may lead to iodide goiter with or without hypothyroidism. Absent autoregulation may be a feature of longstanding multinodular goiter, and the provision of excess iodine in this circumstance may induce thyrotoxicosis (Jod-Basedow disease). The pathologic consequences of iodine excess will resolve when the source of iodine has been dissipated. In addition to its role in reversing iodine deficiency, iodine is used as adjunctive therapy for hyperthyroidism. By inhibiting the proteolytic release of iodothyronines from thyroglobulin, it induces a prompt slowing of thyroid hormone secretion. This effect is exploited in the treatment of thyrotoxic crisis or severe thyrocardiac disease. Iodine also reduces thyroid cellularity and vascularity and therefore is used in the preparation of the patient for thyroidectomy. Finally, by exploiting the failure of escape from the Wolff-Chaikoff effect, iodine may also be used in the early management of radioiodine-treated Graves' hyperthyroidism.

THYROID DISORDERS IN NEWBORNS IN IODINE DEFICIENT AREAS AFTER DISCONTINUATION OF IODINE SUPLMENTATION

Sub-Carpathian region in Poland is known as an Iodine deficient area. 5 groups of babies with thyroid gland disfunction were selected on HT screening: Congenital hypothyroidisn was detected in 15 cases (1:5011) the transient hypothyroidism in three (1:25551) and 88 patients were diagnosed as having IDD (Iodine Deficiency Disorders)including 42with transient hyperthyrotropinemia, 46 with goiter with or without concomittant hyperthyrotropinemia. The high incidence of IDD in this area seems to be connected wth the insufficient Iodine suplementation in the years 1981-87. The Iodine urine excretion confirmed the moderate environmental Iodine deficiency in the studied area. Conclusions: 1/ The prevalence of congenital hypothyroidism in Kraków district is 1:5011. 2/Kraków belongs to the class II Iodine deficient areas. 3/The incidence of the IDD in this area is 1:824. 4/The correction by Iodine salt suplementation seems urgent.