Effect of Iodine Nutrition on Pregnancy Outcomes in an Iodine-Sufficient Area in China

Many studies focused on the association between thyroid disease and pregnancy outcomes. The present study explored the effect of iodine nutrition during the first trimester on pregnancy outcomes. One thousand five hundred sixty-nine pregnant, euthyroid women at ≤12 weeks of gestation in an iodine-sufficient area in China were recruited. According to the World Health Organization (WHO) criteria for iodine nutrition during pregnancy, participants were divided into four groups: adequate iodine (median urinary iodine concentration (UIC), 150–249 μg/L), mild deficiency (UIC, 100–150 μg/L), moderate and severe deficiency (UIC, <100 μg/L), and more than adequate and excessive (UIC, ≥250 μg/L) groups. Pregnancy outcomes, including abortion, gestational hypertension, pre-eclampsia, gestational diabetes mellitus (GDM), placenta previa, placental abruption, preterm labor, low birth weight infants, macrosomia, breech presentation, and cord entanglement, were obtained during follow-up. The results showed that there was no significant difference in general characteristics, including age, body mass index, abdominal circumference, systolic blood pressure, diastolic blood pressure, heart rate, smoking rate, and drinking rate, among the four groups. In the more than adequate and excessive group, thyroid-stimulating hormone (TSH) was greater and free thyroxine (FT4) was lower than any other groups but still within normal range. The thyroglobulin (Tg) level was greater in the moderate and severe deficiency group. The incidence of GDM was significantly greater in women with mild iodine deficiency than in women with adequate iodine nutriture (18.38 vs. 13.70%, p < 0.05). Compared with the adequate group, incidence of macrosomia was significantly greater in the more than adequate and excessive group (12.42 vs. 9.79%, p < 0.05). Mild iodine deficiency was an independent risk factor for GDM (odds ratio = 1.566, 95% confidence interval = 1.060–2.313, p = 0.024); more than adequate and excessive iodine was an independent risk factor for macrosomia (OR = 1.917, CI = 1.128–3.256, p = 0.016). In summary, during 1st trimester, both mild iodine deficiency and excessive iodine intake had adverse impacts on pregnancy outcomes in an iodine-sufficient area.     

硒缺乏与甲状腺激素代谢及功能

Ｉ型脱碘酶为含硒酶,缺硒时,该酶活性下降,使循环Ｔ４增高,外周组织Ｔ３水平下降。缺硒可加速甲状腺组织碘的耗竭,并加重某些缺碘的生物学效应,缺硒还可能与碘缺乏病的发生发展有关。以缺硒为主要病因的克山病存在甲状腺激素代谢异常,其心肌呼吸酶活性变化与缺碘引起的甲状腺功能低下相似,缺碘可缺硒引起的甲状腺激素代谢改变与克山病的发生可能有关。     

The importance of selenium and the effects of its deficiency in animal health

Selenium (Se) is an essential trace element in animal nutrition, and exerts multiple actions related to animal production, fertility and disease prevention. Glutathione peroxidase (GSH-PX) enzyme was the first proven selenoenzyme that can prevent oxidative damage of the cellular membrane. Actually more than 30 selenoenzymes have been described and a hierarchy process for expression in the animal has been established. White muscle disease (WMD) was the first recognized condition associated with Se deficiency. WMD causes new born mortality, especially in ruminants, and impaired production condition in growing and adult animals. Selenium is critical to thyroid hormone synthesis and it is also very important for converting T4 (thyroxin inactive form) to T3 (active form). A good immune response requires Se too. Selenium status in soil, plants and animal blood and tissue can be used in the diagnosis of Se deficiency. Diverse forms of Se supplements are available, but many factors affect their activity and efficacy, such as its chemical form and animal's health and production condition. The relationships between foetus Se metabolism and pregnant dam Se status are critical for productivity and need further research.     

Iodine and zinc, but not selenium and copper, deficiency exists in a male Turkish population with endemic goiter

Although endemic goiter has been shown to have a high prevalence in Turkey, little is known about the concentration of urinary iodine, plasma selenium (Se), copper (Cu), and zinc (Zn) in these patients. We studied on 140 male patient with endemic goiter (mean age: 22.2 ± 0.19 yr) and 140 healthy male subjects (mean age: 21.8 ± 0.28 yr). Daily urinary iodine excretion was determined by the ionometric method. Plasma Se, Zn, and Cu were determined by using atomic absorption spectrometry. Daily urinary iodine excretion was found to be significantly lower in the patient group (38.7 ± 2.26 μg/d) than that of controls (50.73 ± 2.56 μg/day,p = 0.001). Plasma Zn concentrations were also found to be significantly lower in the patient group (1.04 ± 0.03 μg/mL) than that of controls (1.16 ± 0.02 μg/mL,p = 0.001). No significant difference was determined in Se and Cu concentrations between the patient and control groups. Our study shows that a moderate iodine deficiency exists in both patients with endemic goiter and control subjects, which indicates the important role of iodine deficiency in the etiopathogenesis of endemic goiter in Turkey. Zinc deficiency may also contribute to the pathogenesis of endemic goiter. However, Se and Cu do not seem to have any role in the etiopathogenesis of endemic goiter in Turkey. A community-based iodine fortification program throughout the country may be proposed to take over the problem, which also can prevent the contributing effects of other element deficiencies that occur when iodine deficiency is the prevailing factor.     

Selenium in total parenteral nutrition

In clinical practice, selenium deficiency may arise under conditions of chronic malnutrition and especially after long-term total parenteral nutrition (TPN). In infants receiving long-term TPN, we observed plasma selenium levels as low as those previously reported in Chinese children with Keshan disease. Low plasma selenium levels were also usually associated with very low activities of glutathione peroxidase. Although clinical symptoms of selenium deficiency did not occur in our patients, several cases have been described in the literature, indicating the need for supplementation in TPN. In order to derive at the appropriate dosage, it is proposed to correlate it with the total protein supply. According to our present knowledge, .5–1.0 μg selenium/g of protein appears to be adequate to keep patients in Se balance. For Se repletion of body stores, this dosage has been increased up to 3 μg of Se/g of protein. Advantages and disadvantages of selenite and of selenomethionine as possible supplemental forms of Se for TPN solutions are discussed.     

Selenium accumulation in lettuce germplasm

Selenium (Se) is an essential micronutrient for animals and humans. Increasing Se content in food crops offers an effective approach to reduce the widespread selenium deficiency problem in many parts of the world. In this study, we evaluated 30 diverse accessions of lettuce (Lactuca sativa L.) for their capacity to accumulate Se and their responses to different forms of Se in terms of plant growth, nutritional characteristics, and gene expression. Lettuce accessions responded differently to selenate and selenite treatment, and selenate is superior to selenite in inducing total Se accumulation. At least over twofold change in total Se levels between cultivars with high and low Se content was found. Synergistic relationship between Se and sulfur accumulation was observed in nearly all accessions at the selenate dosage applied. The change in shoot biomass varied between lettuce accessions and the forms of Se used. The growth-stimulated effect by selenate and the growth-inhibited effect by selenite were found to be correlated with the alteration of antioxidant enzyme activities. The different ability of lettuce accessions to accumulate Se following selenate treatment appeared to be associated with an altered expression of genes involved in Se/S uptake and assimilation. Our results provide important information for the effects of different forms of Se on plant growth and metabolism. They will also be of help in selecting and developing better cultivars for Se biofortification in lettuce.     

Oxidative DNA base damage, antioxidant enzyme activities and selenium status in highly iodine-deficient goitrous children

The objective of this study was to investigate oxidative DNA damage, and the levels of antioxidant enzymes (AOE) and selenium (Se) in relation to iodine deficiency and/or goiter in children. The study was performed in a group of goitrous high school children (15-18 years of age) ( n =14) with severe or moderate iodine deficiency. Thyroid hormones (TSH, FT 4 , TT 4 , FT 3 , TT 3 ), urinary iodine (UI) and plasma Se levels, and erythrocyte glutathione peroxidase (GSHPx), superoxide dismutase (SOD) and catalase (CAT) activities were determined and compared with those of a control group consisting of non-goitrous high school children ( n =14) with normal UI levels or mild iodine deficiency. In the goitrous group, concentrations of FT 4 , TT 4 , plasma Se and UI, and activities of GSHPx and SOD were found to be significantly lower. Six typical hydroxyl radical-induced base lesions in genomic DNA of peripheral blood were identified and quantified by gas chromatography/isotope-dilution mass spectrometry (GC/IDMS), and higher levels of DNA base lesions were observed in the goitrous group. The results suggest that highly iodine-deficient goitrous children may be under oxidative stress, which may lead to greater level of oxidative damage to DNA. This study supports the evidence for the reported relationship between iodine deficiency and the increased incidence of thyroid malignancies.     

Iodized oil as a complement to iodized salt in schoolchildren in endemic goiter in Romania

OBJECTIVE: To evaluate the long-term efficacy and possible side effects of low doses of iodized oil on iodine nutrition and thyroid function in endemic goiter in Romania. METHODS: Random selection of 214 schoolchildren aged 6-14 years. Serial measurements of urinary iodine, thyroid volume with ultrasound, serum concentrations of thyrotropin, free thyroxine, thyroglobulin and thyroid autoantibodies before and up to 2 years after the oral administration of 200 mg iodine in iodized oil. RESULTS: Urinary iodine concentrations indicated a moderate iodine deficiency before therapy, sharply increased soon after therapy and slowly decreased thereafter but remained within the normal range up to more than 1 year after therapy. The prevalence of goiter was 29% before the administration of iodized oil and 9% 1 year later. Thyroid function tests and autoantibodies were normal before and up to 2 years after therapy. CONCLUSION: A single dose of 200 mg iodine from oral Lipiodol appears adequate and safe for correcting moderate iodine deficiency in children.     

Bioelement effects on thyroid gland in children living in iodine-adequate territory

Endemic goitre is a primary pathology of thyroid gland and critical medico social problem in many countries. A dominant cause of endemic goitre is iodine deficiency. However, besides primary iodine deficiency, the goitre may probably develop due to effects of other bioelement imbalances, essential to thyroid function maintenance. Here we studied 44 cases of endemic goitre in prepubertal children (7–10 y.o.) living in iodine-adequate territory. Thyroid volume was estimated by ultrasonometry. Main bioelements (Al, Ca, Cd, Co, Cr, Cu, Fe, Hg, I, Mg, Mn, Pb, Se, Si, Zn) were determined in hair samples by ICP-OES/ICP-MS method. Relationships between hair content of bioelements and thyroid gland size were estimated by multiple regressions. The regression model revealed significant positive relations between thyroid volume and Cr, Si, Mn contents. However, the actual factor of thyroid gland increase was only Si excess in organism. Significant negative relations of thyroid volume were revealed with I, Mg, Zn, Se, Co and Cd. In spite of this, the actual factors of thyroid gland volume increasing were I, Co, Mg and Se deficiency. Total bioelement contribution in thyroid impairment was estimated as 24%. Thus, it was suggested that endemic goitre in iodine-adequate territory can be formed by bioelement imbalances, namely Si excess and Co, Mg, Se shortage as well as endogenous I deficiency in spite of iodine-adequate environment.     

Iodine Deficiency and Excess in Children: Worldwide Status in 2013

ObjectiveAssessing iodine nutrition at the population level is usually done by measuring the urinary iodine concentration (UIC) and, in some countries, by estimating household coverage of adequately iodized salt (HHIS). Using these indicators, the objective of this review is to assess global and national iodine status in 2013.MethodsThe most recent data on HHIS were obtained from the United Nations Children's Fund. The most recent data on UICs were obtained from the International Council for the Control of Iodine Deficiency Disorders Global Network and the World Health Organization (WHO). Median UIC was used to classify national iodine status based on the current WHO classification system, with the following modification: the “adequate (100 to 199 μg/L)” and “more than adequate (200 to 299 μg/L)” categories of median UIC in school-aged children were combined into a single category of “adequate” iodine intake (100 to 299 μg/L).ResultsOver the past decade, the number of countries that are iodine deficient has fallen from 54 to 30. The number iodine-sufficient countries has increased from 67 to 112, while the number with excessive iodine intake has increased from 5 to 10. In most countries with excess intake, this is due to overiodization of salt and/or poor monitoring of salt iodization. Out of 128 countries with HHIS data, at least 90% of households in 37 countries consume adequately iodized salt, but in 39 countries, coverage rates are below 50%. Overall, about 70% of households worldwide have access to iodized salt.ConclusionThere has been substantial recent progress in the global effort to control iodine deficiency. However, iodized salt programs need to be carefully monitored to ensure adequate iodine intake while avoiding iodine excess. (Endocr Pract. 2013;19:839-846)     

植物铁代谢及植物铁蛋白结构与功能研究进展

铁在生命过程中起着很重要的作用,植物缺铁后叶绿素合成受阻而导致的黄化症状已成为世界性植物营养失调问题。与之相随,人类铁营养的缺乏也极为严重,因此研究植物铁代谢并且开发安全、天然、高效的补铁因子具有重要的意义。到目前为止,在已经发现的植物中,只有豆科类植物是将其种子中～90％的铁储藏在铁蛋白中,所以来源于豆科类植物的铁蛋白是一个理想的补铁资源。与动物铁蛋白相比,植物铁蛋白具有两个显著的特点：首先,植物铁蛋白在其N端具有一个独特的EP肽段;其次,植物铁蛋白只含有H型亚基,且有两种不同的H型亚基组成。主要阐述有关植物铁代谢及铁蛋白的结构、功能的最新研究进展。     

Iodine Status of Preterm Infants Born in an Area of Iodine Sufficiency: Are They at Risk of Iodine Deficiency?

ObjectiveTo the assess the iodine status of preterm infants born in an area of iodine sufficiency using the urinary iodine concentration (UIC) and thyroid-stimulating hormone (TSH) levels and compare these values across different feeding practices during the first 7 days of life.MethodsIn this cross-sectional study, 88 preterm infants born at 30 to 34 weeks of gestation and admitted to the neonatal intensive care unit of a referral hospital in Tehran (Iran) were included. The infant UIC and TSH levels and breast milk iodine concentration in mothers who were exclusively breastfeeding were measured.ResultsMedian (interquartile range [IQR]) UIC and TSH levels in the study population were 81 (39-189) μg/L and 1.60 (0.80-2.85) mIU/L, respectively. When preterm infants were stratified by the type of feeding, the median (IQR) UICs were 64 (42-126) μg/L in parenteral nutrition, 125 (41-195) μg/L in exclusively breastfeeding, 57 (28-123) μg/L in formula feeding, and 45 (35-132) μg/L in mixed feeding, with no statistically significant difference between the groups (P = .31). The median (IQR) breast milk iodine concentration was 271 (177-521) μg/L in preterm infants exclusively fed their mothers’ own milk. There was no significant difference in the proportion of the TSH levels of >5 mIU/L between preterm infants who received enteral and parenteral nutrition (P = .27).ConclusionPreterm infants are at risk of iodine deficiency even in an area where the general population has adequate iodine. Only the preterm infants who received exclusively their mothers’ own milk had marginally adequate iodine status. Further studies are warranted to determine the necessity of iodine supplementation for this vulnerable group.     

Status of selenium and antioxidant enzymes of goitrous children is lower than healthy controls and nongoitrous children with high iodine deficiency

In order to investigate the relations of iodine deficiency and/or goiter with selenium (Se) and antioxidant enzyme (AOE) status, we determined the relevant parameters of goitrous high school children living in an endemic goiter area of Turkey. Subjects were selected by a simple random sampling technique after screening the whole population of the high schools of two towns by neck palpation. The results of the goitrous group (n = 48, aged 15-18 yr) were compared with those of nongoitrous control children (n = 49) from the same populations, and with an outside control group (n = 24) from a lower-goiter-prevalence area. The overall prevalence of goiter was 39.6% in the high school population of the area. Activities of erythrocyte AOE (glutathion peroxidase, catalase, and superoxide dismutase) and concentrations of plasma and erythrocyte Se and urinary iodine were found to be significantly lower in goitrous children than both in-region and out-region of the control groups. When the whole study group was reclassified according to the severity of iodine deficiency, it was found that the AOE and Se status of those control children without goiter but with high iodine deficiency was significantly higher than goitrous children, although they did not differ from nondeficient control group. This might be the result of the possibility that goitrous children are exposed of oxidative stress, which may introduce alterations to the antioxidant defense system and/or the antioxidant status is relatively lower in goitrous children than those children who are highly iodine-deficient but did not develop goiter. The results of this study seem to support the view that the risk of goiter development may be higher in highly iodine-deficient children with lower enzymatic antioxidant and Se status.     

The impact of mineral nutrients in food crops on global human health

Nutrient sufficiency is the basis of good health, productive lives and longevity for everyone. Nutrient availability to people is primarily determined by the output of foods produced from agricultural systems. If agricultural systems fail to provide enough food diversity and quantity to satisfy all the nutrients essential to human life, people will suffer, societies will deteriorate and national development efforts will stagnate. Importantly, plant foods provide most of the nutrients that feed the developing world. Unfortunately, as a result of population pressures, many global food systems are not currently providing enough micronutrients to assure adequate micronutrient intakes for all people. This has resulted in an increasing prevalence of micronutrient deficiencies (e.g., iron deficiency, vitamin A deficiency, and iodine deficiency disorders) that now afflicts over three billion people globally mostly among resource-poor women, infants and children in developing countries. The consequences of micronutrient malnutrition are profound and alarming for human existence. Agricultural approaches to finding sustainable solutions to this problem are urgently needed. This review presents some ways in which plant nutritionists can contribute to preventing micronutrient malnutrition in sustainable ways.     

Attenuation of LDL receptor gene expression by selenium deficiency during hypercholesterolemia

Selenium deficiency has been associated with hypercholesterolemia. Present study was aimed to determine the effect of selenium (Se) deficiency on LDL receptor (LDL-R) activity as well as mRNA expression during experimental hypercholesterolemia in SD male rats. Animals were fed Se adequate (0.2 ppm) and deficient (0.02 ppm) control diet as well as high cholesterol (2%) diet (HCD) for 1 and 2 months. LDL-R activity was measured in vivo by injecting radiolabeled LDL to rats and percent decrease in cpm with time was taken as a measure of LDL clearance and in turn LDL-R activity. LDL-R mRNA expression was studied by RT-PCR. LDL-R activity and mRNA expression decreased significantly on HCD feeding in both Se deficient and adequate diet fed rats after 2 months. In Se deficiency receptor activity and mRNA expression decreased significantly. After 2 months LDL-R activity and expression decreased in both the Se deficient groups and in Se adequate HCD fed group in comparison to 1 month data. But after 4 month there was no significant difference observed in LDL-R activity and mRNA expression in selenium deficiency as well as on HCD feeding. So the present results demonstrate that Se deficiency act synergistically with hypercholesterolemia to downregulate LDL-R activity as well as mRNA expression.     

Iodine nutrition and breast feeding

A survey of the databanks Medline and Web of science identified studies dealing with maternal and infant iodine nutrition during breast feeding. The iodine concentration of human milk varies widely due to maternal iodine intake. Mean breast milk iodine concentrations are reported as ranging from 5.4 to 2170 μg/L (median 62 μg/L) in worldwide studies. In the few studies that compared length of lactation, gestation length, and parity number, these factors did not significantly affect milk-iodine concentrations. In studies of maternal iodine deficiency, untreated goiter had no impact on breast milk iodine when compared with controls. Iodine in human milk responds quickly to dietary iodine intake, either supplemented or consumed in natural foods. Easily absorbable iodine from foods, supplemental sources, iodine-based medication or iodine-based antiseptic solutions used during parturition, is taken up by the maternal thyroid and mammary glands through the Na⁺/I⁻ symporter system. This transmembrane carrier protein transports iodine against a high concentration gradient. Hormonal iodine in breast milk occurs mainly as T-4, but depending on maternal iodine intake, high concentrations of the inorganic form (iodide) are found. In less developed countries, where natural-food-iodine intake is low, adequate maternal iodine nutritional status depends exclusively on enforcement of food iodination. In industrialized countries, maternal iodine intake has increased as a function of increasing consumption of dairy products. The human infant is sensitive to maternal iodine nutrition during fetal development and later during breast feeding. Environmental factors, not directly related to maternal iodine intake, such as intake of selenium and organochlorine pollutants, can affect thyroid hormone homeostasis in breast-fed infants. In spite of low iodine concentrations found in milk of mothers consuming low-iodine natural foods, long lasting or even life-lasting benefits to the breast-fed infant are demonstrable.     

Effect of selenium and protein deficiency on selenium and glutathione peroxidase in rats

Twenty-four weanling male Wistar rats were divided into four groups fed diets containing adequate or deficient levels of selenium (0.5 ppm [+ Se] or <0.02 ppm [−Se] and protein (15% [+Pro] or 5% [−Pro]), but adequate levels of all other nutrients for 4 wk to determine the effects of Se deficiency and protein deficiency on tissue Se and glutathione peroxidase (GSHPx) activity in rats. Plasma, heart, liver, and kidney Se and GSHPx were significantly lower in Se-deficient groups in relation to Se-sufficient groups. In Se-deficient groups, Se and GSHPx were significantly higher in −Se−Pro rats in heart, liver, and kidney. Data analysis showed that there were significant interaction effects between dietary Se and protein on Se and GSHPx of rats. It is assumed that under the condition of Se deficiency. a low level of protein may decrease Se and GSHPx utilization, increase GSHPx synthesis, and result in Se redistribution. This could account for high levels of Se and GSHPx in the −Se−Pro rats compared to −Se+Pro rats.     

Etiologic factors and pathologic alterations in selenium-vitamin E deficiency and excess in animals and humans

The etiology of selenium-vitamin E (Se-E) deficiency diseases may be complex. Many of the syndromes involve combined deficiency of selenium and vitamin E. Selenium moves into the animal and human food chain from soil and plants, which may contain inadequate amounts of the nutrient in many areas of the world. Vitamin E may be in low concentration in many animal feeds unless supplements are added. Some syndromes, such as steatitis in cats, result from an increased requirement of vitamin E in diets that contain large amounts of polyunsaturated fatty acids, and these diseases will only respond to vitamin E administration. Deficiency syndromes in animals owing to pure Se deficiency are infrequent and have been produced mainly by laboratory studies utilizing extreme deficiency conditions. Other factors that may affect the occurrence of these deficiency diseases are concurrent dietary deficiency of S-containing amino acids, bioavailability of different forms of dietary Se, intake of compounds that antagonize Se (e.g., silver salts), and exposure to various prooxidant substances (e.g., iron compounds, oxygen, ozone, and various drugs). A wide variety of pathologic alterations occur in animals and humans with Se-E deficiency. Myocardial lesions are seen most frequently in calves, lambs, pigs, turkey poults, and ducklings. In humans, Keshan disease, an endemic cardiomyopathy in China, is attributed to Se deficiency. Necrosis of skeletal muscle is the most frequent lesion observed in animal species. Necrosis of smooth muscle of the gizzard and intestine may be a prominent lesion in turkey poults, ducklings, and quail. Other Se-E deficiency lesions include hepatic necrosis, gastric ulceration, intestinal and uterine lipofuscinosis, pancreatic damage, steatitis, exudative diathesis, encephalomalacia, and testicular necrosis. Selenium toxicosis is well characterized in animals and humans by neurological, hoof, and hair alterations.     

The implications of selenium deficiency for wild herbivore conservation: a review

Selenium (Se) is required at a fundamental physiological level in all animals. Adequate levels of Se are necessary for proper bone metabolism, iodine metabolism, immune function, reproductive success, and recruitment. Selenium is a component of enzymes which scavenge oxidative free radicals that would otherwise degrade cell membranes. Severe deficiency results in obvious symptoms such as white muscle disease in ungulates. However, more frequently, deficiency may be chronic and subclinical. Individuals then display no obvious signs of malady, yet performance suffers until their populations decline without apparent cause or through proximate factors which obscure underlying primary factors. Although well known in domestic stock, the link between population performance and Se deficiency in wild populations has been difficult to firmly establish. Confounding factors include the role of vitamin E, which also acts as an antioxidant to mitigate the need for Se under some circumstances; changing Se requirements at changing times in animal life history; changing Se requirements in relation to pollution levels and other factors causing oxidative stress; and the non-uniform distribution of Se in its various chemical forms in the environment. The latter point is especially important to wild populations that have been reduced to remnant portions of their previous range. Here, we have reviewed the literature of Se in wildlife as well as provided an introduction to Se in physiology and Se behavior in the environment for the wildlife researcher and manager. We conclude that unrecognized Se deficiency may often impede optimal population performance, and we provide recommendations for habitat analysis with regard to Se which can be used in future research. Finally, evidence that the amount of available Se in the environment is decreasing from anthropogenic causes is shown.