In infants and young children in Sub-Saharan Africa, iron-deficiency anemia (IDA) is common, and many complementary foods are low in bioavailable iron. In-home fortification of complementary foods ...using iron-containing micronutrient powders (MNPs) and oral iron supplementation are both effective strategies to increase iron intakes and reduce IDA at this age. However, these interventions produce large increases in colonic iron because the absorption of their high iron dose (≥12.5 mg) is typically <20%. We reviewed studies in infants and young children on the effects of iron supplements and iron fortification with MNPs on the gut microbiome and diarrhea. Iron-containing MNPs and iron supplements can modestly increase diarrhea risk, and in vitro and in vivo studies have suggested that this occurs because increases in colonic iron adversely affect the gut microbiome in that they decrease abundances of beneficial barrier commensal gut bacteria (e.g., bifidobacteria and lactobacilli) and increase the abundance of enterobacteria including entropathogenic Escherichia coli. These changes are associated with increased gut inflammation. Therefore, safer formulations of iron-containing supplements and MNPs are needed. To improve MNP safety, the iron dose of these formulations should be reduced while maximizing absorption to retain efficacy. Also, the addition of prebiotics to MNPs is a promising approach to mitigate the adverse effects of iron on the infant gut.
Iodine Deficiency Zimmermann, Michael B
Endocrine reviews,
2009-June, Letnik:
30, Številka:
4
Journal Article
Recenzirano
Odprti dostop
Iodine deficiency has multiple adverse effects in humans, termed iodine deficiency disorders, due to inadequate thyroid hormone production. Globally, it is estimated that 2 billion individuals have ...an insufficient iodine intake, and South Asia and sub-Saharan Africa are particularly affected. However, about 50% of Europe remains mildly iodine deficient, and iodine intakes in other industrialized countries, including the United States and Australia, have fallen in recent years. Iodine deficiency during pregnancy and infancy may impair growth and neurodevelopment of the offspring and increase infant mortality. Deficiency during childhood reduces somatic growth and cognitive and motor function. Assessment methods include urinary iodine concentration, goiter, newborn TSH, and blood thyroglobulin. But assessment of iodine status in pregnancy is difficult, and it remains unclear whether iodine intakes are sufficient in this group, leading to calls for iodine supplementation during pregnancy in several industrialized countries. In most countries, the best strategy to control iodine deficiency in populations is carefully monitored universal salt iodization, one of the most cost-effective ways to contribute to economic and social development. Achieving optimal iodine intakes from iodized salt (in the range of 150–250 μg/d for adults) may minimize the amount of thyroid dysfunction in populations. Ensuring adequate iodine status during parenteral nutrition has become important, particularly in preterm infants, as the use of povidone-iodine disinfectants has declined. Introduction of iodized salt to regions of chronic iodine deficiency may transiently increase the incidence of thyroid disorders, but overall, the relatively small risks of iodine excess are far outweighed by the substantial risks of iodine deficiency.
Iodine is essential for thyroid hormone synthesis. High iodine intakes are well tolerated by most healthy individuals, but in some people, excess iodine intakes may precipitate hyperthyroidism, ...hypothyroidism, goiter, and/or thyroid autoimmunity. Individuals with preexisting thyroid disease or those previously exposed to iodine deficiency may be more susceptible to thyroid disorders due to an increase in iodine intake, in some cases at intakes only slightly above physiological needs. Thyroid dysfunction due to excess iodine intake is usually mild and transient, but iodine‐induced hyperthyroidism can be life‐threatening in some individuals. At the population level, excess iodine intakes may arise from consumption of overiodized salt, drinking water, animal milk rich in iodine, certain seaweeds, iodine‐containing dietary supplements, and from a combination of these sources. The median urinary iodine concentration (UIC) of a population reflects the total iodine intake from all sources and can accurately identify populations with excessive iodine intakes. Our review describes the association between excess iodine intake and thyroid function. We outline potential sources of excess iodine intake and the physiological responses and consequences of excess iodine intakes. We provide guidance on choice of biomarkers to assess iodine intake, with an emphasis on the UIC and thyroglobulin.
High iodine intakes are well tolerated by most healthy individuals, but in some people, excess iodine intakes may precipitate morbidity. Our review describes the association between excess iodine intake and thyroid function. We outline potential sources of excess iodine intake, and the physiological responses and consequences of excess iodine intakes. We provide guidance on the choice of biomarkers to assess iodine intake, with an emphasis on the UIC and thyroglobulin.
Iodine requirements are increased ≥50% during pregnancy. Iodine deficiency during pregnancy can cause maternal and fetal hypothyroidism and impair neurological development of the fetus. The ...consequences depend upon the timing and severity of the hypothyroidism; the most severe manifestation is cretinism. In moderate‐to‐severely iodine‐deficient areas, controlled studies have demonstrated that iodine supplementation before or during early pregnancy eliminates new cases of cretinism, increases birthweight, reduces rates of perinatal and infant mortality and generally increases developmental scores in young children by 10–20%. Mild maternal iodine deficiency can cause thyroid dysfunction but whether it impairs cognitive and/or neurologic function in the offspring remains uncertain. Two meta‐analyses have estimated that iodine‐deficient populations experience a mean reduction in IQ of 12–13.5 points. In nearly all regions affected by iodine deficiency, salt iodisation is the most cost‐effective way of delivering iodine and improving maternal and infant health.
Iodine status has been historically assessed by palpation of the thyroid and reported as goiter rates. Goiter is a functional biomarker that can be applied to both individuals and populations, but it ...is subjective. Iodine status is now assessed using an objective biomarker of exposure, i.e., urinary iodine concentrations (UICs) in spot samples and comparison of the median UIC to UIC cut‐offs to categorize population status. This has improved standardization, but inappropriate use of the crude proportion of UICs below the cut‐off level of 100 µg/L to estimate the number of iodine‐deficient children has led to an overestimation of the prevalence of iodine deficiency. In this review, a new approach is proposed in which UIC data are extrapolated to iodine intakes, adjusted for intraindividual variation, and then interpreted using the estimated average requirement cut‐point model. This may allow national programs to define the prevalence of iodine deficiency in the population and to quantify the necessary increase in iodine intakes to ensure sufficiency. In addition, thyroglobulin can be measured on dried blood spots to provide an additional sensitive functional biomarker of iodine status.
Salt iodization has been introduced in many countries to control iodine deficiency. Our aim was to assess global and regional iodine status as of 2011 and compare it to previous WHO estimates from ...2003 and 2007. Using the network of national focal points of the International Council for the Control of Iodine Deficiency Disorders as well as a literature search, we compiled new national data on urinary iodine concentration (UIC) to add to the existing data in the WHO Vitamin and Mineral Nutrition Information System Micronutrients Database. The most recent data on UIC, primarily national data in school-age children (SAC), were analyzed. The median UIC was used to classify national iodine status and the UIC distribution to estimate the number of individuals with low iodine intakes by severity categories. Survey data on UIC cover 96.1% of the world's population of SAC, and since 2007, new national data are available for 58 countries, including Canada, Pakistan, the U.K., and the U.S.. At the national level, there has been major progress: from 2003 to 2011, the number of iodine-deficient countries decreased from 54 to 32 and the number of countries with adequate iodine intake increased from 67 to 105. However, globally, 29.8% (95% CI = 29.4, 30.1) of SAC (241 million) are estimated to have insufficient iodine intakes. Sharp regional differences persist; southeast Asia has the largest number of SAC with low iodine intakes (76 million) and there has been little progress in Africa, where 39% (58 million) have inadequate iodine intakes. In summary, although iodine nutrition has been improving since 2003, global progress may be slowing. Intervention programs need to be extended to reach the nearly one-third of the global population that still has inadequate iodine intakes.
► I review the role of iodine in growth and development. ► The major impact of hypothyroidism due to iodine deficiency is impaired neurodevelopment, particularly early in life. ► Offspring of ...deficient mothers are at high risk for cognitive disability. ► Correction of iodine deficiency in children improves cognitive and motor function. ► Iodine prophylaxis can prevent the adverse effects of iodine deficiency throughout the life cycle.
Iodine is an essential component of the hormones produced by the thyroid gland. Thyroid hormones, and therefore iodine, are essential for mammalian life. Iodine deficiency is a major public health problem; globally, it is estimated that two billion individuals have an insufficient iodine intake. Although goiter is the most visible sequelae of iodine deficiency, the major impact of hypothyroidism due to iodine deficiency is impaired neurodevelopment, particularly early in life. In the fetal brain, inadequate thyroid hormone impairs myelination, cell migration, differentiation and maturation. Moderate-to-severe iodine deficiency during pregnancy increases rates of spontaneous abortion, reduces birth weight, and increases infant mortality. Offspring of deficient mothers are at high risk for cognitive disability, with cretinism being the most severe manifestation. It remains unclear if development of the offspring is affected by mild maternal iodine deficiency. Moderate-to-severe iodine deficiency during childhood reduces somatic growth. Correction of mild-to-moderate iodine deficiency in primary school aged children improves cognitive and motor function. Iodine prophylaxis of deficient populations with periodic monitoring is an extremely cost effective approach to reduce the substantial adverse effects of iodine deficiency throughout the life cycle.
Iodine deficiency and thyroid disorders Zimmermann, Michael B; Boelaert, Kristien
The lancet. Diabetes & endocrinology,
04/2015, Letnik:
3, Številka:
4
Journal Article
Recenzirano
Iodine deficiency early in life impairs cognition and growth, but iodine status is also a key determinant of thyroid disorders in adults. Severe iodine deficiency causes goitre and hypothyroidism ...because, despite an increase in thyroid activity to maximise iodine uptake and recycling in this setting, iodine concentrations are still too low to enable production of thyroid hormone. In mild-to-moderate iodine deficiency, increased thyroid activity can compensate for low iodine intake and maintain euthyroidism in most individuals, but at a price: chronic thyroid stimulation results in an increase in the prevalence of toxic nodular goitre and hyperthyroidism in populations. This high prevalence of nodular autonomy usually results in a further increase in the prevalence of hyperthyroidism if iodine intake is subsequently increased by salt iodisation. However, this increase is transient because iodine sufficiency normalises thyroid activity which, in the long term, reduces nodular autonomy. Increased iodine intake in an iodine-deficient population is associated with a small increase in the prevalence of subclinical hypothyroidism and thyroid autoimmunity; whether these increases are also transient is unclear. Variations in population iodine intake do not affect risk for Graves' disease or thyroid cancer, but correction of iodine deficiency might shift thyroid cancer subtypes toward less malignant forms. Thus, optimisation of population iodine intake is an important component of preventive health care to reduce the prevalence of thyroid disorders.
Nutritional iron deficiency Zimmermann, Michael B, Dr; Hurrell, Richard F, PhD
Lancet,
08/2007, Letnik:
370, Številka:
9586
Journal Article, Book Review
Recenzirano
Summary Iron deficiency is one of the leading risk factors for disability and death worldwide, affecting an estimated 2 billion people. Nutritional iron deficiency arises when physiological ...requirements cannot be met by iron absorption from diet. Dietary iron bioavailability is low in populations consuming monotonous plant-based diets. The high prevalence of iron deficiency in the developing world has substantial health and economic costs, including poor pregnancy outcome, impaired school performance, and decreased productivity. Recent studies have reported how the body regulates iron absorption and metabolism in response to changing iron status by upregulation or downregulation of key intestinal and hepatic proteins. Targeted iron supplementation, iron fortification of foods, or both, can control iron deficiency in populations. Although technical challenges limit the amount of bioavailable iron compounds that can be used in food fortification, studies show that iron fortification can be an effective strategy against nutritional iron deficiency. Specific laboratory measures of iron status should be used to assess the need for fortification and to monitor these interventions. Selective plant breeding and genetic engineering are promising new approaches to improve dietary iron nutritional quality.
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