Iodine insufficiency in pregnant women from the State of São Paulo

Ferreira, Sabrina Maria Saueia; Navarro, Anderson Marliere; Magalhães, P. K. R.; Maciel, Léa Maria Zanini

doi:10.1590/0004-2730000002979

Cited by 33 publications

(39 citation statements)

References 28 publications

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“…In some areas, mild iodine deficiency is still a public health problem. It is particularly worth mentioning that, according to monitoring data, there exists a large percentage of women of reproductive age with an UIC of 100-150 μg/L [111,112]. This UIC level is just slightly lower than the standard (150-249 μg/L) and is considered a marginal iodine deficiency, a milder status of iodine deficiency.…”

Section: Future Directionsmentioning

confidence: 99%

Maternal Hypothyroxinemia-Induced Neurodevelopmental Impairments in the Progeny

et al. 2015

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Maternal hypothyroxinemia can induce neurodevelopmental impairments in the developing fetus. We here review recent studies on the epidemiology and molecular mechanisms associated with this important public health issue. In 2011, the American Thyroid Association defined maternal hypothyroxinemia as low serum free thyroxine (FT4) levels (<5th or <10th percentile) existing in conjunction with normal serum free triiodothyronine (FT3) or thyroid stimulating hormone (TSH) levels during pregnancy. Compared to clinical or subclinical hypothyroidism, hypothyroxinemia is more commonly found in pregnant women. Hypothyroxinemia usually ensues in response to several factors, such as mild iodine deficiency, environmental endocrine disrupters, or certain thyroid diseases. Unequivocal evidence demonstrates that maternal hypothyroxinemia leads to negative effects on fetal brain development, increasing the risks for cognitive deficits and poor psychomotor development in resulting progeny. In support of this, rodent models provide direct evidence of neurodevelopmental damage induced by maternal hypothyroxinemia, including dendritic and axonal growth limitation, neural abnormal location, and synaptic function alteration. The neurodevelopmental impairments induced by hypothyroxinemia suggest an independent role of T4. Increasing evidence indicates that adequate thyroxine is required for the mothers in order to protect against the abnormal brain development in their progeny.

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Section: Future Directionsmentioning

confidence: 99%

Maternal Hypothyroxinemia-Induced Neurodevelopmental Impairments in the Progeny

et al. 2015

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“…Interestingly, in this study, 19 (9.9%) pregnant women had UIE > 250 μg/L, 63 (33%) had UIE within the normal range (150-250 μg/L), and 109 (57.1%) had UIE < 150 μg /L. 16 So, there is a part of the pregnant women population that is at risk of IDD and should probably receive supplementation. On the other hand, the majority of the general population and the pregnant women population, specifically, are iodine sufficient, in which case supplementation could induce adverse effects, such as Wolff-Chaikoff effect and neonatal hypothyroidism.…”

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confidence: 50%

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2018

Rev Bras Ginecol Obstet

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Iodine is an essential micronutrient required for the production of thyroid hormones, which are critical for homeostasis and neurodevelopment. Because of increased thyroid hormone production, renal iodine excretion and fetal iodine requirements, dietary iodine requirements are higher in pregnancy than they are for nonpregnant adults. 1 Based on this, the World Health Organization (WHO) and the American Thyroid Association (ATA) recommend a daily iodine intake of 250 µg for pregnant and lactating women. 2,3 Iodine deficiency disorder (IDD) in pregnant women could result in harmful effects, including goiter, cretinism, hypothyroidism, growth retardation, pregnancy loss, and infant mortality. Moreover, inadequate iodine intake during pregnancy may lead to neurodevelopmental deficits in offspring, and iodine deficiency is currently considered the leading preventable cause of intellectual impairment worldwide. 4 On the other hand, the excess of iodine may result in fetal goiter and hypothyroidism. Exposures as minor as the vaginal application of povidone-iodine during delivery or local use of disinfectant in newborns can lead to increased serum TSH concentrations 5 and transient neonatal hypothyroidism. 6 With this information in mind, we read with great interest the 2017 Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease during Pregnancy and the Postpartum. 7 Among other topics, the nutritional aspects related to iodine sufficiency are addressed in section IV, and a supplementation with 150 μg of potassium iodine per day is suggested on Recommendation 6 for women, in most regions of the world, who are planning a pregnancy or currently pregnant. This is optimally started 3 months in advance of planned pregnancy (strong recommendation, moderate-quality evidence). Could this recommendation improve the quality of the prenatal care of Brazilian pregnant women?The most efficient method of IDD prevention is salt iodination. Also, ongoing monitoring of population biomarkers, such as urinary iodine concentration, is essential to ensure that population iodine intakes are optimized. In Brazil, the salt iodination is controlled by federal law in partnership with the National Agency for Sanitary Surveillance (Anvisa, in the Portuguese acronym) and the salt productive sector. 8-10 Unfortunately, data on the iodine nutritional status are scarce and contradictory in Brazil. The national project of salt iodination (PNAIsal, in the Portuguese acronym) (which evaluated 477 locations and a total of 18,978 school children) identified Brazil as a country of "more than appropriate" iodine consumption, with a mean urinary iodine excretion (UIE) concentration of 276 µg/L. 11,12 A recent meta-analysis concluded that the majority of the data on this subject are derived from the population in the south/southeast region of Brazil, but the actual overall IDD prevalence is unknown and might still be high in some areas. 13 Regarding the pregnant population, three studies were published prior to Anvis...

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“…Although universal salt iodization has taken several decades, there are also a large percentage of women of reproductive age suffering from marginal or mild ID (Ferreir et al, 2014; Méndez-Villa et al, 2014). Therefore, we should concern about the impacts on the fetus following maternal mild and marginal ID.…”

Section: Discussionmentioning

confidence: 99%

“…Even in some developed countries and regions, mild ID, and marginal ID are largely ignored problems for women of child bearing age (Morreale de Escobar et al, 2000; Hollowell and Haddow, 2007; Perrine et al, 2010; Pearce et al, 2013). Monitoring data have indicated that a large percentage of women during pregnancy and lactation have UIC of 100–150 μg/l in the developing country, which is slightly lower than the WHO criteria for sufficient iodine supply (World Health Organization/UNICEF/ICCIDD, 2007; Ferreir et al, 2014; Méndez-Villa et al, 2014). Mild ID is identified as one of the most frequent causes of maternal and neonatal hypothyroxinemia (Morreale de Escobar et al, 2000; Vermiglio et al, 2004; Stagnaro-Green et al, 2011; Henrichs et al, 2013).…”

Section: Introductionmentioning

confidence: 93%

Maternal Different Degrees of Iodine Deficiency during Pregnant and Lactation Impair the Development of Cerebellar Pinceau in Offspring

et al. 2017

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Aims: Iodine is critical for synthesis of thyroid hormones (TH). And iodine deficiency (ID) is one of the most significant reasons of intellectual disability and motor memory impairment, although the potential mechanisms are still under investigation. Presently, mild ID and marginal ID are largely ignored problems for women of child bearing age. Mild ID is a subtle form of TH deficiency, which shows low levels of free thyroxine (FT4) and relatively normal free triiodothyronine (FT3) or thyroid stimulation hormone (TSH). And marginal ID is a milder form of ID with decreased total T4 (TT4) but relatively normal FT3, FT4, and TSH. Therefore, we investigated the effects of maternal different degrees of ID on the development of pinceau in cerebellar purkinje cells (PCs) and studied the expression of pinceau related protein, which is crucial for the development and maturation of pinceau.Methods and Results: Three developmental iodine deficient rat models were created by feeding dam rats with an iodine-deficient diet and deionized water supplemented with potassiumiodide. Our study showed that different degrees of ID inhibited cerebellar pinceau synapse development and maturation on postnatal day (PN) 14 and PN21. What's more, mild and severe ID reduced the expression of AnkG, β4-spectrin, neurofascin186 and NrCAM on PN7, PN14, and PN21. However, marginal ID rarely altered expression of these proteins in the offspring.Conclusion: These results suggested that maternal mild and severe ID impaired the development and maturation of cerebellar pinceau, which may be attributed to the decrease of AnkG, β4-spectrin, neurofascin 186, and NrCAM. And the alteration of development and maturation in cerebellar pinceau in the offspring were also observed following maternal marginal ID, which is slighter than that of mild ID.

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Iodine insufficiency in pregnant women from the State of São Paulo

Cited by 33 publications

References 28 publications

Maternal Hypothyroxinemia-Induced Neurodevelopmental Impairments in the Progeny

Maternal Hypothyroxinemia-Induced Neurodevelopmental Impairments in the Progeny

Untitled

Maternal Different Degrees of Iodine Deficiency during Pregnant and Lactation Impair the Development of Cerebellar Pinceau in Offspring

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