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The Assessment and Prevention of Gestational Iodine Deficiency and Its Adverse Fetal Consequences: A Focus on Mild Iodine Deficiency

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A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: closed (28 July 2019) | Viewed by 26744

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Prof. John Burgess

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School of Medicine, University of Tasmania. Department of Endocrinology, Royal Hobart Hospital.Hobart, Tasmania 7000, Australia
Interests: Iodine Nutrition; Iodine Deficiency in Pregnancy; Fetal neurocognitive sequelae of iodine deficiency; Epidemiology of Thyroid Disease; Endocrine Neoplasia

Special Issue Information

Dear Colleagues,

Whilst great strides have been made in the quest to eliminate iodine deficiency disorders, there remains a largely unresolved challenge. The purpose of this Special Issue of Nutrients is to provide a collective focus for nutritional scientists, epidemiologists, neuroscientists, educationalists and public health experts to consider the challenge of mild iodine deficiency in pregnancy and lactation. Despite most previously iodine deficient populations benefiting from programs to eliminate iodine deficiency in childhood, the adequacy of iodine nutrition during pregnancy and lactation often remains unclear or manifestly inadequate in many jurisdictions. In part, methods for population assessment of iodine nutrition as well as modes of public health iodine supplementation account for this, with iodine vectors used for targeting children and the general population often ill-suited for women of reproductive age. Moreover, despite numerous small and often observational studies indicating an adverse impact of mild gestational iodine deficiency on fetal neurocognitive development and the later educational performance of the child, our knowledge of the underlying neurobiology, effect magnitude and appropriate public health mitigations is surprisingly inadequate given the potential societal consequences of mild gestational iodine deficiency. The opportunity and necessity exists to raise the research, public health and educational profile of what largely remains inadequately understood and untreated “mild” iodine deficiency in pregnancy and lactation. Given your expertise and highly respected commitment in this field, it’s my pleasure to warmly invite you to contribute to this Special Issue of Nutrients which aims to further multidisciplinary awareness and collaboration in relation to “The Assessment and Prevention of Gestational Iodine Deficiency and its Adverse Fetal Consequences: a focus on mild iodine deficiency”.

Prof. John Burgess
Guest Editor

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Keywords

Iodine Deficiency
Pregnancy
Gestational iodine deficiency
Neurocognitive sequelae
Prenatal
Iodine supplementation
Urine iodine concentration
Educational performance
IQ

Published Papers (4 papers)

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Research

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13 pages, 859 KiB

Open AccessArticle

The Effects of Iodine Supplementation in Pregnancy on Iodine Status, Thyroglobulin Levels and Thyroid Function Parameters: Results from a Randomized Controlled Clinical Trial in a Mild-to-Moderate Iodine Deficiency Area

by Simona Censi, Sara Watutantrige-Fernando, Giulia Groccia, Jacopo Manso, Mario Plebani, Diego Faggian, Monica Maria Mion, Roberta Venturini, Alessandra Andrisani, Anna Casaro, Pietro Vita, Alessandra Avogadro, Marta Camilot, Carla Scaroni, Loris Bertazza, Susi Barollo and Caterina Mian

Nutrients 2019, 11(11), 2639; https://doi.org/10.3390/nu11112639 - 4 Nov 2019

Cited by 29 | Viewed by 7334

Abstract

Background: Iodine supplementation during pregnancy in areas with mild-to-moderate iodine deficiency is still debated. Methods: A single-center, randomized, single-blind and placebo-controlled (3:2) trial was conducted. We enrolled 90 women before 12 weeks of gestation. From enrollment up until 8 weeks after delivery, 52 women were given an iodine supplement (225 ug/day, potassium iodide tablets) and 38 were given placebo. At recruitment (T0), in the second (T1) and third trimesters (T2), and 8 weeks after delivery (T3), we measured participants’ urinary iodine-to-creatinine ratio (UI/Creat), thyroid function parameters (thyroglobulin (Tg), TSH, FT3, and FT4), and thyroid volume (TV). The newborns’ urinary iodine concentrations were evaluated in 16 cases. Results: Median UI/Creat at recruitment was 53.3 ug/g. UI/Creat was significantly higher in supplemented women at T1 and T2. Tg levels were lower at T1 and T2 in women with UI/Creat ≥ 150 ug/g, and in the Iodine group at T2 (p = 0.02). There was a negative correlation between Tg and UI/Creat throughout the study (p = 0.03, r = −0.1268). A lower TSH level was found in the Iodine group at T3 (p = 0.001). TV increased by +Δ7.43% in the Iodine group, and by +Δ11.17% in the Placebo group. No differences were found between the newborns’ TSH levels on screening the two groups. Conclusion: Tg proved a good parameter for measuring iodine intake in our placebo-controlled series. Iodine supplementation did not prove harmful to pregnancy in areas of mild-to-moderate iodine deficiency, with no appreciable harmful effect on thyroid function. Full article

(This article belongs to the Special Issue The Assessment and Prevention of Gestational Iodine Deficiency and Its Adverse Fetal Consequences: A Focus on Mild Iodine Deficiency)

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10 pages, 235 KiB

Open AccessArticle

Women Remain at Risk of Iodine Deficiency during Pregnancy: The Importance of Iodine Supplementation before Conception and Throughout Gestation

by Kristen L. Hynes, Judy A. Seal, Petr Otahal, Wendy H. Oddy and John R. Burgess

Nutrients 2019, 11(1), 172; https://doi.org/10.3390/nu11010172 - 15 Jan 2019

Cited by 28 | Viewed by 5924

Abstract

In Australia, pregnant women are advised to take an iodine supplement (I-supp) (150 µg/day) to reduce risks to the foetus associated with iodine deficiency (ID). To examine the impact of this recommendation on iodine status, and to identify factors that contribute to adequacy during gestation, supplement use and Urinary Iodine Concentration (UIC) was measured in 255 pregnant women (gestation range 6 to 41 weeks) in Tasmania. The median UIC (MUIC) of 133 µg/L (Inter-quartile range 82–233) was indicative of ID, being below the 150–249 µg/L range for adequacy during pregnancy. Women taking an iodine-containing-supplement (I-supp) had a significantly higher MUIC (155 µg/L) (n = 171) compared to the combined MUIC (112.5 µg/L) (n = 84) of those who had never (120 µg/L) (n = 61) or were no longer taking an I-supp (90 µg/L) (n = 23) (p = 0.017). Among women reporting I-supp use, the MUIC of those commencing the recommended 150 µg/day prior to conception was significantly higher than those starting supplementation following pregnancy confirmation: 196 (98–315) µg/L (n = 45) versus 137.5 (82.5–233.5) µg/L (n = 124), p = 0.032. Despite recommendations for iodine supplementation pregnant Tasmanian women remain at risk of ID. Commencing an I-supp of 150 µg/day prior to conception and continuing throughout pregnancy is required to ensure adequacy. Timely advice regarding the importance of adequate iodine nutrition, including supplementation is needed to reduce the risk of irreversible in utero neurocognitive damage to the foetus. Full article

(This article belongs to the Special Issue The Assessment and Prevention of Gestational Iodine Deficiency and Its Adverse Fetal Consequences: A Focus on Mild Iodine Deficiency)

Review

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18 pages, 718 KiB

Open AccessReview

Optimal Assessment and Quantification of Iodine Nutrition in Pregnancy and Lactation: Laboratory and Clinical Methods, Controversies and Future Directions

by Creswell J Eastman, Gary Ma and Mu Li

Nutrients 2019, 11(10), 2378; https://doi.org/10.3390/nu11102378 - 5 Oct 2019

Cited by 30 | Viewed by 7845

Abstract

Iodine intake must be boosted during pregnancy to meet the demands for increased production and placental transfer of thyroid hormone essential for optimal foetal development. Failure to meet this challenge results in irreversible brain damage, manifested in severity from neurological cretinism to minor or subtle deficits of intelligence and behavioural disorders. Attention is now being focused on explaining observational studies of an association between insufficient iodine intake during pregnancy and mild degrees of intellectual impairment in the offspring and confirming a cause and effect relationship with impaired maternal thyroid function. The current qualitative categorisation of iodine deficiency into mild, moderate and severe by the measurement of the median urinary iodine concentration (MUIC) in a population of school-age children, as a proxy measure of dietary iodine intake, is inappropriate for defining the degree or severity of gestational iodine deficiency and needs to be replaced. This review examines progress in analytical techniques for the measurement of urinary iodine concentration and the application of this technology to epidemiological studies of iodine deficiency with a focus on gestational iodine deficiency. We recommend that more precise definitions and measurements of gestational iodine deficiency, beyond a spot UIC, need to be developed. We review the evidence for hypothyroxinaemia as the cause of intrauterine foetal brain damage in gestational iodine deficiency and discuss the many unanswered questions, from which we propose that further clinical studies need to be designed to address the pathogenesis of neurodevelopmental impairments in the foetus and infant. Agreement on the testing instruments and standardization of processes and procedures for Intelligence Quotient (IQ) and psychomotor tests needs to be reached by investigators, so that valid comparisons can be made among studies of gestational iodine deficiency and neurocognitive outcomes. Finally, the timing, safety and the efficacy of prophylactic iodine supplementation for pregnant and lactating women needs to be established and confirmation that excess intake of iodine during pregnancy is to be avoided. Full article

(This article belongs to the Special Issue The Assessment and Prevention of Gestational Iodine Deficiency and Its Adverse Fetal Consequences: A Focus on Mild Iodine Deficiency)

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20 pages, 320 KiB

Open AccessConcept Paper

Mild-to-Moderate Gestational Iodine Deficiency Processing Disorder

by Ian Hay, Kristen L. Hynes and John R. Burgess

Nutrients 2019, 11(9), 1974; https://doi.org/10.3390/nu11091974 - 22 Aug 2019

Cited by 16 | Viewed by 4902

Abstract

This synopsis paper aims to identify if a common pattern of learning and social difficulties can be conceptualized across recent longitudinal studies investigating the influence of mild-to-moderate gestational iodine deficiency (GID) on offspring’s optimal cognitive and psycho-social development. The main studies investigated are: The Southampton Women’s Study (SWS)—United Kingdom; the Avon Longitudinal Study of Parents and Children (ALSPAC)—United Kingdom; the Gestational Iodine Cohort Longitudinal Study—Tasmania, Australia, and the Danish National Birth Cohort Case-Control Study—Denmark. In contrast to severe GID where there is a global negative impact on neurodevelopment, mild-to-moderate intrauterine iodine deficiency has subtler, but nonetheless important, permanent cognitive and psycho-social consequences on the offspring. This paper links the results from each study and maintains that mild-to-moderate GID is associated with a disorder that is characterized by speed of neural transmitting difficulties that are typically associated with working memory capacity difficulties and attention and response inhibition. The authors maintain that this disorder is better identified as Gestational Iodine Deficiency Processing Disorder (GIDPD), rather than, what to date has often been identified as ‘suboptimal development’. The Autistic Spectrum Disorder (ASD), Attention Deficit, Hyperactivity Disorder (ADHD), language and literacy disorders (learning disabilities and dyslexia) are the main manifestations associated with GIDPD. GIDPD is identified on IQ measures, but selectively and mainly on verbal reasoning IQ subtests, with individuals with GIDPD still operating within the ‘normal’ full-scale IQ range. Greater consideration needs to be given by public health professionals, policy makers and educators about the important and preventable consequences of GID. Specifically, more emphasis should be placed on adequate iodine intake in women prior to pregnancy, as well as during pregnancy and when lactating. Secondly, researchers and others need to further extend, refine and clarify whether GIDPD, as a nosological (medical classification) entity, is a valid disorder and concept for consideration. Full article

(This article belongs to the Special Issue The Assessment and Prevention of Gestational Iodine Deficiency and Its Adverse Fetal Consequences: A Focus on Mild Iodine Deficiency)

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