Iodine is an essential micronutrient that is required for thyroid hormone (TH) synthesis. However, adequate maternal thyroid function is critical for fetal growth and neurodevelopment. Pregnancy increases iodine requirements due to enhanced renal clearance, higher maternal TH production, and transplacental transfer, making pregnant women especially vulnerable to iodine deficiency. In this review, we examine the molecular mechanisms of TH synthesis and regulation, placental transport and metabolism, and the physiological adaptations of thyroid function during gestation. We also analyze the clinical and public health consequences of iodine imbalances, ranging from deficiency to excess. Evidence indicates that mild iodine deficiency—which is common even in developed countries—can lead to maternal thyroid overstimulation, increased thyroglobulin levels, altered T3/T4 ratios, and enlarged thyroid volume, while severe deficiency results in maternal and fetal hypothyroidism with irreversible neurocognitive impairment in the offspring. Conversely, excessive iodine intake may impair fetal thyroid function through mechanisms such as the Wolff–Chaikoff effect. In conclusion, ensuring balanced iodine intake through iodized salt, supplementation, and routine thyroid monitoring during pregnancy is essential to protect maternal health and optimize early neurodevelopment.

In 1895, iodine was characterized as an essential element of thyroid tissue by Baumann. The efficacy of iodine to prevent goiter was demonstrated by Marine in Northern USA in 1916-1920. Severe endemic goiter and cretinism had been almost entirely eliminated from continental Western Europe and Northern America before the 1930's; however large populations elsewhere and even some places in Western Europe (Sicily) were still affected up to the 2000's. Public health consequences of iodine deficiency are not limited to endemic goiter and cretinism. Iodine deficiency disorders include also increased neonatal death rate and decreased intellectual development, although these consequences are not included in the current estimation of the Global Burden Disease related to iodine deficiency. Severe iodine deficiency as a public health problem is now largely under control worldwide, but can still affect isolated places, in hard-to-reach and/or politically neglected populations. We emphasize the importance of maintaining international cooperation efforts, in order to monitor iodine status where iodine deficiency is now adequately controlled, and identify at-risk population where it is not. The goal should be now global eradication of severe iodine deficiency. Commercial distribution of iodized salt remains the most appropriate strategy. A randomized clinical trial in New Guinea clearly showed in the 1970's that correcting severe iodine deficiency early in pregnancy prevents endemic neurological cretinism. This supports the essential role of thyroid hormones of maternal origin on the normal fetal development, during the first trimester of pregnancy (i.e. when fetal thyroid is still not functional). A randomized clinical trial in Congo (RD) in the 1970's also showed that correcting severe iodine deficiency during pregnancy prevents myxœdematous cretinism, particularly prevalent in affected Congolese areas.

The aim of the present study was to calculate the distribution of total iodine intake among Flemish preschoolers and to identify the major sources contributing to iodine intake. A simulation model using a combination of deterministic and probabilistic techniques was utilised. Scenario analyses were performed to assess iodine intake via dairy products, industrially added iodised salt in bread and discretionarily added iodised household salt. Relevant data from 3-d estimated dietary records of 696 preschoolers 2·5–6·5 years old were used. Usual iodine intakes were calculated using the Iowa State University method. With a more generalised utilisation of iodised salt in bread (44 % of the bakers in 2011 instead of 12 % in 2002), mean iodine intake increased from 159 to 164 μg/d using the McCance and Widdowson's food composition table and from 104 to 109 μg/d using the German food composition table. The percentage of preschoolers with an iodine intake below the estimated average requirement (65 μg/d) decreased from 5–12 to 4–9 %, while the percentage of preschoolers with an iodine intake above the tolerable upper intake level (300 μg/d) remained constant (0·3–4 %). Mean iodine intake via food supplements was 4·2 μg/d (total population) and 16·9 μg/d (consumers only). Both in 2002 and 2011, sugared dairy products, milk and iodised salt (21·4, 13·1, and 8·7 %, respectively in 2011) were the main contributors to total iodine intake. In conclusion, dietary iodine intake could still be improved in Flemish preschoolers. The use of adequately iodised household salt and the more generalised use of iodised salt by bakers should be further encouraged.

Iodine is a crucial component of thyroid hormones (THs), specifically triiodothyronine (T3) and thyroxine (T4) and is vital for normal thyroid function. During pregnancy, a deficiency in iodine can result in inadequate production of THs, leading to hypothyroidism. This con-dition can negatively impact the intellectual development of the newborn. Numerous stud-ies have demonstrated that iodine deficiency during pregnancy correlates with lower IQ levels in children. This deficiency can hinder critical processes such as neurogenesis, neu-ronal migration, and myelination, all of which are essential for proper cognitive develop-ment. Research indicates that children born to iodine-deficient mothers are at a higher risk of having lower IQs compared to those whose mothers received iodine supplements during pregnancy. Therefore, ensuring sufficient iodine levels and optimal TH function during pregnancy is crucial for the cognitive development of children. This highlights the im-portance of nutrition and regular monitoring of thyroid health in pregnant women. This re-view focuses on the key mechanisms of thyroid hormone homeostasis and discusses the implications of iodine deficiency during pregnancy.

Background: Thyroglobulin (Tg) is a biomarker of iodine status. Newborn Tg is a more sensitive marker than neonatal TSH in detecting variations in iodine intake. This study aims to validate an enzyme-linked immunosorbent assay (ELISA) for Tg determination on dried blood spots (DBS) in newborns. This study also sets out to assess the stability of Tg and the influence of newborns’ hematocrit on Tg determination. Methods: A commercially available ELISA Tg assay was adapted for use on DBS. DBS-Tg in cord blood was measured in 209 newborns delivered from healthy euthyroid pregnant women. Sensitivity, linearity, repeatability, and intermediate fidelity were determined using the appropriate standards and quality control materials. Results: The limit of detection of the DBS-Tg assay was 2.4 µg/L, and the limit of quantification was 5.8 µg/L. Repeatability and intermediate fidelity were 7.7–8.3% and 11.0–11.2%, respectively. The median cord plasma Tg and DBS-Tg values in newborns were not significantly different, 30.2 (21.3–44.4) µg/L and 31.6 (19.3–48.7) µg/L (P = 0.48) with the ELISA, respectively, and 76.5 (40.0–101.5) µg/L with the Elecsys assay with an R = 0.88. DBS-Tg concentrations decrease with increasing hematocrit values (P < 0.05). DBS-Tg values were stable at a concentration of 25 µg/L for 12 months at −20ºC and 4ºC. Conclusion: This DBS-Tg assay demonstrated good analytical performance over a wide range of Tg concentrations, suggesting it is well suited to detecting variations in Tg concentrations. Studies comparing populations with different prevalence of anemia should consider the effect of hematocrit on DBS-Tg determination. The availability of a DBS-Tg assay for newborns makes it possible to integrate iodine status monitoring with newborn screening for inherited metabolic diseases.