Fully two billion women and children worldwide are thought to be Fe deficient [89].
The American Congress of Obstetricians and Gynecologists (ACOG) currently rec- ommends prenatal Fe supplementation and universal anemia screening [90]. Recent systematic review of current Fe supplementation practices noted that while Fe sup- plementation did have a positive impact on maternal Fe status, there is inconclusive evidence at present to link this practice to improvements in maternal or infant clini- cal outcomes [66, 91]. Clearly more data are needed to evaluate the relative impact of Fe supplementation practices across gestation and to determine which obstetric and Fe status groups are most likely to benefit from this supplementation. Maternal Fe absorption across gestation is regulated in response to maternal Fe stores and to systemic hepcidin concentrations. There may be threshold effects of Fe
supplementation in that the magnitude of the response to supplementation is likely to be dependent on baseline maternal Fe status. In spite of the availability of multi- ple Fe status biomarkers, very little variability in Fe absorption can currently be captured using the multiple Fe status biomarkers and the systemic Fe regulatory hormones that have been identified to date. More information is needed to under- stand the genetic determinants of maternal and neonatal Fe status so that targeted approaches to supplementation can eventually be developed. In addition, basic research is needed to evaluate the impact of maternal Fe supplementation on in utero fetal development to identify if there are key gestational windows at which time Fe availability may be most integral to fetal development and to characterize mechanisms by which Fe status impacts maternal birth outcomes.
Current data on maternal Fe status in relation to birth outcomes may be challeng- ing to summarize, given the variability in the baseline Fe status of the populations studied, the variable timing of the pregnancy measures obtained, and the need to adjust for inflammation if relying on Fe status indicators that also function as acute phase proteins. In addition, optimal requirements necessary to support maternal and fetal health may not correspond to the amount of Fe required to prevent maternal anemia. As the field moves forward, answers to these questions will inform subse- quent recommendations designed to promote Fe status and maternal and fetal health during this key life stage.
Acknowledgment This work was supported by a USDA National Research Initiative Grant (2008–0857) and by The Gerber Foundation.
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© Springer International Publishing AG, part of Springer Nature 2018 C. J. Lammi-Keefe et al. (eds.), Handbook of Nutrition and Pregnancy, Nutrition and Health, https://doi.org/10.1007/978-3-319-90988-2_3
Sun Y. Lee and Elizabeth N. Pearce
Keywords Iodine · Pregnancy · Iodine in pregnancy · Iodine in foods
Iodine deficiency in pregnancy · Iodine excess in pregnancy · Iodine supplement
Key Points
• Iodine is an essential micronutrient for thyroid hormone production.
• Pregnant women have increased iodine requirements due to increased maternal thyroid hormone production, increased maternal urinary losses, and fetal thyroid hormone production later in pregnancy.
• Adequate thyroid hormone is critically important for normal fetal development.
• Maternal iodine deficiency can lead to adverse pregnancy and offspring neurode- velopmental outcomes.
• Both iodine deficiency and iodine excess may lead to maternal thyroid dysfunction.
• Use of iodized salt is the mainstay of worldwide efforts to eradicate iodine defi- ciency, but mild-to-moderate iodine deficiency persists in many countries.
• Although the general population in the USA is considered iodine sufficient, pregnant women are mildly iodine deficient.
• Professional societies recommend that women in many regions should take sup- plements containing 150 mcg of iodine daily during preconception, pregnancy, and lactation.
S. Y. Lee · E. N. Pearce (*)
Section of Endocrinology, Diabetes, and Nutrition, Boston University School of Medicine, Boston, MA, USA
e-mail: [email protected]; [email protected]
Introduction
Iodine is an essential micronutrient which is required for thyroid hormone produc- tion. Thyroid hormone, which depends on iodine for function, in turn, is critically important for regulation of energy expenditure in adults and children and also for growth and development of the fetus. Iodine is found ubiquitously in soil and groundwater, and the ocean is especially rich in iodine that has been leached from soil through glaciation, snow, and rain. Iodine content in soil and water varies geo- graphically, and thus, crops and livestock grown in different areas may have sub- stantially different iodine content [1, 2]. Once consumed through food or supplements, iodine is readily absorbed through the stomach and duodenum. Iodine, in the form of iodide, is then either transported to the thyroid gland in varying amounts (10–80%) depending on an individual’s iodine nutritional status or is excreted through the kidney. When taken up by the thyroid gland, iodide is used to make thyroid hormones. Renal clearance accounts for more than 90% of iodine excretion, making urinary iodine concentration (UIC) a good marker for recent iodine intake [2–4].
The public health ramifications of chronic iodine deficiency (ID) have long been recognized [5]. Cretinism, found only in the most iodine deficient regions, is char- acterized by mental deficiency, goiter (thyroid gland enlargement), and abnormali- ties in motor and neurodevelopment. In the twentieth century, the efficacy of iodine supplementation in preventing cretinism was shown in several landmark trials in Papua New Guinea, Zaire, and China [6]. In the early twentieth century, the high (26–70%) prevalence of goiter due to chronic ID in children from the Great Lakes, Appalachia, and Northwestern regions of the USA led to this region of the USA being referred to as the “goiter belt.” [7] In the 1980s, the term “iodine deficiency disorders” (IDD) was introduced, with worldwide recognition of the broad effects of ID such as decreased intelligence quotient (IQ) and adverse obstetric outcomes, in addition to goiter. By the early 1990s, it was estimated that more than 1.5 billion people worldwide were living in iodine-deficient areas, and the World Summit for Children at the United Nations established the global elimination of IDD as a goal [8]. A subsequent worldwide campaign for universal salt iodization (USI) has achieved a significant decrease in the prevalence of IDD. However, a global survey by the Iodine Global Network (IGN), formerly known as the International Council for the Control of Iodine Deficiency Disorders (ICCIDD), in 2013 showed that pregnant women were deemed to be iodine- sufficient in only 8 of the 21 countries studied [1].
This chapter will review measurement of thyroid function, iodine physiology in pregnancy, methods to assess population iodine status in pregnancy, the effects of iodine deficiency in pregnancy, data regarding iodine supplementation in pregnancy, the effects of iodine excess in pregnancy, current recommendations for iodine sup- plementation in pregnancy, the current iodine nutrition status of pregnant women, and dietary sources of iodine.