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.
Highlights
The trace element iodine is an essential dietary micronutrient for the synthesis of thyroid hormones
Pino et al recommended using the less hazardous ammonium persulphate as the oxidising agent with subsequent good correlation shown between the two methods [16]. This modified method has been recommended by the World Health Organization (WHO) the United Nations Childrens Fund (UNICEF) and the International Council for Control of Iodine Deficiency Disorders (ICCIDD) for epidemiological assessment of a population and it is the most popular method of choice today [17]
The assumption underlying the recommendations for increasing iodine intake during pregnancy is that the estimated 50% increase in maternal thyroid hormone production requires a commensurate increase in iodine intake from the daily pre-pregnant recommended dietary intake (RDI) of 150 μg to 225 μg, rounded out to 250 μg, by many expert guidelines [57,58]
Summary
The trace element iodine is an essential dietary micronutrient for the synthesis of thyroid hormones. Deficiency Disorders (IDDs), comprising multiple physical, neurological and intellectual deficits with the clinical expression dependent upon the severity, duration and timing of the dietary iodine deficiency at specific life-stages, especially occurring during foetal and infant development [1,2]. While this is true for severe, nutritional iodine deficiency, the effects of mild to moderate iodine deficiency during pregnancy on neurodevelopmental outcomes of the offspring continue to be debated and have recently become a focus of increased interest and research [3]. With the widespread acceptance and implementation of prophylactic universal salt iodisation, severe iodine deficiency has been eradicated from most of the developing world, causing a paradigm shift in the epidemiology of IDDs from endemic goitre and cretinism, so well-studied in regions of severe iodine deficiency, to focus on the effects of less severe iodine deficiency, in the developed world [5]
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