Mild to moderate iodine deficiency

Abstract

Measurement of iodine excretion in urine is the accepted surrogate marker for dietary iodine intake. Results of these measurements are used to classify and report the spectrum of iodine deficiency in a population as mild, moderate or severe, but the evidence supporting these definitions is imprecise and questionable. The current practice of describing a population as being iodine deficient is based on single spot urine iodine excretion measurements, rather than measuring habitual iodine intake. We examine and question current practices of extrapolating spot urine iodine results, obtained in school-age children, to other segments of a population as being representative of iodine deficiency in the population as a whole. We suggest that the time has come for a review of definitions and a revised classification system for iodine deficiency rather than repeating the historical imprecise descriptors of mild, moderate and severe iodine deficiency. While the crippling, adverse consequences of severe iodine deficiency are indisputable, the frequency and extent of damage - the iodine deficiency disorders (IDD) - caused by the currently accepted definitions of mild to moderate iodine deficiency remains uncertain. Enlargement of the thyroid gland in response to continuing iodine deficiency is a normal physiological adaptation designed to maintain normal secretion of thyroid hormones and prevent deficiency disorders. It only becomes a pathological entity when the body can no longer compensate for inadequate iodine intake and irreversible pathological changes occur. Underpinning our understanding of IDD is the assumption that all of the damage to the central nervous system and other organs occurring in association with iodine deficiency is a consequence of deficient thyroid hormone secretion and action. There is evidence for this assumption in populations suffering from severe iodine deficiency but a paucity of good evidence for any significant effect in mild to moderate iodine deficiency. Of particular interest is the recent findings, in the United Kingdom and Tasmania Australia, of neurocognitive impairment in the offspring of children born to mothers who were documented to have mild iodine deficiency during pregnancy. While we cannot readily explain these findings as no data was collected on maternal and fetal thyroid function, good clinical practice should ensure that iodine intake during pregnancy is optimised while we await the outcome of randomised controlled trials of iodine supplementation during pregnancy.