Iodine nutrition in early life and childhood neurodevelopment and growth

Abstract

Iodine is a micronutrient required for optimal development and growth. Mandatory iodine fortification of bread was implemented in Australia in October 2009 following the re-emergence of iodine deficiency. However, there are limited data on the iodine status of South Australians and populations at risk, particularly pregnant women. There is a concern about the inconsistent classification of iodine status in the general population and pregnant women by different markers. Evidence on the association between iodine nutrition in early life, and neurodevelopment and growth in populations with mild iodine deficiency to iodine sufficiency, is inconsistent. Newborn thyroid stimulating hormone (TSH) concentration has been suggested as a marker of iodine nutrition in early life. This thesis aims to assess: 1) the agreement between markers of iodine status, 2) iodine status (including pregnant women) in South Australia, before and after the mandatory iodine fortification using the newborn TSH concentration and urinary iodine concentration (UIC), and 3) associations between newborn TSH concentration and childhood neurodevelopment and growth. A systematic review was conducted to assess agreement between markers of population-level iodine status (median UIC, newborn TSH concentration and goitre prevalence), while urinary iodine data, including an estimated 24-h urinary iodine excretion (UIE), UIC, iodine-to-creatinine ratio (I/Cr), and UIC-corrected for creatinine, were used to assess agreement between markers of individual-level iodine status in pregnant women. The results of the systematic review showed that at a population level, newborn TSH concentration >5 mIU/L greater than 3% had a better agreement with goitre prevalence than median UIC to define iodine deficiency in populations. At an individual level, I/Cr from spot urine samples had a better agreement with the estimated 24-h UIE compared with UIC or UIC~Cr markers in pregnant women. Based on the newborn TSH concentration, South Australia was classified as mildly iodine deficient in both pre- and post-fortification periods in contrast to iodine sufficiency defined by median UIC post-fortification. Iodine status of pregnant women was classified as iodine deficiency pre-fortification and iodine sufficiency post-fortification by the UIC marker. Utilising developmental outcome data from two studies, a null association was observed between newborn TSH and childhood neurodevelopment or growth at 18 months. However, poorer neurodevelopment or growth in infants with high TSH in a borderline iodine deficient setting and better neurodevelopment in infants with high TSH in iodine sufficient setting cannot be excluded. In conclusion, monitoring of iodine status using multiple markers is required to identify populations or population groups at increased risk of iodine deficiency disorders. Re-evaluation of current TSH criteria for classifying iodine status in populations is suggested. As neurodevelopmental assessments at 18 months of age may not be stable, data-linkage studies that utilise newborn TSH data and examine neurodevelopmental outcomes at later ages are warranted in populations where newborn screening is routinely performed.