Investigating the relationship between maternal iodine intake in pregnancy and iodine status or thyroid function of mothers and infants: a prospective cohort study.

Abstract

Iodine is crucial for thyroid hormone production which is essential for growth and development. Iodine deficiency in pregnancy can lead to cognitive impairment, poor growth, congenital abnormalities and in severe situations cretinism. Mild iodine deficiency re-emerged in Australia in the last decade. To address this issue, in 2009 mandatory iodine fortification of bread was implemented and in 2010 routine iodine supplementation in pregnancy was recommended. Since mandatory iodine fortification there has been limited data on the iodine intake and iodine status of Australians, including pregnant women. Intervention trials in iodine deficient populations have shown a higher maternal and infant urine iodine concentration (UIC) in iodine supplemented groups compared to controls, with the effect on thyroid function being less clear. However, no studies have assessed the relationships between maternal iodine intake from food and supplements in pregnancy and maternal or infant iodine status and thyroid function in mildly iodine deficient or sufficient populations. The primary aims of the thesis were to examine the associations between maternal iodine intake/iodine status/thyroid function in pregnancy and markers of maternal and infant iodine status/thyroid function. The secondary aims were to examine the associations between maternal iodine intake/thyroid function in pregnancy and pregnancy/birth outcomes, infant growth and the general health of pregnant and postnatal women. 783 pregnant women in South Australia participated in the study. An iodine specific food frequency questionnaire (I-FFQ) was developed and validated to assess dietary iodine intake at baseline (<20 weeks’ gestation) and 28 weeks’ gestation. Maternal UIC, maternal thyroid function and the general health and wellbeing of pregnant and postpartum women was assessed at baseline, 28 weeks’ gestation and 3 months postpartum. Breast milk iodine concentration (BMIC) was assessed at birth and 3 months postpartum. Thyroid stimulating hormone (TSH) was collected from newborn screening at birth. Pregnancy/birth outcome data and infant anthropometrics at birth were collected from the women’s and infant’s medical records and infant UIC, infant thyroid function and infant growth was measured at 3 months of age. Based on the median UIC, pregnant women in this study were classified as iodine sufficient, both with or without the use of iodine supplements during pregnancy. Maternal iodine intake in pregnancy was positively associated with maternal UIC and BMIC (Chapter 4), while no association was found with maternal thyroid function (Chapter 4), infant UIC, infant thyroid function (Chapter 5) or clinical outcomes (Chapter 6). At 28 weeks’ gestation maternal free triiodothyronine (fT3) was positively associated with infant fT3 at 3 months of age, while maternal fT3 and thyroglobulin (Tg) was inversely associated with infant TSH at 3 months of age (Chapter 5). Furthermore, markers of maternal thyroid function at 28 weeks gestation was associated with the mental and physical health of women at 3 months postpartum as well as the severity of stress at 28 weeks gestation (Chapter 6). In summary, maternal iodine intake in pregnancy is not associated with maternal or infant thyroid function in an iodine sufficient population, although maternal thyroid function at 28 weeks’ gestation is associated with infant thyroid function at 3 months of age and with aspects of the general health and wellbeing of pregnant and postnatal women. Further research is needed to better understand these relationships in populations with various iodine status and their impact on infant development.