Thyroid autoimmunity impacts up to one in five pregnant women and impairs fertility and pregnancy success. Women with thyroid autoimmunity that do fall pregnant, remain at an increased risk of gestational diabetes mellitus, preterm birth, preeclampsia and fetal growth restriction (FGR) even when all other thyroid parameters are within a healthy reference. While these pregnancy disorders are known to be linked with placental dysfunction, why they occur in women with thyroid autoimmunity is unknown. We have undertaken several approaches to investigate how thyroid autoimmunity leads to adverse pregnancy outcomes and investigated potential treatment options. We have begun to characterise how thyroid antibodies bind to trophoblast cells and impact cellular function in vitro and are looking at how these antibodies impact rat and human vessel function. We have established rat models of thyroid autoimmunity to investigate physiological processes. Rats that are thyroid antibody positive have alterations in estrous cycling prior to pregnancy and we are continuing to investigate how this might occur. Pregnant rats with thyroid antibodies develop changes to glucose metabolism, fetal growth and litter size. In our current rat project, we are focused on examining how these antibodies impact preeclampsia like outcomes. Having gained some understanding of how thyroid antibodies mediate adverse pregnancy outcomes, we are also investigating potential treatments. More than 32 randomised control trials have tested the effectiveness of selenium at reducing thyroid antibody levels and overall, these studies have been successful. Yet clinical recommendation for use in pregnancy requires preclinical animal studies. As such, we are currently assessing the relationship between thyroid autoimmunity and selenobiology. We are also treating our thyroid antibody positive rats with selenium to see if it prevents adverse pregnancy outcomes.