This article reviews recent studies dealing with thyroid physiology and pathophysiology in the pregnant woman, with special emphasis on the important role of relative iodine deficiency, which is still characteristic today of many areas in Europe. Iodine restriction limits the capacity of the thyroid gland to meet the metabolic challenge presented by pregnancy, yielding important repercussions for both the maternal and fetal-thyroid functions. Although iodine sufficiency (and perhaps even excess) in the United States (US) probably explains the failure of US reports to confirm significant changes in the size of the thyroid gland occurring during pregnancy, the iodine restriction frequently observed in Europe constitutes the basis for explaining gestational goitrogenesis, as well as glandular hyperplasia at birth in neonates born to mothers who have not benefitted from iodine supplementation during pregnancy. In Europe with only a moderate iodine restriction, the condition leads to goiter formation, but it rarely leads to hypothyroidism in otherwise healthy patients. In other parts of the world with more severe iodine deficiency, both maternal and neonatal hypothyroidism are frequently present, endemic cretinism represents the most dramatic expression of these abnormalities.