The main change in thyroid function associated with the pregnant state is the requirement of an increased production of thyroid hormone that depends directly upon the adequate availability of dietary iodine and integrity of the glandular machinery. Physiologic adaptation takes place when the iodine intake is adequate, while this is replaced by pathologic alterations when there is a deficient iodine intake. Pregnancy acts typically, therefore, as a revelator of underlying iodine restriction. Iodine deficiency (ID) has important repercussions for both the mother and the fetus, leading to sustained glandular stimulation, hypothyroxinemia and goitrogenesis. Furthermore, because severe ID may be associated with an impairment in the psycho-neuro-intellectual outcome in the progeny—because both mother and offspring are exposed to ID during gestation (and the postnatal period), and because ID is still prevalent today in several European countries—it has been proposed already in the early 1990s that iodine supplements be given systematically to pregnant and breast-feeding women. Particular attention is required to ensure that pregnant women receive an adequate iodine supply, by administering multivitamin tablets containing iodine supplements, in order to achieve the ideal recommended dietary allowance of 200–250 μg iodine/day.