Hormonal changes and metabolic demands during pregnancy result in profound alterations in the biochemical parameters of thyroid function. For thyroid economy, the main events occurring during pregnancy are a marked increase in serum thyroxine-binding globulin levels; a marginal decrease in free hormone concentrations (in iodine-sufficient areas) that is significantly amplified when there is iodine restriction or overt iodine deficiency; a frequent trend toward a slight rise in basal thyrotropin (TSH) values between the first trimester and term; a transient stimulation of the maternal thyroid gland by elevated levels of human chorionic gonadotropin (hCG) resulting in a rise in free thyroid hormones and decrement in serum TSH concentrations during the first trimester; and finally, modifications of the peripheral metabolism of maternal thyroid hormones. Together, metabolic changes associated with the progression of gestation in its first half constitute a transient phase from preconception steady state to pregnancy steady state. In order to be met, these metabolic changes require an increased hormonal output by the maternal thyroid gland. Once the new equilibrium is reached, increased hormonal demands are maintained until term, probably through transplacental passage of maternal thyroid hormones and increased turnover of maternal thyroxine (T4), presumably under the influence of the placental (type 3) deiodinase. For healthy pregnant women with iodine sufficiency, the challenge of the maternal thyroid gland is to adjust the hormonal output in order to achieve the new equilibrium state, and thereafter maintain the equilibrium until term. In contrast, the metabolic adjustment cannot easily be reached during pregnancy when the functional capacity of the thyroid gland is impaired because of iodine deficiency. The ideal dietary allowance of iodine recommended by World Health Organization (WHO) is 200 microg of iodine per day for pregnant women. In conditions with iodine restriction, enhanced thyroidal stimulation is revealed by relative hypothyroxinernia and goitrogenesis. Goiters formed during gestation may only partially regress after parturition. Pregnancy, therefore, represents one of the environmental factors that may help explain the higher prevalence of goiter and thyroid disorders in women compared with men. An iodine-deficient status in the mother also leads to goiter formation in the progeny and neuropsycho-intellectual impairment in the offspring. When adequate iodine supplementation is given early during pregnancy, it allows for the correction and almost complete prevention of maternal and neonatal goitrogenesis. In summary, pregnancy is accompanied by profound alterations in the thyroid economy, resulting from a complex combination of factors specific to the pregnant state, which together concur to stimulate the maternal thyroid machinery. Increased thyroidal stimulation induces, in turn, a sequence of events leading from physiological adaptation of the thyroidal economy observed in healthy iodine-sufficient pregnant women to pathological alterations affecting both thyroid function and the anatomical integrity of the thyroid gland, when gestation takes place in conditions with iodine restriction or deficiency: the more severe the iodine deficiency, the more obvious, frequent, and profound the potential maternal and fetal repercussions.