Congenital hypothyroidism (CH) is also known as endemic cretinism, goiter cretinism, and sporadic cretinism. Iodine deficiency is the main cause of endemic cretinism. Congenital hypothyroidism is currently defined as any low thyroid function present at birth. Untreated CH causes growth retardation, impaired intelligence and metabolic abnormalities during childhood and adolescence. Normal brain and mental development during fetal development and at 2 to 3 years of age depends on thyroid hormones, and any delay in treatment will reduce final IQ. One study reported that 80% of children treated before 3 months of life had a final IQ greater than 90, while only 45% were treated after 3 months of life. Clearly, early diagnosis and treatment are needed. Since the 1960s and 1970s, advances in sensitive TSH and thyroid hormone immunoassay methods have made it possible to study the physiology of fetal and prenatal thyroid function in animals and humans, and to find that TSH does not cross the placenta, that there is limited transport of thyroid hormones from the mother to the fetus, and that the fetal pituitary-thyroid system functions independently of the mother. The fetal pituitary-thyroid system functions independently of the mother. Studies of neonatal thyroid function have demonstrated that the rapid cooling of the external environment after birth stimulates early TSH elevation resulting in increased physiological thyroid activity. Therefore, the best time to test newborns is 3 to 5 days after birth, when the physiological TSH peak has been suppressed. By analyzing the literature, researchers evaluated 675 treated CH infants and 570 control infants, resulting in a mean reduction in IQ of 6.3. Several recent studies of infants and children treated to minimize the impact on IQ have found that the most important prognostic factor is thyrotropin. factors were the dose of thyroxine and the timing of initiation of treatment.