Cretinism is a severe disorder caused by congenital hypothyroidism, a condition in which the thyroid gland fails to produce sufficient amounts of thyroid hormones from birth. Thyroid hormones, mainly thyroxine (T4) and triiodothyronine (T3), are essential for normal growth, brain development, metabolism, and maturation of body tissues. If this deficiency is not detected and treated during early infancy, it results in permanent physical and mental disabilities. The term "cretinism" is now largely replaced in medical practice by the term congenital hypothyroidism because it is more accurate and less stigmatizing. However, the term cretinism is still used in educational and historical contexts to describe the severe manifestations of untreated congenital hypothyroidism. From the perspective of community nutrition, cretinism is an important public health problem because one of its major causes is iodine deficiency. Iodine is an essential micronutrient required for the synthesis of thyroid hormones. In regions where the soil and water are deficient in iodine, people consume inadequate amounts of this nutrient, leading to iodine deficiency disorders (IDD). Cretinism represents the most severe form of iodine deficiency disorder. It is entirely preventable through adequate iodine intake and effective public health interventions. There are two major forms of cretinism. The first is neurological cretinism, which is characterized by severe intellectual disability, deaf-mutism, squint, spasticity, and motor abnormalities. This type mainly results from iodine deficiency during early pregnancy when fetal brain development depends on maternal thyroid hormones. The second is myxedematous cretinism, which is characterized by severe hypothyroidism, short stature, delayed skeletal development, dry skin, puffy face, and mental retardation. Individuals with this form may also have enlarged thyroid glands or goiter due to prolonged iodine deficiency. The causes of cretinism include congenital absence of the thyroid gland (athyreosis), underdeveloped thyroid gland (hypoplasia), abnormal development or location of the thyroid gland (ectopic thyroid), inherited defects in thyroid hormone synthesis, maternal iodine deficiency during pregnancy, maternal use of antithyroid drugs, radioactive iodine exposure, congenital defects in hormone metabolism, and severe iodine deficiency in the community. Among these causes, iodine deficiency remains the most significant nutritional factor, especially in developing countries. Iodine deficiency develops when dietary intake of iodine is consistently below the body's requirement. Since the human body cannot synthesize iodine, it must be obtained from food and water. The recommended dietary allowance varies according to age and physiological status. Pregnant and lactating women require higher amounts because iodine is needed for fetal growth and breast milk production. Inadequate maternal iodine intake during pregnancy results in reduced thyroid hormone production, impairing fetal brain development and increasing the risk of miscarriage, stillbirth, congenital anomalies, and cretinism. The thyroid gland plays an important role in regulating metabolism, protein synthesis, growth, and neurological development. Thyroid hormones influence cell differentiation, myelination of nerve fibers, maturation of the central nervous system, bone growth, muscle function, cardiovascular activity, and energy metabolism. During fetal life and the first two years after birth, adequate thyroid hormone levels are especially critical because this period represents rapid brain development. Deficiency during this sensitive period causes irreversible neurological damage. Risk factors for cretinism include living in iodine-deficient regions, lack of iodized salt consumption, poor socioeconomic conditions, inadequate antenatal care, maternal malnutrition, repeated pregnancies without nutritional supplementation, family history of thyroid disorders, premature birth, low birth weight, maternal autoimmune thyroid disease, and lack of newborn screening programs. Remote mountainous regions and flood-prone areas are particularly vulnerable because iodine is often washed away from the soil, resulting in iodine-deficient crops. The clinical features of cretinism vary depending on the severity of thyroid hormone deficiency and the age at diagnosis. Newborns may appear normal at birth because maternal thyroid hormones partially protect the fetus during pregnancy. As maternal hormone levels decline after birth, symptoms gradually become apparent. Early signs include prolonged neonatal jaundice, excessive sleepiness, poor feeding, constipation, hoarse cry, large tongue (macroglossia), umbilical hernia, puffy face, dry skin, low body temperature, slow heart rate, and poor muscle tone. As the child grows, untreated congenital hypothyroidism produces more obvious manifestations. Growth becomes markedly delayed, resulting in dwarfism or short stature. Bone age remains delayed, and skeletal maturation is impaired. Intellectual disability becomes progressively severe. Speech development is delayed, and many children have learning disabilities. Motor milestones such as sitting, standing, and walking occur much later than expected. Muscle weakness, sluggish movements, and poor coordination are common. Hearing impairment and deaf-mutism may develop in neurological cretinism. Dental eruption is delayed, and facial features become coarse with thick lips, broad