AbstractThe primary role of iodine deficiency in goitrogenesis and the prevention and treatment of endemic goiter by iodine supplementation is firmly established. Unfortunately, implementation of iodine prophylaxis programs has met with considerable technical and socioeconomic difficulties. Besides, lack of knowledge concerning some of the other causative factors of endemic goiter has prevented development of appropriate measures for its complete eradication in those areas where goiter persists in spite of prolonged and adequate iodine supplementation. At present, no less than 5% of the world's population have goiters and associated disorders, resulting in a public health and socioeconomic problem of major proportions. Seventy‐five percent of people with goiter live in less developed countries where iodine deficiency is prevalent. Goiter prevalence rates of more than 50% and the highest frequency of severe cases of iodine deficiency disorders, namely, cretinism, congenital hypothyroidism, and various degrees of impairment of growth and mental development are found in endemic areas with extreme iodine deficiency. Goiters are usually multinodular and of very large size, producing, on occasion, signs of compression that require surgery. Recurrence rates are as high as 25–30% and second surgery accounts for 16% of all thyroidectomies. Unfortunately, most of these goiters occur in areas with highly restricted medical and surgical facilities. Twenty‐five percent of people with goiters live in more developed countries where goiter continues to occur in certain areas despite iodine prophylaxis. Iodine‐sufficient goiters are associated with autoimmune thyroiditis, hypothyroidism, hyperthyroidism, and thyroid carcinoma. Goiter is of considerable surgical significance in iodine‐sufficient endemic areas and, to a lesser degree, in nonendemic areas where it is called “sporadic” goiter. Recurrence rates of iodine‐sufficient goiter are 10–19% following thyroidectomy. Since most of these goiters grow by mechanisms other than increased thyrotropin (TSH) stimulation, treatment with suppressive doses of L‐thyroxine is inefficient and, because of possible complications, not recommended. Although Graves' hyperthyroidism is not directly related to endemic goiter, it does relate adversely with ingestion or administration of iodine. At present, Graves' disease is treated with131I or antithyroid drugs in more than 90% of the cases. The incidence rates of papillary, follicular, and anaplastic thyroid carcinomas appear to be related to endemic goiter and iodine supplementation, with surgery being required in essentially all of these cases.