The first case of goiter caused by high iodine was reported in 1938 and was first found in the Hokkaido area of Japan, accounting for 6-12% of the population. Later, it was also reported in China’s coastal Bohai Bay, and more than 200 cases have been reported so far. It is most common among fishermen and their families, who consume an average of 50-200 mg of iodine per day. Although goiter is obvious, thyroid function is normal, and when iodine intake is stopped for 1 to 2 weeks, urinary iodine, serum iodine and thyroid iodine uptake rate can return to normal, and in a few patients, goiter is significantly reduced. Epidemiological data show that in the population when urinary iodine is <45 µg/day, goiter is inversely proportional to urinary iodine; when urinary iodine is >1000 µg/day, goiter is positively correlated with urinary iodine in a U-shaped curve. Hyperiodogenic goiter is almost always a diffuse goiter with mild to moderate enlargement and a firm texture. The onset of iodine-induced goiter varies from a few months to several years after iodine ingestion. Laboratory tests reveal increased urinary iodine excretion, often >800 micrograms/liter, low 24-hour iodine uptake, often less than 10%, positive potassium perchlorate excretion test, and normal thyroid function. The cause of iodine-induced goitre is unclear and may be due to late inability to undergo escape; or excess iodine destroys thyroglobulin; or excess iodine persistently inhibits thyroid peroxidase activity. Thyroid autoantibodies can often be measured in the serum, suggesting the presence of an underlying thyroid autoimmune phenomenon. Hyperiodination to goiter tends to occur in patients with a history of thyroid disease or thyroid disorders, such as hyperthyroidism, slow onset thyroiditis, or after surgical treatment of hyperthyroidism with 131 iodine or. The mechanism of hypo-iodothyroidism is similar to that of hyper-iodine goiter, except that it is more severe or combined with other thyroid disorders, such as chronic lymphatic thyroiditis, and the enlarged thyroid gland does not compensate to normal function, so hypofunction occurs. The risk of hypo-iodothyroidism is greatly increased by congenital or acquired iodine organic deficiency of the thyroid gland, and patients with simple goiter caused by iodine organic deficiency are most likely to develop hypo-iodothyroidism. A prospective study of iodine administration to patients with slow onset thyroiditis who had normal thyroid function could produce hypothyroidism with high iodine, and after stopping iodine intake, thyroid function returned to normal. The incidence of hypothyroidism or goiter in combination with chronic thyroiditis has been increasing in the United States in recent years and is thought to be due to increased amounts of iodine in food and medications. Hypo-iodothyroidism is also likely to occur in patients with diffuse goiter previously treated with 131 iodine or surgery, but not all patients will cause hypo-iodothyroidism, which may be due to an underlying iodine organic disorder of its own, exacerbated by radiation therapy. Fetuses and newborns are also susceptible to hyperiodothyroidism. The clinical features of hyperiodogenic hypothyroidism are varied, with goiter being the most common, mostly moderate to severe diffuse enlargement of the thyroid gland, often with a previous history of slow onset thyroiditis, diffuse goiter disease, or thyroid macrosomia. Signs and symptoms of hypothyroidism are lacking, serum T4 and thyrotropin values are normal or lower limit of normal, and thyrotropin-releasing hormone excitation tests show abnormally enhanced thyrotropin. The thyroid iodine uptake rate of 131 can be reduced, normal or elevated and does not contribute to the differential diagnosis. The strongest diagnostic basis is that excessive iodine uptake causes goiter or hypothyroidism, and that thyroid size and function return to normal when iodine uptake is stopped. Most patients are positive for thyroid antibodies, which indicates that these patients have an underlying slow onset of thyroiditis and an underlying thyroid dysfunction that is sensitive to excess iodine. The incidence of hypothyroidism due to high iodine is not known and is higher in women than in men. The time of presentation of hypothyroidism also varies, from months to years. Since iodine supplementation to prevent endemic goiter, iodine-induced hyperthyroidism has been reported, with the first case of iodine-induced hyperthyroidism reported in 1821. Epidemiological data found that the incidence of hyperthyroidism was significantly higher after iodine supplementation in the Netherlands, Yugoslavia, and Tasmsnia (Australia) than before supplementation. The incidence of hyperthyroidism increased after 6 months of long-term iodine supplementation, peaked at 1 to 3 years, and returned to pre-iodine supplementation levels in 6 to 10 years, but no increase in the incidence of hyperthyroidism after iodine supplementation has been reported in areas with endemic goiter. Drug treatment of hyperthyroidism in iodine-deficient areas is easier than in iodine-rich areas and is less likely to recur after discontinuation of the drug. After discontinuation of thyrotropin-releasing hormone patients, iodine supplementation was more likely to cause recurrence of hyperthyroidism than non-iodine supplementation. The recurrence rate of postoperative hyperthyroidism in thyrotropin-releasing hormone patients is five times higher in iodine-rich areas and five times lower in hypothyroidism than in iodine-deficient areas. Iodine-induced hyperthyroidism generally occurs after 6 months of iodine administration, but can also occur after 1 to 2 months of iodine administration, with a peak of 1 to 3 months, and the incidence of hyperthyroidism gradually decreases to normal after 6 to 10 months of iodine supplementation. The mechanism of iodine-induced hyperthyroidism is not known for sure. It may be due to the lack of self-feedback regulation of excess iodine in the thyroid gland, where large doses of iodine in the thyroid gland cannot be fed back to inhibit further iodine uptake, causing the thyroid gland to produce excess thyroid hormone, leading to hyperthyroidism. Alternatively, in areas with endemic goiter, subclinical functionally autonomous high-functioning thyroid adenomas existed before iodine supplementation, and iodine supplementation promoted the development of hyperthyroidism. However, most patients with goiter do not develop iodine-induced hyperthyroidism, so patients with goiter are not contraindicated to oral iodine-containing drugs or iodine contrast agents. The clinical features of iodine hyperthyroidism are similar to those of diffuse goiter, except that the former is associated with an older age. Rarely, there is diffuse goiter ophthalmopathy. It is characterized by a reduced iodine uptake rate of the thyroid gland, with a 24-hour thyroid uptake rate of <3%. Measurement of urinary iodine is not very helpful in diagnosis because of the wide range of normal values of urinary iodine. Iodine-induced hyperthyroidism is relatively self-remitting, and treatment requires cessation of iodine intake. Hyperthyroidism often lasts for several weeks to months and can resolve spontaneously. In mild cases, beta-blockers alone may be used, in severe cases antithyroid drugs are applied, and surgery is usually not required. Due to the low iodine uptake rate of the thyroid gland, radioactive iodine therapy is not recommended. Simultaneous administration of potassium perchlorate and antithyroid drugs can facilitate the excretion of iodine accumulated in the thyroid gland, which is beneficial to the treatment of iodine-induced hyperthyroidism, but there are also reported results from different perspectives. Numerous studies have shown that iodine has a close relationship with thyroid autoimmune disease before. The incidence of thyroid autoimmune disease is higher in iodine-rich areas than in iodine-deficient areas; lymphocyte infiltration is rarely seen in thyroid surgery for endemic goiter, but becomes apparent after sulfur supplementation, along with a significant increase in thyroid antibodies; feeding a low iodine diet to Os chickens genetically susceptible to slow onychomycosis can lead to a decrease in thyroid antibodies in the blood. However, the opposite has also been reported, with some authors finding higher blood thyroid antibodies in iodine-deficient areas than in iodine-rich areas. In addition, lymphocytic infiltration is not uncommon in some patients with endemic goiter. In Finland, increasing food iodine intake in iodine-deficient areas did not increase the incidence of slow onychomycosis and hypothyroidism. Although low iodine reduced thyroid antibodies in the blood of Os chickens, excess iodine had no effect in genetically non-susceptible rats, further demonstrating that the effect of iodine must occur in genetically susceptible individuals. The incidence of slow onychomycosis in the United States has increased each year in recent years, and it is widely believed that this may be due to increased intake of iodine in food additives. The mechanism by which iodine induces thyroiditis is uncertain. Studies have shown that iodine binding to thyroglobulin can increase the immunogenicity of thyroglobulin, and that iodine-rich thyroglobulin has strong immunogenicity; it has also been shown that iodine can stimulate B lymphocytes to produce immunoglobulin; iodine can also stimulate the ability of phagocytes to engulf thyroglobulin. The incidence of thyroid cancer has been reported to be higher in areas with endemic goiter, but iodine-rich diets have also been reported to contribute to the development of thyroid cancer. Thyroid follicles are common in iodine deficient areas, while papillary thyroid carcinoma is more common in iodine rich areas. However, most authors have a negative attitude towards the relationship between iodine and thyroid cancer, and there are relatively few studies in this area. Iodine deficiency has an impact on human health, while too much iodine has the same impact on human health. Insufficient intake of nutrients can make us less resistant to infectious diseases, vitamin deficiency, rickets and other diseases; on the contrary, too much intake of nutrients can cause hypertension, diabetes, cardiovascular and cerebrovascular diseases. We can neither iodine deficiency nor too much iodine.