The Ministry of Health announced the national food safety standard “Iodine Content of Edible Salt (Exposure Draft)” on July 26, 2010, which intends to lower the upper limit value of iodine content of table salt in China, and at the same time, the concentration of iodized salt will no longer be unified across the country. Over the years, China has made three adjustments to the iodine content of salt, and this will be the fourth adjustment. The first adjustment was made in 1996. 1995 national iodine nutritional monitoring found that because there was no upper limit value for the iodine content in salt, the salt iodine content in some areas was too high, some as high as 100 mg/kg. For this reason, it was stipulated in 1996 that the upper limit of iodine content should not exceed 60 mg/kg. The second adjustment was made in 1997, when the results of the 1997 national iodine nutritional monitoring showed that children’s urinary iodine levels were 330 micrograms per liter, suggesting that children’s urinary iodine levels had risen sharply as a result of indiscriminate iodine supplementation (indiscriminate use of iodized health care and iodized oil pills) to key populations. The Ministry of Health promptly requested that most areas where iodized salt coverage had already been greatly increased stop taking iodized oil pills, and at the same time put forward the principle and slogan of “scientific iodine supplementation”. The third adjustment was made in 1999. In that year, the results of the national iodine nutritional monitoring found that children’s urinary iodine level was 306 micrograms per liter, which was on the high side. After discussion and argumentation, our experts proposed for the first time in the world that lowering the level of urinary iodine to less than 300 micrograms/liter was an acceptable level of iodine nutrition, which would provide sufficient iodine to the population and minimize the risk of side effects. In 2000, we downgraded the iodine level in the production chain from not less than 40 mg/kg ex-factory to an average of 35 mg/kg. Iodine in the thyroid gland is not only involved in the synthesis and release of thyroid hormones, but also regulates the synthesis and release of thyroid hormones. It is well known that there is a close association between iodine deficiency or excessive intake and thyroid disease. Here is a superficial understanding of iodine and thyroid disease. The earliest understanding of iodine deficiency started with endemic goiter, commonly known as “big neck disease”, which is still remembered as a figurative description of this condition in a childhood ballad: “Drinking the water from XX (name of the place), the neck becomes thicker and the legs shorter”. Later, in the 1980s, it was discovered that the effects of iodine deficiency on people were more mainly on intelligence and growth. In iodine-deficient areas, the IQ, height and weight of adolescents were lower than those in non-iodine-deficient areas, so the concept of “iodine deficiency disorders” was replaced by the concept of “iodine-induced endemic goiter”. Iodine deficiency disorders include diseases caused by insufficient iodine intake, such as impaired mental development, goiter, impaired growth and development, or congenital deafness or congenital dementia. A mild iodine deficiency can cause an enlarged thyroid gland, but if the iodine deficiency is severe, or if the enlarged thyroid gland fails to compensate for its normal function, hypothyroidism (hypothyroidism) can occur. Congenital untreated hypothyroidism can severely affect fetal growth and development, manifested by severe congenital mental and/or hearing impairments called cretinism. Although iodine deficiency disorders can affect all age groups, the most severe effects are mainly on fetuses, newborns and infants. This is because these are the periods of rapid development. Iodine deficiency disorders affect the fetus by increasing stillbirths, miscarriages and congenital malformations, and iodine supplementation can reduce these complications. Similarly, excessive iodine intake has been strongly associated with thyroid disorders. The first case of iodine-induced goiter was found in 1938 in the Hokkaido area of Japan. It was later reported in the Bohai Bay area of China, and was most common in fishermen and their families. When iodine intake was stopped for 1-2 weeks, the goiter subsided in a few patients. High iodine goiter is almost always diffuse goiter, which is mildly to moderately enlarged and hard. We all know that low iodine can lead to hypothyroidism, but many people will not realize that high iodine can also lead to hypothyroidism, only the degree is more serious, or at the same time combined with other thyroid dysfunction, such as combined with chronic lymphocytic thyroiditis, the function of the enlarged thyroid gland can not be compensated for the normal, so hypothyroidism has occurred. In recent years, the incidence of chronic thyroiditis combined with hypothyroidism or goiter has been increasing in the United States, and some American scholars believe that it is due to the increase in the amount of iodine in food and drugs. However, not all patients cause hyperiodinemia, which may be an underlying disorder of iodine organicization itself. The clinical features of iodine-induced hypothyroidism are varied, with goiter being the most common, and most having moderate to severe diffuse enlargement of the thyroid gland, often with a past history of chronic thyroiditis and diffuse goiter. There is a close relationship between iodine and thyroid autoimmune disease, with iodine-rich areas having a higher incidence of thyroid autoimmune disease than iodine-deficient areas; in the United States in recent years, the incidence of chronic lymphocytic thyroiditis (Hashimoto’s disease) has increased annually, and it is widely believed that this may be due to increased iodine intake in food additives. A certain percentage of patients with Hashimoto’s disease have thyroid cancer foci, and some scholars believe that it is a precancerous lesion of thyroid cancer. The mechanism of iodine-induced thyroiditis is currently uncertain. It has been reported that the incidence of thyroid cancer in endemic goiter areas is higher than that in other areas, and that iodine-rich diets can contribute to the development of thyroid cancer, but many scholars are opposed to the relationship between iodine and thyroid cancer. Most scholars think that iodine is related to the type of thyroid cancer, follicular thyroid cancer is common in iodine-deficient areas, and papillary thyroid cancer is common in iodine-enriched areas, while the epidemiological investigation of thyroid cancer by domestic scholars in recent years also shows that follicular thyroid cancer has been declining in recent years, and papillary thyroid cancer has been obviously rising. With the continuous progress of medical science, the adjustment of the national standard of iodine content in edible salt reflects our government’s active concern for the health of the general public. Similarly, each of us should start from the smallest detail in our daily life. On the one hand, we should rationalize our diet to ensure sufficient iodine intake to prevent iodine deficiency diseases. On the other hand, we should pay attention to the amount of iodine supplementation, that is, the low iodine and low sodium diet recommended by doctors in practice, and should not blindly supplement iodine excessively, in order to prevent various diseases caused by high iodine.