The most common type of hyperthyroidism is toxic diffuse goiter (Graves’ disease), which accounts for about 88% of all hyperthyroid patients. This is followed by toxic multinodular goiter and toxic thyroid adenocarcinoma. There are other types of hyperthyroidism, iodinated hyperthyroidism and pharmacological hyperthyroidism, which are less common. Because the pathogenesis of many types of hyperthyroidism has not been fully elucidated, prevention of its development is difficult. The development of toxic diffuse goiter is closely related to autoimmunity, and the autoimmune response is associated with genetic and environmental factors. In hyperthyroidism, the cause of the autoimmune reaction is uncertain, but there are two considerations: ① An autoimmune reaction occurs because the antigenicity of the thyroid cells is altered and the immune system treats it as a foreign substance. The thyroid cells may change due to radiation, injury, viral infection, etc. ② Due to changes in immunologically active cells and the immune stabilization function of the body, it is thought that the immunologically active cells may mutate and lymphocytes that target their own thyroid gland may appear. Due to a genetic defect in immune surveillance function, these mutated cells cannot be eliminated immediately, allowing them to survive and causing autoimmunity. Clinical observation shows that mental stimulation and infection are related to the development of hyperthyroidism. Long-term trauma or strong mental stimulation, such as worry, panic and stress, can often promote the development of the disease. It has been reported that 62% of hyperthyroidism patients have mental irritation factors. The relationship between these triggers and autoimmunity is still unclear. Some experimental studies have tentatively indicated that mental stimulation can cause changes in immune function. In conclusion, the occurrence and development of autoimmunity is still unclear, and the background and mode of genetic inheritance have also been elucidated, so it is difficult to find ways to prevent hyperthyroidism from autoimmunity and genetic aspects. Therefore, it is difficult to find ways to prevent hyperthyroidism from autoimmune and genetic aspects. Therefore, we can only look for prevention methods from environmental factors, which mainly include various triggering factors for the development of hyperthyroidism. The common triggering factors of hyperthyroidism are ① Infection, various bacterial and viral infections, such as cold, tonsillitis, pneumonia, etc. (2) Mental stimulation, such as stress, trauma, anxiety, panic, etc., (3) Radiation injury, (4) Trauma, such as trauma, car accidents, (5) Overexertion, exertion, etc. In addition, hyperthyroidism can be triggered or aggravated in early pregnancy; excessive iodine intake, such as the consumption of large amounts of seafood like kelp and seaweed, and oral administration of drugs containing high iodine such as gliodinone, can also trigger hyperthyroidism. If the above triggering factors can be avoided, the onset of hyperthyroidism can be prevented or alleviated in some patients. Of course, these triggering factors are difficult to avoid in a lifetime, and some of them are difficult to prevent. In conclusion, minimizing the above triggers may reduce the probability of occurrence or recurrence of hyperthyroidism.