Ann W. et al. found that the risk of prostate cancer was significantly higher in patients with hyperinsulinemia and insulin resistance. Seely et al. found that high sugar intake led to an increased incidence of breast cancer, which they attributed to increased insulin secretion due to high sugar intake. Heuson JC et al. found that the use of tetraoxonine after carcinogenic agents prevented the development of tumors. The results of all the above trials suggest that insulin is involved in the pathogenesis of tumors and plays an important role in the development of tumors. Insulin resistance in patients with malignant tumors was first found in patients with malignant tumors accompanied by cachexia. Subsequently, insulin resistance was also found in cancer patients without cachexia and without metastasis.Copeland et al. injected different concentrations of insulin into 10 colon cancer patients and 10 healthy individuals matched for age, sex, and nutritional status, and as a result, all of the tumor groups showed a significant reduction in glucose handling capacity. Another study found that glucose uptake gradually returned to normal in patients after complete removal of the tumor tissue. Yoshikawa T et al. further investigated the relationship between insulin resistance and malignancy and found that insulin resistance was not related to weight loss but to the tumor itself. They also studied the relationship between tumor site, tumor stage and insulin resistance, and found that insulin sensitivity in the body decreases at the early stage of tumor development, but insulin resistance is not related to the stage and site of tumor. According to the above test results, on the one hand, hyperinsulinemia or insulin resistance can contribute to the development of cancer; on the other hand, malignant tumors can lead to insulin resistance, thus constituting a vicious circle. The cause of cancer caused by high levels of insulin in peripheral blood may be related to the effect of insulin on the cell cycle. The G1 phase restriction point in the cell cycle has the role of preventing DNA replication in cells with damaged DNA from entering S phase. As discussed previously, insulin allows cells to rapidly pass through the G1 phase restriction point into S phase, which makes it possible for some cells with damaged or mutated DNA to avoid the G1 phase restriction point to enter S phase and undergo DNA replication. Insulin shortens the cell proliferation cycle and disrupts the cell cycle regulatory mechanism, allowing cells to proliferate abnormally at a faster rate, all of which may contribute to the development of cancer. In addition, as mentioned earlier insulin can lead to abnormally high expression of cyclinD, and studies have shown that abnormal cyclinD expression is closely associated with tumorigenesis. In addition, high levels of insulin in peripheral blood can lead to increased activity of IGF-1, which can contribute to cell growth and proliferation and convert cells to a malignant phenotype. Extensive studies have been conducted on IGF-1 both domestically and internationally. A large amount of information indicates that IGF-1 plays an important role in the development of tumors. Pharmacology has also found that the application of drugs that reduce IGF-1 concentration can reduce the occurrence of malignant tumors. The cause of hyperinsulinemia and insulin resistance due to malignant tumors may be related to increased levels of tumor necrosis factor and decreased expression of glucose labile transport carrier 4 (GLUT4) in malignant tumors.