Gout can be divided into two categories: primary gout and secondary gout, both of which have different causes, but both can lead to hyperuricemia, resulting in urate crystal deposits and thus gout attacks. Primary gout is caused by a combination of environmental and genetic factors and has a certain degree of family heritability. Except for a very small number of cases caused by congenital defects in purine metabolizing enzymes, the rest are mostly associated with a high purine diet and often co-exist with obesity, hypertension, diabetes mellitus and coronary heart disease. Secondary gout is mainly caused by kidney diseases that lead to reduced uric acid excretion, certain drugs that inhibit uric acid excretion, and myeloproliferative diseases that lead to increased uric acid production due to radiotherapy. At present, with the improvement of material living standard, high purine diet has become one of the main causes of gout. Drinking alcohol, seafood, animal offal, beef and mutton, and sweet drinks are the main types of high purine diet. Long-term high purine diet can cause elevated blood uric acid and lead to hyperuricemia. If the blood uric acid level is elevated for a long time, the concentration of urate increases and crystals are formed and deposited in joints and kidneys, leading to gout attacks. However, it is important to note that elevated blood uric acid alone does not equal gout; gout must occur with the formation and deposition of urate crystals. Therefore, all factors that can cause hyperuricemia can be considered to be the cause of gout, and hyperuricemia is the basis for the development of gout.