Polycystic ovary syndrome (PCOS) is a major cause of ovulatory infertility. There are various etiological hypotheses about PCOS, which are summarized as follows: 1. The origin of hyperinsulinemia Obesity in childhood increases the release of insulin, and the combined effect of insulin and gonadotropins promotes the synthesis of androgens in the ovaries, which may lead to ovulation disorders and hirsutism. Hyperinsulinemia in adulthood can increase androgen secretion in the ovaries and induce early arrest of follicular development. Insulin can also inhibit the production of sex hormone binding globulin in the liver, which in turn may increase the level of free androgens in the blood, leading to some of the features of PCOS. Genetic abnormalities originate in 30-50% of PCOS patients whose immediate family members have also been diagnosed with PCOS. studies in identical twins have found a co-morbidity rate of PCOS of up to 65%. Genetic analysis using candidate gene strategies has identified over 100 candidate genes that may be associated with PCOS, and studies continue to report functional associations of candidate genes with PCOS. However, the predictive value of genetic risk scores for PCOS remains weak, suggesting that key genes have not been identified or that genetic abnormalities are not the origin of the disease. 3. Epigenetic alterations In addition to genetic alterations, alterations in gene expression caused by modifications that do not alter the primary DNA sequence, i.e. epigenetic alterations, including DNA methylation and histone modifications, may sometimes occur. When needed, these alterations can persist throughout life in the absence of a continuous source of stimulation. There is a hypothesis that PCOS originates from epigenetic alterations. 4. The hypothesis of fetal origin of adult disease with intrauterine hyperandrogenic exposure, also known as the Barker hypothesis, suggests that the effects of adverse factors during intrauterine development can lead to permanent physiological and metabolic abnormalities. Fetal exposure to androgens during a critical period of embryonic development can lead to masculinization of the anatomy and behavior of both female and male offspring. Evidence from both clinical and preclinical studies supports that intrauterine Kaohsiung exposure increases the propensity of female offspring to develop a PCOS phenotype after the onset of pubertal development.