PCOS (Polycystic Ovarian Syndrome) affects the health, reproduction, and quality of life of many women of childbearing age, but we still don’t know its causes. Once its cause is understood, it could play a key role in improving the quality of life for women with PCOS. Let’s share the insights from an article that explores whether fetal overexposure to androgens causes PCOS. According to recent data, exposure of female fetuses to high levels of androgens during in utero development may predispose them to develop PCOS after puberty.The study, which used rhesus monkeys, which were injected with testosterone during gestation, and whose offspring developed polycystic ovaries, scanty menstruation, high LH levels, and insulin resistance, constitutes the strongest evidence for the theory to date. There is evidence of androgen excess in the intrauterine environment of pregnant women with PCOS, and this hyperandrogenism may be caused by elevated maternal androgen concentrations. Normally, maternal androgens or fetal adrenal androgens are rapidly converted to estrogens by placental aromatase. In placental tissue of women with PCOS, 3β-HSD-1 activity is elevated and P450 aromatase activity is decreased, which would increase androgen production during pregnancy. PCOS is known to be largely familial, but there are no clear genetic mutations associated with it. It is hypothesized that epigenetic factors such as methylation of PCOS-related genes play an important role in its etiology. Methylation is known to play a key role in regulating gene expression. AMH has a mysterious role in the pathogenesis of PCOS and increased AMH levels are a common feature of PCOS. Hypomethylation of the AMH gene may lead to intrinsic overexpression of the AMH gene and increased production of AMH in PCOS. Increased AMH leads to anovulation by inhibiting the follicle growth-promoting effects of FSH, and AMH is positively correlated with testosterone and LH serum concentrations. It can be hypothesized that AMH methylation may represent another epigenetic alteration related to the hormonal environment in the uterus. There are data from animal experiments suggesting that an androgen-excessive intrauterine environment also predisposes to insulin resistance in the offspring of mothers with PCOS, ultimately giving rise to the metabolic features of PCOS. In summary, fetal overexposure to the androgenic environment in utero plays a central role in the etiology of PCOS.