Polycystic ovary syndrome (PCOS) is associated with a high prevalence of mental health disorders, including depression, anxiety and eating disorders. There are numerous clinic-based and population studies from around the world showing a high prevalence of both depressive symptoms and depression in reproductive-age women with PCOS compared to controls. These studies indicate that the risk of depression may be independent of obesity and associated with clinical and biochemical hyperandrogenism, with genetic data supporting closely linked biological pathways. Similarly, the risk of anxiety is significantly higher in women with PCOS as compared to a control population. Longitudinal studies depicted a persistence of both depression and anxiety symptoms in women with PCOS over time. First-line treatments for PCOS, including weight-loss interventions and use of hormonal contraceptives, may improve depression and anxiety scores. Recent publications indicate an increased risk of disordered eating and eating disorders in women with PCOS. Given that lifestyle modifications are a first-line treatment for PCOS, early screening and treatment of depression, anxiety and disordered eating are essential for comprehensive management of this population.

Polycystic ovary syndrome (PCOS) is characterized by clinical or biochemical hyperandrogenism, oligo-anovulation and polycystic ovarian morphology on ultrasound. Although the ovaries are the primary source of hyperandrogenism in PCOS, between 20% and 30% of patients with PCOS demonstrate adrenal androgen (AA) excess, as reflected by the circulating dehydroepiandrosterone sulfate (DHEAS) levels. The contribution of AA excess to the development or phenotypic expression of PCOS is not fully understood. Women with PCOS, particularly those with hyperandrogenic subphenotypes, show generalized hypersecretion of adrenocortical products, basally and in response to adrenocorticotropic hormone (ACTH). Alterations in adrenocortical biosynthesis, an exaggeration in the responsivity to ACTH, defects in cortisol metabolism and extra-adrenal factors, including obesity, insulin and glucose levels, and ovarian secretions play a limited role in increased AA production observed in PCOS. Adrenal androgen (AA) levels and their response to ACTH stimulation are highly individualized and relatively constant over time, suggesting that AA hypersecretion may be an inherited trait. Familial aggregation of AA excess in both brothers and sisters of patients with PCOS also supports heritability. However, studies to date have failed to identify specific genetic defects in adrenocortical dysfunction of PCOS due to the genetic and phenotypic heterogeneity of the syndrome and the lack of insufficiently large cohorts.

The genetic underpinnings of polycystic ovary syndrome (PCOS) implicate neuroendocrine, metabolic and reproductive pathways in the pathogenesis of disease. Although specific phenotype stratified analyses are needed, genetic findings were surprisingly consistent across the diagnostic classifications using former National Institute of Health (NIH) , Rotterdam or AE-PCOS criteria suggesting a common genetic architecture underlying the different phenotypes. Genes identified until now all in some ways involved ovarian function and folliculogenesis. Indeed most of the identified single nucleotide polymorphisms (SNPs) were significantly associated with ovulatory dysfunction, hyperandrogenism and polycystic ovarian morphology (PCOM). Furthermore, there was also genetic evidence for shared biologic pathways between PCOS and a number of metabolic disorders, menopause, depression and male-pattern balding, a putative male phenotype.

Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women during reproductive life. The aetiology of the syndrome is unknown; however, many endocrine changes occur, such as insulin resistance and hyperinsulinaemia, hyperandrogenaemia, elevated LH and increased anti-Müllerian hormone, which contribute to the pathogenesis of the syndrome. There are three main characteristics which play key roles in the definition of the syndrome – menstrual irregularities, hyperandrogenism and polycystic morphology of the ovaries – but there is no consensus as to the gravity of each of these features. The management of the syndrome depends on the prevailing symptom and whether the woman is interested in becoming pregnant or not. Combined oral contraceptive pills, diet, lifestyle changes, ovulation-inducing drugs and in-vitro fertilization are the main means of treating the syndrome. Treatment should also take into account possible long-term consequences of this condition, such as metabolic syndrome and cancer development.