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Polycystic Ovary Syndrome (PCOS) is a complex endocrine disorder characterized by an interplay between genetic, metabolic, and hormonal abnormalities that lead to ovarian dysfunction, hyperandrogenism, and metabolic disturbances. The pathophysiology begins with insulin resistance, which occurs in many but not all women with PCOS and contributes significantly to its endocrine and metabolic features.
The treatment of polycystic ovary syndrome (PCOS) is multifaceted because the condition involves hormonal imbalance, metabolic dysfunction, and reproductive irregularities. Management typically begins with lifestyle modification, as even a modest 5–10% weight reduction can significantly improve ovulation, insulin sensitivity, and androgen levels.
Epigenetic mechanisms appear to play a significant role in the pathophysiology of polycystic ovary syndrome (PCOS), helping explain how genetic susceptibility interacts with environmental and developmental factors to produce the syndrome’s diverse reproductive and metabolic manifestations.
Polycystic Ovary Syndrome (PCOS) is intricately linked to hyperinsulinemia and an increased risk of developing type 2 diabetes, primarily due to the role of insulin resistance in the condition's pathophysiology. Hyperinsulinemia, a condition characterized by elevated levels of insulin in the blood, plays a pivotal role in the development of insulin resistance through a complex interplay of cellular and molecular mechanisms.
Endometriosis and PCOS are the Yin and Yang of reproductive medicine. Endometriosis is driven by relatively low levels of prenatal and postnatal testosterone. Testosterone affects the developing hypothalamic–pituitary–ovarian (HPO) axis, and at low levels, it can result in an altered trajectory of reproductive and physiological phenotypes that can mediate the symptoms of endometriosis. Polycystic ovary syndrome, by contrast, is known to be caused primarily by high prenatal and postnatal testosterone, and it demonstrates a set of phenotypes opposite to those found in endometriosis.
Endometriosis is driven by relatively low levels of prenatal and postnatal testosterone. Testosterone affects the developing hypothalamic–pituitary–ovarian (HPO) axis (defined below), and at low levels and it can result in an altered trajectory of reproductive and physiological phenotypes that can mediate the symptoms of endometriosis. A phenotype is defined as a person’s observable characteristics resulting from the interaction of their genetic makeup and the environment. Polycystic ovary syndrome, by contrast, is known to be caused primarily by high prenatal and postnatal testosterone, and it demonstrates a set of phenotypes that are diametrically opposite to those found in endometriosis.
Epigenetics plays an important role in the development of many metabolic diseases and since these alternations to the underlying DNA are reversible, restoring the DNA to normal provides opportunities for developing pharmacotherapies for many metabolic diseases.
Polycystic Ovary Syndrome (PCOS) is a common metabolic and reproductive disorder of women characterized by high levels of male hormones (androgens), insulin resistance, and ovulatory dysfunction. High levels of male hormones manifest themselves in excessive coarse and dark hair growth in women where hair is typically minimal or absent, such as the face, chest, and back, referred to as hirsutism. Acne or scalp hair loss can also occur in combination with hirsutism. Long recognized as a reproductive disorder, PCOS is now well established as a metabolic disorder with long-term health risks, including type 2 diabetes and cardiovascular disease.