Polycystic Ovary Syndrome (PCOS) is a common endocrine disorder affecting women during their reproductive years. This complex condition involves a significant hormonal imbalance that impacts various body systems. PCOS is one of the most frequent hormonal disorders in this demographic, affecting 5% to 18% of women worldwide. It is characterized by a mix of reproductive and metabolic disturbances.
Defining Characteristics and Manifestations
The clinical presentation of PCOS generally falls into three main categories. The first is a disturbance in the menstrual cycle, often presenting as oligo- or amenorrhea. This means a woman may experience infrequent periods (cycles longer than 35 days) or a complete absence of menstruation for several months. These irregularities occur because hormonal imbalance prevents the ovary from regularly releasing an egg, a process known as anovulation.
The second manifestation is hyperandrogenism, which refers to clinical or biochemical evidence of excess androgens, such as testosterone. Clinical signs include hirsutism, the growth of coarse, dark hair in a male-like pattern on the face, chest, or back. Severe, persistent acne and male-pattern hair thinning or loss on the scalp (androgenic alopecia) are also common symptoms.
The third characteristic is the presence of polycystic ovaries, visualized on an ultrasound. These are not true cysts, but numerous small, underdeveloped sacs called follicles. A polycystic ovary typically contains 12 to 20 or more follicles, often arranged around the periphery, giving a “string of pearls” appearance. These immature egg sacs fail to develop and rupture, which is the underlying reason for the irregular cycles.
Underlying Biological Drivers
The root causes of PCOS involve a complex interaction between genetic, hormonal, and metabolic factors. A central driving force is insulin resistance, present in a majority of women with the condition. Insulin resistance causes the pancreas to produce excessive amounts of insulin to maintain normal blood sugar levels, a state known as hyperinsulinemia.
This excess insulin acts on the ovaries, directly stimulating the production and release of androgens. Insulin enhances the activity of enzymes in ovarian cells responsible for synthesizing androgens. Hyperinsulinemia also reduces the liver’s production of Sex Hormone-Binding Globulin (SHBG), a protein that binds to androgens in the bloodstream.
A lower level of SHBG results in a higher amount of free, biologically active androgen circulating in the body, driving symptoms like hirsutism and acne. The resulting excess androgen disrupts the normal process of ovulation. High androgen levels impair the growth and maturation of ovarian follicles, preventing the release of an egg. This follicular arrest leads to the accumulation of immature follicles and causes the chronic anovulation resulting in irregular periods.
Establishing a Diagnosis
PCOS diagnosis is one of exclusion, requiring other conditions that mimic its symptoms, such as thyroid dysfunction or elevated prolactin levels, to be ruled out. Healthcare providers use the Rotterdam Criteria, a set of internationally accepted guidelines, to formally diagnose the condition. A diagnosis requires the presence of at least two out of three specific criteria:
- Oligo- or anovulation, evidenced by irregular or absent menstrual periods.
- Hyperandrogenism, determined clinically (excess hair growth or acne) or biochemically (elevated levels of free or total testosterone).
- The presence of polycystic ovaries on an ultrasound examination.
Blood tests are necessary to assess hormone levels and exclude other conditions. These tests often measure androgens and sometimes Sex Hormone-Binding Globulin to calculate free androgen levels. Metabolic screening, such as fasting glucose, insulin, and a lipid panel, is also performed to assess the risks of insulin resistance and heart disease.
Therapeutic Approaches
The management of PCOS is individualized, focusing on controlling symptoms, reducing long-term health risks, and addressing specific goals, such as achieving pregnancy. Lifestyle modifications form the foundational, first-line treatment. Weight management, even a modest reduction of 5% to 10% of body weight, can significantly improve insulin sensitivity and may restore regular ovulation.
A healthy diet, often focusing on low glycemic index foods and caloric restriction, combined with regular physical activity, is recommended. Exercise, including aerobic and resistance training, helps lower insulin levels and improve the body’s response to insulin. These changes address the underlying metabolic drivers and help alleviate reproductive and physical symptoms of androgen excess.
Medical interventions manage specific symptoms alongside lifestyle changes. Hormonal birth control, typically combination pills, is frequently prescribed to regulate the menstrual cycle and reduce the risk of endometrial hyperplasia. These medications also decrease androgen levels, improving acne and hirsutism. Anti-androgen medications, such as spironolactone, can directly block the effects of androgens on the skin and hair follicles, offering further relief.
Insulin-sensitizing medications, like metformin, are commonly used to improve insulin use and reduce hyperinsulinemia. By lowering insulin levels, metformin can decrease androgen production and may help restore ovulatory cycles. For women who wish to become pregnant, fertility treatments are utilized, with medications like clomiphene citrate or letrozole often used to stimulate the ovaries and induce ovulation.