The exact etiology of PCOS is unknown, although it is known to be a metabolic disorder that affects several hormones including: insulin (hyperinsulinemia), androgen hormones (e.g. testosterone), luteinizing hormone (LH) and follicle stimulating hormone (FSH) (McCance and Huether, 2019). There are no specific pain sensations that patients experience, although they do experience more psychosocial factors such as interpersonal sensitivity, depression, and sexual dysfunction (Elsenbruch et al., 2003).
Normal ovaries produce a single dominant follicle that results in a single ovulation per menstrual cycle. This dominant follicle is responsible for estradiol synthesis during the follicular phase of the menstruation cycle; after ovulation, the dominant follicle forms into the corpus luteum, which secretes high levels of progesterone during the luteal phase of the menstrual cycle. Then, estradiol and progesterone act on the uterus to prepare for implantation of the human embryo (Williams and Erickson, 2012). Under normal circumstances, ovarian follicles contain egg cells which are released during ovulation. In polycystic ovary syndrome, the ovarian cycle and the folliculogenesis process are disrupted. Abnormal hormone levels prevent follicles from growing and maturing to release egg cells. Instead, these immature follicles accumulate in the ovaries. Affected women can have 12 or more of these follicles (Genetics Home Reference, 2019).
Hyperandrogenism: In PCOS, elevated androgens, or hyperandrogenism, is a key feature. Androgens are considered male hormones that are made by the adrenal cortex, and in women are also produced by the ovaries. In women, these hormones are further broken down into estrogen (in large amounts) and testosterone (in smaller amounts). All women have testosterone, and in small amounts this serves a purpose, especially for reproduction, bone health, and libido. Androgen excess initiates premature luteinization, hindering ovulation by impairing the selection of dominant follicles (McCance and Huether, 2019). Excess androgen levels can also explain the excess hair growth and acne present in some PCOS cases. Excess androgens also reduce the synthesis of estradiol, growth hormones of tissues of the reproductive organs, which are required for the full development of antral follicles. The “cysts” on the ovaries are antral follicles that are prematurely developed. Polycystic ovaries are characterized by theca cell hyperplasia, ovarian cortical thickening, and the increase in antral follicles and ovarian stoma. The theca cells secrete higher levels of androgens – both basally and in response to LH and insulin (Diamanti-Kandarakis and Dunaif, 2012). Polycystic ovaries are present in up to 33% of PCOS cases (Barthelmess and Naz, 2014).
LH/FSH: Luteinizing hormone (LH) and follicle stimulating hormone (FSH) are made and secreted by a part of the brain called the pituitary gland. These hormones are essential to reproduction as they are necessary for the expression of gonadal steroidogenic enzymes and sex hormone secretion. The primary goal of LH is to stimulate and produce androgens. FSH is responsible for the stimulation and maturation of an egg before it is released during ovulation. In PCOS, these hormones are imbalanced. There is an increase in the production of LH, which produces too much androgens that convert to testosterone and a decrease in FSH, which prevents the stimulation, maturation, and release of an egg during ovulation (McCance and Huether, 2019).
Insulin Resistance and Hyperinsulinemia: It should be noted that though insulin resistance is not included in the diagnostic criteria for PCOS, it is highly prevalent among PCOS cases. Sixty to eighty percent of PCOS cases have insulin resistance (Barthelmess and Naz, 2014). In insulin resistance, the body’s cells are unable to use the hormone insulin to metabolize glucose for energy. When there is an excess amount of glucose in the body, it is stored in the body as fat. This is what contributes to weight gain in some women with PCOS. Insulin is also a big factor in the secretion of androgen (male) hormones. When there is an excess amount of insulin in the body that is not being used, it stimulates the overproduction of androgens (McCance and Huether, 2019). Acanthosis nigricans is also present in some PCOS cases. This condition may create velvet-likes skin lesions and correlated to insulin resistance, as insulin causes excess keratinocyte growth, leading to the abnormal skin patches (Diamanti-Kandarakis and Dunaif, 2012).
All of the above factors contribute to the development of PCOS in women.
Picture in Voice Thread retrieved from: https://ghr.nlm.nih.gov/condition/polycystic-ovary-syndrome