Polycystic Ovary Syndrome (PCOS) is a common endocrine disorder characterized by hormonal imbalances, ovulatory dysfunction, and metabolic irregularities. It affects reproductive-age women globally and is the most frequent cause of anovulatory infertility. A defining feature in many women with this condition is an alteration in the neuroendocrine system, marked by an elevation of Luteinizing Hormone (LH) relative to Follicle-Stimulating Hormone (FSH). Understanding this hormonal shift is central to grasping the pathophysiology of PCOS.
Luteinizing Hormone’s Normal Role
Luteinizing Hormone is a glycoprotein secreted by the pituitary gland, serving as a regulator of reproductive function in women. Its primary function is to stimulate the ovaries to produce steroid hormones and manage the timing of the menstrual cycle. In the first half of the cycle, LH works with FSH to stimulate the growth of ovarian follicles and the production of estrogen.
The most dramatic event driven by LH is the pre-ovulatory surge, a rapid rise in its concentration. This surge triggers the final maturation of the egg and causes the dominant follicle to rupture, releasing the egg (ovulation). Following ovulation, LH supports the corpus luteum, stimulating it to produce progesterone to prepare the uterus for potential pregnancy.
The LH/FSH Imbalance in PCOS
In a healthy reproductive cycle, LH and FSH levels are typically similar in the early follicular phase, resulting in a ratio near 1:1. Women with PCOS often exhibit a chronic, non-surging elevation of LH, while FSH levels remain normal or relatively low. This disparity creates an elevated LH to FSH ratio, a characteristic hormonal profile in many cases of PCOS.
This ratio frequently exceeds 2:1. The relative lack of FSH, which is needed for the full maturation of ovarian follicles, combined with chronic LH stimulation, causes the follicles to stall in their development. This failure leads to the accumulation of small, fluid-filled sacs, contributing to the polycystic ovary morphology seen on ultrasound.
Key Drivers of Elevated LH
The primary reason for the disproportionate LH elevation in PCOS is an alteration in the signaling pathway controlling the pituitary gland. This control originates in the hypothalamus, which releases Gonadotropin-Releasing Hormone (GnRH) in discrete pulses. In women with PCOS, the frequency of these GnRH pulses is significantly faster than normal, often increasing from a typical 90-minute interval to approximately one pulse per hour.
This rapid GnRH pulsatility preferentially stimulates the pituitary gland to synthesize and release LH over FSH. Since FSH requires slower, less frequent GnRH pulses for optimal production, the faster pace results in a relative deficiency of FSH. The resulting high LH levels then overstimulate the ovarian theca cells, causing them to produce excessive amounts of androgens, such as testosterone.
The high levels of androgens feed back to the hypothalamus, reinforcing the rapid GnRH pulse frequency. Androgens reduce the sensitivity of the GnRH pulse generator to negative feedback signals from sex steroids. This perpetuates the cycle of high GnRH pulse frequency and elevated LH, creating a self-sustaining neuroendocrine environment that favors hyperandrogenism.
The Impact of Hyperinsulinemia
Metabolic dysfunction is intertwined with PCOS hormonal abnormalities, as insulin resistance leads to compensatory hyperinsulinemia in many women. This high concentration of circulating insulin acts as a co-gonadotropin, significantly contributing to elevated LH effects. Insulin molecules bind to receptors on ovarian theca cells, acting synergistically with LH to accelerate androgen production.
The theca cells in women with PCOS show heightened sensitivity to both insulin and LH, meaning even physiological doses of insulin can trigger excessive androgen synthesis. This connection links the metabolic and endocrine aspects of the syndrome.
Hyperinsulinemia also directly impacts the liver’s production of Sex Hormone-Binding Globulin (SHBG), a protein that binds to and inactivates androgens. High insulin suppresses SHBG synthesis, leading to lower levels of this binding protein. This reduction increases the amount of free, biologically active androgen, which exacerbates clinical symptoms of hyperandrogenism, such as hirsutism and acne.
Consequences of Chronic LH Elevation
The sustained, non-surging elevation of LH disrupts the sequence of events required for a normal ovulatory cycle. Since LH levels are chronically high, the ovary cannot generate the sharp, pre-ovulatory LH surge necessary to trigger egg release. This failure results in chronic anovulation, a common cause of infertility and irregular menstrual periods in PCOS.
The constant overstimulation by LH promotes the growth of thecal cells and increases their production of androgens. These excessive androgens prevent the final development of ovarian follicles, causing them to arrest prematurely and form the characteristic small cysts. This environment of high LH and high androgens drives the outward manifestations of the syndrome, including excessive hair growth and persistent acne.