Polycystic Ovary Syndrome (PCOS) is a common hormonal disorder affecting women, characterized by a range of symptoms including irregular periods, anovulation, and often, elevated levels of androgens. Among these, testosterone levels are frequently found to be high in women with PCOS. This article explains the biological reasons for increased testosterone production in PCOS.
The Body’s Natural Testosterone Production
In women, testosterone is primarily produced in the ovaries, with smaller amounts also originating from the adrenal glands. This hormone plays an important role in female health, contributing to bone density, muscle mass, energy levels, and libido. The production of testosterone is tightly regulated by a complex feedback system involving the brain’s hypothalamus and pituitary gland.
The pituitary gland releases two key hormones: Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH). These hormones stimulate the ovaries to produce estrogen and progesterone, but LH also plays a direct role in stimulating the ovarian cells responsible for androgen production. In a typical menstrual cycle, the balance and pulsatile release of LH and FSH are crucial for healthy ovarian function and hormone synthesis.
Insulin’s Central Role in Androgen Excess
One of the key drivers behind elevated testosterone levels in PCOS is insulin resistance, a condition where the body’s cells do not respond effectively to insulin. When cells become resistant, the pancreas compensates by producing more insulin to maintain normal blood sugar levels. This results in chronically high circulating insulin levels.
These elevated insulin levels directly stimulate the theca cells within the ovaries. Insulin acts as a co-gonadotropin, enhancing the effects of LH on these cells, leading to an overproduction of androgens, including testosterone. This direct stimulation bypasses normal regulatory mechanisms, driving up androgen synthesis within the ovaries.
High insulin levels also impact testosterone levels by affecting the liver. The liver produces Sex Hormone-Binding Globulin (SHBG), a protein that binds to testosterone and other sex hormones in the bloodstream, rendering them inactive. Elevated insulin levels suppress the liver’s production of SHBG. A reduction in SHBG means that more “free” or unbound testosterone is available in the circulation, which is the biologically active form of the hormone.
Ovarian Dysfunction and LH Signaling
Beyond insulin’s influence, ovarian dysfunction and abnormal Luteinizing Hormone (LH) signaling are key contributors to high testosterone in PCOS. In women with PCOS, there is an altered pattern of LH secretion from the pituitary gland. This often manifests as higher baseline LH levels and an increased pulse frequency.
This elevated and dysregulated LH excessively stimulates the ovarian theca cells, prompting them to produce excess androgens. The ovaries in women with PCOS also exhibit an altered enzymatic environment. There is increased activity of enzymes like cytochrome P450c17a, which favor the synthesis of androgens over the production of estrogens.
This excessive androgen production within the ovaries disrupts the normal development of ovarian follicles. Instead of maturing and releasing a single egg, many follicles remain small and underdeveloped, forming the characteristic “cysts” in PCOS. This follicular arrest further contributes to the hormonal imbalance and anovulation.
Additional Factors Contributing to High Testosterone
While insulin resistance and ovarian dysfunction are key drivers, other factors can also contribute to elevated testosterone levels. In some women, the adrenal glands also contribute to increased androgen production. These glands can produce adrenal androgens like DHEA-S (dehydroepiandrosterone sulfate), which can be converted to testosterone.
Genetic predisposition also plays a role in PCOS; certain inherited variations influence how a woman’s body produces or regulates hormones. These genetic factors affect insulin sensitivity, ovarian enzymes, or the pituitary’s regulation of LH, all of which impact androgen synthesis.
Chronic low-grade inflammation can also worsen the condition. Inflammation can worsen insulin resistance, increasing androgen production by the ovaries. It can also directly stimulate the adrenal glands or ovaries to produce more androgens, further contributing to high testosterone.