Polycystic ovaries develop when a combination of genetic, hormonal, and metabolic factors cause the ovaries to produce too many androgens (often called “male hormones,” though all women produce them in small amounts). This excess disrupts normal egg development, leaving multiple small, fluid-filled follicles on the ovaries instead of releasing a mature egg each cycle. PCOS affects an estimated 10 to 13% of women of reproductive age worldwide, and up to 70% of those women don’t know they have it.
There is no single cause. PCOS emerges from several overlapping mechanisms that reinforce each other, which is part of why it looks different from person to person. Here’s what drives it.
Genetics Play the Largest Role
Twin studies estimate that PCOS is roughly 70% heritable, meaning your genes account for the majority of your risk. If your mother or sister has PCOS, your chances of developing it are significantly higher than average. Researchers have identified several gene regions linked to the condition, with the strongest evidence pointing to genes involved in hormone signaling and insulin processing: THADA, FSHR, INS-VNTR, and DENND1A.
The genetics are complex. Different populations carry different risk variants. For example, specific variations in the DENND1A gene are associated with PCOS in women of Han Chinese and broader Asian ancestry, while a different variation in the same gene drives risk in women of European ancestry. Family studies have also uncovered rare genetic variants in DENND1A that contribute specifically to hormonal imbalances but wouldn’t show up in large population-wide scans. This helps explain why PCOS can run strongly in some families even when standard genetic tests don’t flag anything obvious.
Insulin Resistance Drives Androgen Production
Insulin resistance is one of the most important mechanisms behind PCOS, and it affects women with the condition regardless of their weight. When your cells don’t respond well to insulin, your body compensates by producing more of it. That extra circulating insulin acts directly on the ovaries, stimulating the cells that produce androgens to ramp up production. Insulin does this by increasing the activity of a key enzyme in the androgen-making pathway, essentially turning up the volume on testosterone production at the source.
High insulin also suppresses your liver’s production of a protein that binds to testosterone in the bloodstream and keeps it inactive. With less of this binding protein available, more testosterone circulates freely and actively affects your body, contributing to symptoms like acne, excess hair growth, and disrupted ovulation.
This is why insulin resistance matters even in women who are not overweight. Studies show that insulin resistance in fat tissue is present and positively correlated with androgen levels even in normal-weight women with PCOS. The metabolic dysfunction isn’t just a side effect of carrying extra weight; it’s woven into the condition itself.
A Hormonal Feedback Loop That Reinforces Itself
In a typical menstrual cycle, the brain releases two key hormones in a balanced ratio: luteinizing hormone (LH), which triggers ovulation, and follicle-stimulating hormone (FSH), which helps eggs mature. In PCOS, the brain’s signaling pulses faster than normal, producing relatively more LH and less FSH. About 71% of women with PCOS have an LH-to-FSH ratio above 1.0, when the two should be roughly balanced.
This imbalance has a direct consequence: excess LH pushes the ovaries to produce more androgens, while insufficient FSH means follicles never fully mature. They stall partway through development, accumulating as the small cysts visible on an ultrasound. The androgens produced by this process then feed back to the brain, reducing the normal braking signals that would slow LH production down. The result is a self-reinforcing cycle where high androgens drive high LH, which drives more androgens. Breaking this loop is one of the central goals of PCOS treatment.
How Body Fat Adds Fuel
Fat tissue isn’t just passive storage. It’s an active hormone-producing organ with the full machinery to manufacture androgens on its own. In women with PCOS, fat tissue beneath the skin shows increased activity of enzymes that build testosterone while simultaneously showing decreased activity of the enzyme that converts androgens into estrogen. The net effect: fat tissue becomes another source of excess androgens on top of what the ovaries are already producing.
Deeper abdominal fat creates additional problems. Androgens promote the breakdown of fat stored in this area, releasing fatty acids that get deposited in the liver and muscles. This worsens insulin resistance, which in turn drives more insulin production and more ovarian androgen output. Fat cells exposed to high androgens also become enlarged and inflamed, attracting immune cells that release inflammatory signals. This creates yet another feedback loop layered on top of the hormonal one.
Importantly, weight gain doesn’t cause PCOS, but it can significantly amplify every mechanism involved. Losing even a modest amount of weight, around 5 to 10%, can meaningfully reduce androgen levels and improve ovulation in many women with the condition.
Chronic Low-Grade Inflammation
Women with PCOS tend to have elevated levels of inflammatory molecules circulating in their blood. This isn’t the kind of inflammation you can feel, like a swollen ankle. It’s a subtle, persistent activation of the immune system that operates in the background.
Several of these inflammatory signals directly interfere with hormone balance. One (IL-6) reduces the activity of the enzyme that converts androgens to estrogen in the ovary’s supporting cells, leading to androgen buildup. Others correlate directly with testosterone levels, and even basic markers like white blood cell counts track with free androgen levels in women with PCOS. Advanced glycation end-products, compounds that form when blood sugar is chronically elevated, also correlate with circulating androgen levels. Inflammation doesn’t just accompany PCOS; it actively participates in maintaining the hormonal disruption.
The Adrenal Glands Contribute in Some Women
The ovaries are the primary source of excess androgens in PCOS, but they’re not the only source. Between 20% and 30% of women with PCOS also have elevated androgens coming from the adrenal glands, the small organs that sit on top of your kidneys. This is reflected by high levels of a specific adrenal androgen called DHEAS in the blood.
For these women, the adrenal contribution means that treatments targeting only the ovaries may not fully resolve symptoms. It also helps explain why some women with PCOS continue to experience androgen-driven symptoms like hair growth or acne even when their ovarian function is well managed.
Exposure Before Birth May Set the Stage
There’s growing evidence that PCOS can be programmed before birth. Animal studies in rats, mice, sheep, and rhesus monkeys have consistently shown that exposing a female fetus to excess androgens during pregnancy produces a PCOS-like condition in adulthood. Human data supports a similar pattern: second-trimester amniotic fluid from pregnancies of women with PCOS contains higher testosterone levels than controls, and cord blood from newborns of mothers with PCOS shows elevated androgens.
Fetal androgen exposure doesn’t just nudge a few hormone levels. Research shows it alters the expression of hundreds of genes in the developing ovary, with 241 genes upregulated and 112 downregulated compared to unexposed tissue. It also damages the structure and function of mitochondria, the energy-producing components inside cells, increasing oxygen consumption while reducing efficiency. These changes are detectable within the first day of life and can lead to a PCOS phenotype in adulthood, even without obesity. This means some women may be predisposed to PCOS from the earliest stages of development, well before any lifestyle factors come into play.
What Counts as Polycystic Ovaries on Imaging
Having polycystic-appearing ovaries on ultrasound is common and doesn’t automatically mean you have PCOS. Current international guidelines define polycystic ovarian morphology as 20 or more follicles in at least one ovary when using modern transvaginal ultrasound, or an ovarian volume of 10 ml or greater. With older ultrasound equipment or when using a transabdominal approach, the threshold drops to 10 follicles per cross-section or a volume of 10 ml.
For adolescents, there are no definitive ultrasound criteria, and imaging isn’t recommended as part of diagnosis in that age group. Many young women naturally have ovaries that appear “polycystic” without having the syndrome. A PCOS diagnosis requires at least two of three features: irregular or absent periods, signs of excess androgens (either on blood tests or visible symptoms), and polycystic ovarian morphology. The ultrasound finding alone is just one piece of the picture.