PCOS is a metabolic condition that happens to involve the ovaries

Polycystic ovary syndrome is badly named. The "cysts" are not cysts — they are small immature follicles that have stalled part-way through development. Plenty of people with the condition do not have them at all, and plenty of people who do have them do not have the condition.

What PCOS actually is: the most common endocrine disorder in people of reproductive age, affecting somewhere between 8 and 13 percent, and a condition whose consequences are as much metabolic and cardiovascular as reproductive.

How it is diagnosed

The Rotterdam criteria require two of three, with other causes excluded:

1. Irregular or absent ovulation — typically cycles longer than 35 days, fewer than eight or nine periods a year, or none
2. Clinical or biochemical androgen excess — hirsutism, persistent acne, scalp hair thinning, or raised testosterone on a blood test
3. Polycystic ovarian morphology on ultrasound, or a raised AMH level

Because only two of three are required, the condition presents very differently between people. Someone with irregular cycles and raised testosterone has PCOS without any ultrasound finding. Someone with regular cycles and no androgen features does not have PCOS just because a scan looked polycystic.

In adolescents, ultrasound is not used at all, because multifollicular ovaries are normal in the years after periods begin.

The engine underneath

Two mechanisms drive most of it.

Insulin resistance. A majority of people with PCOS have some degree of it, including many at a normal weight — this is important, because lean PCOS is routinely missed. Higher circulating insulin does two things: it drives the ovarian theca cells to produce more androgens, and it lowers sex hormone binding globulin, which means more of the testosterone present is free and active. So insulin resistance amplifies androgen excess twice over.

Disordered gonadotrophin signalling. LH pulses run faster and higher relative to FSH. Follicles start developing but none is properly selected to mature and ovulate, so they accumulate as the small follicles seen on a scan. No ovulation means no corpus luteum, no progesterone, and no proper luteal phase.

That last point explains a lot of the day-to-day experience. Without progesterone, the uterine lining builds under unopposed oestrogen and eventually sheds unpredictably and heavily. It is also why the ordinary rhythm described in what a normal cycle looks like is absent, and why an app predicting periods from an average is close to useless here.

It also explains why LH ovulation tests behave strangely — chronically elevated LH produces persistent or repeated positives that do not correspond to ovulation. How to tell when you ovulate covers the workaround.

The parts that get left out of the conversation

PCOS is associated with substantially raised risk of impaired glucose tolerance and type 2 diabetes, with dyslipidaemia and hypertension, with non-alcoholic fatty liver disease, and with obstructive sleep apnoea independent of weight. It also carries a raised risk of endometrial hyperplasia when periods are very infrequent, because the lining is exposed to oestrogen for long stretches without progesterone to oppose it. That is why guidelines suggest ensuring a bleed at least every three to four months.

Rates of depression and anxiety are markedly higher too, and not only as a reaction to symptoms.

Current guidelines therefore recommend periodic screening for glucose tolerance and cardiovascular risk factors in everyone with PCOS, at any weight. Many people are never offered it.

What treatment should target

Treatment depends on what you want right now, and that changes over a lifetime.

For cycle regulation and endometrial protection: combined hormonal contraception, or cyclical progestogen. This does not treat the underlying condition, but it makes bleeding predictable and protects the lining.

For androgen symptoms: combined contraception lowers free testosterone; anti-androgens such as spironolactone are added where needed. Both take months, not weeks — hair follicle cycles are slow, and judging response before six months is judging too early.

For insulin resistance: metformin, and inositol supplementation which has reasonable supportive evidence. Resistance training is particularly effective at improving insulin sensitivity, largely independent of weight change — strength training does more for women than any other exercise applies with unusual force here.

For fertility: letrozole is now first-line for ovulation induction, having outperformed clomifene in head-to-head trials.

Weight loss is often recommended, and modest loss does improve ovulation for those carrying excess weight. But it is not the whole answer, it is not relevant for lean PCOS, and being told to lose weight instead of being investigated is one of the most common complaints people with PCOS have about their care. Why women wait longer for a diagnosis is relevant background.

Tracking is unusually useful here

When cycles are long and unpredictable, memory is a poor instrument. Whether you had four periods this year or seven, whether the acne tracks with anything, whether your energy crashes correspond to particular foods or to sleep, whether a treatment started in March actually changed anything by August — these are all answerable from a record and unanswerable without one.

Naked is built for exactly this: logging cycles, symptoms, mood, sleep and energy over the long stretches PCOS demands, and finding the connections between them. With a condition this variable between people, the population average is close to useless. Your own data is the only thing that describes your version of it.