PCOS: Signs, Diagnosis and What Actually Helps

Polycystic ovary syndrome is the most common endocrine disorder in women of reproductive age: it affects 8–13% of women, and up to 70% of them are undiagnosed. The name misleads twice over: there are no cysts involved, and the condition reaches well beyond gynaecology — it is a metabolic syndrome with reproductive manifestations.

What it actually is#

PCOS is not a disease of the ovaries but a systemic regulatory disorder. Two mutually reinforcing mechanisms sit at its centre.

Androgen excess. The ovaries and adrenal glands produce too much androgen. Clinically this shows as hirsutism (male-pattern hair growth), acne and sometimes androgenic alopecia. In the lab it shows as elevated free testosterone or free androgen index.

Insulin resistance. Tissues respond poorly to insulin and the pancreas compensates by secreting more. That hyperinsulinaemia in turn stimulates ovarian androgen production and suppresses hepatic synthesis of sex hormone-binding globulin — so free testosterone rises further. The loop closes.

At the level of the cycle the result is disrupted selection of a dominant follicle. Follicles begin growing but stall at the antral stage; ovulation fails to occur or occurs rarely. Those arrested follicles are exactly what ultrasound shows as "polycystic".

Making the diagnosis#

The Rotterdam criteria require two features out of three:

1. oligo- or anovulation (cycles longer than 35 days, or fewer than 8 cycles a year);
2. clinical or biochemical androgen excess;
3. polycystic ovarian morphology on ultrasound (20 or more follicles of 2–9 mm per ovary, or ovarian volume above 10 ml).

And, without exception, the exclusion of other causes.

What is excluded	How	Why it matters
Thyroid disease	TSH	Hypothyroidism disrupts cycles
Hyperprolactinaemia	Prolactin	A pituitary adenoma is treated differently
Non-classical CAH	17-OH progesterone in early follicular phase	Looks like PCOS, needs different therapy
Cushing's syndrome	Where clinical signs are present	Rare but fundamental
Androgen-secreting tumour	Where virilisation progresses rapidly	Requires urgent workup

Assessment does not stop there. The guidelines mandate a metabolic workup: fasting glucose or an oral glucose tolerance test, lipid panel, blood pressure, waist circumference. This is not defensive medicine — the risk of type 2 diabetes in PCOS is raised three to fourfold.

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What genuinely helps#

Intervention	What it affects	Evidence
5–10% weight reduction	Ovulation, androgens, metabolism	Strong; first-line where weight is elevated
Regular exercise	Insulin sensitivity, body composition	Good; works without weight loss too
Letrozole	Ovulation induction	Strong; superior to clomiphene on live births
Combined oral contraceptives	Cycle, acne, hirsutism	Good, where pregnancy is not being sought
Metformin	Metabolic markers, partly cycle	Moderate; not first-line for fertility
Antiandrogens (spironolactone)	Hirsutism, acne	Good; only with reliable contraception
Inositol	Insulin sensitivity, ovulation	Limited; encouraging data, moderate study quality
GLP-1 agonists	Weight, metabolism	Growing; off-label use remains under discussion

Lifestyle sits first for substantive reasons. A 5–10% reduction in body weight in women carrying excess restores ovulation in roughly half of cases, lowers androgen levels and improves metabolic markers. The mechanism is direct: less visceral fat means less insulin resistance means less androgen stimulation.

There is a caveat frequently skipped in consultations, though. "Just lose weight" is poor advice for a condition that itself makes weight loss harder. Hyperinsulinaemia promotes fat storage and amplifies hunger. What is called for is structured support — nutrition, training, sleep, and pharmacotherapy where indicated — rather than a demand for willpower.

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About diet#

There is no single "PCOS diet", and systematic reviews confirm it: at matched calorie deficits, different patterns produce comparable results. Some principles still follow sensibly from the mechanism:

• adequate protein — better satiety and muscle preservation;
• carbohydrates predominantly from whole sources with fibre, which flattens the glycaemic response;
• regular meals instead of long gaps followed by overeating;
• limiting sweetened drinks and alcohol.

The various "PCOS protocols" that exclude dairy, gluten or nightshades have no evidence base.

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Fertility#

PCOS is the most common cause of anovulatory infertility and simultaneously one of the most correctable. The usual sequence is weight and lifestyle management, then pharmacological ovulation induction, then gonadotrophins or IVF.

The key change of recent years is the move to letrozole as first-line. Compared head-to-head with clomiphene (Legro et al., NEJM, 2014), letrozole produced higher live birth rates in women with PCOS. It is an aromatase inhibitor, and its use in this role was off-label for years, but it is now embedded in international guidance.

Not only hormones#

An often underweighted part of the picture is psychological. The Cooney meta-analysis found substantially higher prevalence of moderate and severe depressive and anxiety symptoms in women with PCOS compared with controls. The causes are layered: biological mechanisms, the effect of hirsutism and acne on body image, and the stress that surrounds fertility.

International guidance explicitly requires screening for anxiety and depression at diagnosis. That is part of standard management rather than an optional extra.

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The long view#

PCOS does not end when the question of pregnancy is settled. Elevated risks persist for type 2 diabetes, metabolic syndrome, non-alcoholic fatty liver disease and — where prolonged anovulation leaves the endometrium unopposed — endometrial hyperplasia.

A practical monitoring minimum: glucose or HbA1c every one to three years depending on risk factors, a lipid panel, blood pressure and weight, and attention to cycle regularity. Where periods are infrequent (fewer than four a year), endometrial protection with progestogens or combined contraception is worth discussing.

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The bottom line#

PCOS sits at the intersection of endocrinology, gynaecology and metabolic medicine. The diagnosis requires two features out of three after excluding other causes, and ultrasound "cysts" are not among the requirements.

At its core is the pairing of androgen excess and insulin resistance, present in women with normal weight as well. Lifestyle is first-line; beyond that the choice depends on the goal — contraception and antiandrogens where pregnancy is not being sought, letrozole where it is. In every case, long-term metabolic monitoring matters, because the reproductive features soften with time while the metabolic ones do not.