PCOS/PMOS Explained: More Than Just Period Problems

If you have ever been told that PCOS is simply a problem with periods, fertility or “cysts on the ovaries”, you have only been given part of the picture.

In May 2026, polycystic ovary syndrome, or PCOS, was officially renamed Polyendocrine Metabolic Ovarian Syndrome, or PMOS. The new name was chosen after an extensive international process involving researchers, healthcare professionals and people living with the condition.

It reflects something increasingly important in our understanding of PMOS: this is a complex endocrine and metabolic condition involving far more than the ovaries. PMOS can affect menstrual cycles and fertility, but it can also influence insulin regulation, androgen production, skin and hair, cardiovascular health, sleep, mental health and longer-term metabolic health.

Understanding those connections can make PMOS feel considerably less mysterious.

What is PMOS?
PMOS is a syndrome, meaning that it describes a collection of features rather than one single symptom. Around one in eight women are thought to be affected worldwide, but PMOS does not look the same in everybody.

Symptoms can include:

• irregular, infrequent or absent periods
• difficulty ovulating or conceiving
• acne and oily skin
• increased facial or body hair
• thinning scalp hair
• weight gain or difficulty managing weight
• insulin resistance or impaired glucose regulation
• darkened, velvety areas of skin, known as acanthosis nigricans
• skin tags
• fatigue
• sleep difficulties and obstructive sleep apnoea
• anxiety, depression and difficulties with body image.

Some women experience many of these. Others have only a few. Importantly, you can have PMOS in a smaller body, have PMOS without acne, and have PMOS without the ultrasound appearance traditionally described as “polycystic ovaries”.

How is PMOS diagnosed?
In adults, current international guidance generally requires two of three features, once other possible causes have been excluded:

1. Ovulatory dysfunction, usually seen as irregular or absent menstrual cycles.
2. Clinical or biochemical hyperandrogenism, meaning symptoms or blood-test evidence of increased androgen activity, eg hirsutism, male pattern hair loss, acne
3. Polycystic ovarian morphology on ultrasound or elevated AMH, where appropriate.

If both irregular cycles and hyperandrogenism are already present, ultrasound or AMH testing may not be required. And despite the old name, these are not ovarian “cysts” in the usual medical sense. They are numerous small follicles.

Diagnosis in teenagers is approached differently because irregular cycles and acne can both occur normally during puberty.

But what actually drives PMOS?
This is where PMOS becomes much more interesting.

There is no single cause. Genetics clearly contribute, but researchers increasingly understand PMOS as the result of interacting hormonal and metabolic pathways.

These can include:

• insulin resistance and higher insulin production
• ovarian and adrenal androgen excess
• altered ovarian hormone signalling
• low-grade inflammation and oxidative stress
• adipose tissue dysfunction
• stress and altered hypothalamic-pituitary-adrenal, or HPA, axis activity

These systems influence one another, potentially creating reinforcing biological loops.

Insulin: not simply a blood sugar issue
Insulin is one of the most important hormones to understand in PMOS.

After we eat foods containing carbohydrate, glucose enters the bloodstream and the pancreas releases insulin. Insulin helps move glucose into cells where it can be used for energy or stored.

With insulin resistance, cells do not respond as effectively to insulin. The pancreas therefore often compensates by producing more. This can result in hyperinsulinaemia or higher circulating insulin levels.

But insulin does far more than manage blood glucose. Higher insulin levels can stimulate ovarian theca cells to produce more androgens. It can also reduce the liver's production of sex hormone-binding globulin, or SHBG, which means more testosterone remains biologically available. The result can be greater androgen activity, which contributes to acne, facial or body hair growth, weight gain, scalp hair thinning, and disruption of normal follicle development and ovulation.

Higher androgen levels may alter body fat distribution and adipose tissue function and contribute to poorer insulin sensitivity. So, we can begin to see a feedback loop between insulin and androgens, rather than one hormone being solely responsible.

Androgens don't only come from the ovaries
Another commonly overlooked part of PMOS is the adrenal glands. Androgens, such as testosterone, are often associated with ovarian production, but the adrenal glands also produce androgen precursors including DHEA and DHEAS. And research suggests that approximately 20–30% of women with PMOS demonstrate excess adrenal precursor androgen production. 

The adrenal glands form part of the body's hypothalamic-pituitary-adrenal, or HPA, axis, which coordinates our physiological stress response. Research has identified altered HPA-axis and stress responsiveness in some women with PMOS.

This gives us another potential connection between stress physiology, adrenal hormone production and androgen symptoms.

What about chronic stress?
Stress is often discussed too simplistically. Cortisol is not a “bad hormone”. We need it to wake up in the morning, maintain blood pressure, mobilise energy and respond appropriately to threats and demands.

Problems really arise when the stress response is activated frequently without adequate recovery.

Cortisol and other stress hormones help make energy available by increasing glucose availability. In the short term, this is useful. Persistently altered stress physiology, however, can interact with insulin sensitivity, appetite regulation, visceral fat deposition, and sleep.

This does not make stress the cause of PMOS, but it does make stress biologically relevant rather than simply an issue of emotional wellbeing.

And there is another important relationship here: PMOS itself can be stressful.

Unpredictable periods, fertility concerns, acne, unwanted hair growth, weight stigma, and years of feeling unheard can create significant psychological stress. Anxiety and depressive symptoms are also considerably more common in women with PMOS.

So again, the relationship may run in both directions.

Where does inflammation fit?
Low-grade inflammation is another important part of the PMOS picture. Inflammation is an essential part of normal immune function. The problem is not inflammation itself, but persistent low-grade inflammatory signalling.

Research has consistently found higher levels of several inflammatory markers in women with PMOS, although body composition and other metabolic factors can contribute. Inflammatory signalling can interfere with insulin signalling, potentially worsening insulin resistance.

Studies have also linked inflammation and oxidative stress with circulating androgen levels, while experimental work has shown that suppressing inflammation and oxidative stress may reduce ovarian androgen hypersecretion.

At the same time, insulin resistance, visceral adipose tissue and androgen excess can themselves encourage inflammatory signalling.

Once again, we have a potential feedback loop.

Inflammation may worsen insulin signalling. Higher insulin may increase ovarian androgen production. Androgen excess and changes in adipose tissue (fat tissue) may then contribute to further metabolic and inflammatory dysfunction.

Why does all this matter?
Because PMOS should never be treated as though the only important questions are: “Are your periods regular?” and “Do you want to get pregnant?”.

Current international guidance recognises increased risks relating to glucose regulation, type 2 diabetes, cardiovascular risk factors, obstructive sleep apnoea, endometrial health and psychological wellbeing.

This does not mean that somebody with PMOS will inevitably develop these conditions. But it does mean there are good reasons to think beyond reproductive symptoms and look at the whole person.

What can we do about it?
There is no single PMOS diet, and current evidence does not show that everyone with PMOS needs to follow one particular dietary pattern.

Instead, nutrition and lifestyle strategies should be individualised.

Depending on the person, priorities might include improving overall diet quality, supporting healthy glucose and insulin regulation, eating adequate protein and fibre, incorporating a diverse range of plant foods, moving regularly, including resistance exercise, improving sleep and addressing chronic stress.

And importantly, the international guideline recognises that healthy lifestyle changes can produce benefits even without weight loss.