It is not often that a diagnosis gets a makeover. Following 14 years of international consultation with more than 50 patient and professional organisations and a survey involving 22,000 respondents, the condition formerly known as polycystic ovary syndrome (PCOS) has been rebranded. The new name, polyendocrine metabolic ovarian syndrome (PMOS), was announced in the Lancet in May.
While the acronym is very similar, it represents a sea-change in the way the syndrome is conceptualised. A hallmark symptom is infrequent or absent menstruation and attendant sub-fertility, which led PMOS to be traditionally considered a gynaecological problem. The old name implied there was something wrong with the ovaries, but the numerous “cysts” commonly seen are not cysts at all. They are egg-bearing follicles whose maturation has been arrested by an abnormal hormone environment. And while high levels of testosterone are another hallmark feature, causing the acne and hirsutism experienced by many patients, there are numerous hormonal irregularities that interact with one another – hence “polyendocrine”. A frequent abnormality is insulin resistance, which underlies the association of PMOS with type 2 diabetes and excess weight.
PMOS currently affects around one in ten women of reproductive age globally. It has a strong genetic basis, but why should evolution have selected them to be so prevalent? It is likely that this particular genetic profile (in both females and males) helped our ancient ancestors survive periods of famine, favouring fat deposition when calories were plentiful and a dialled-down metabolism when they were scarce. In today’s consistent, energy-dense food environment, and when lifestyles are often sedentary, that same genetic make-up now works against us.
PMOS is a complex system of interlocking hormone disturbances best thought of as a cascade, which plays out over years. It is likely to have several potential triggers. An important one seems to be the insulin spikes provoked by contemporary high-carbohydrate diets. There is also emerging evidence that disturbances in the gut microbiome, and the presence of hormonally active chemical pollutants in the environment, might also set it in motion. Once underway, the cascade can be self-fuelling and auto-amplifying.
Given these environmental factors, one would expect the condition to be becoming more common, and indeed the “Global Burden of Disease” (GBD) study suggested an estimated 60 per cent increase between 1990 and 2021. Some of that will be due to greater awareness among clinicians and the public, but there is also genuinely increased prevalence worldwide.
Intriguingly, the GBD study identified one country that is bucking the trend: rates of PMOS are falling in Italy. This may reflect concerted efforts by the Italian health system to pick up signs of the syndrome in adolescents, who are then offered intensive dietary and exercise advice, sometimes in conjunction with medication, to arrest the cascade at an early stage – a modest 5 per cent reduction in weight can be curative. The cultural normalcy of a whole-food Mediterranean diet may also be helpful.
Tackling the syndrome is important not just for current patients: there also appears to be a snowballing effect generationally. While many of us have a PMOS-type genetic profile, whether those genes become expressed depends on environmental activation (so-called epigenetics). A foetus growing in a mother with PMOS appears to become epigenetically primed to switch on their own PMOS profile.
Once thought of primarily as a reproductive issue, PMOS is properly understood as metabolic ill-health that starts playing out during the formative years. The change in name is an important step to refocus attention where it really matters, and where it has the greatest chance of doing the most good.
[Further reading: If the government isn’t careful, GPs could go the way of dentists]
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This article appears in the 17 Jun 2026 issue of the New Statesman, The Race