PCOS has a new name - here's why it matters.

As of May 2026, PCOS has a new name. A global consensus process, published in The Lancet, has formally renamed polycystic ovary syndrome to polyendocrine metabolic ovarian syndrome (PMOS) [1]. This isn't a rebrand for the sake of it. It's the result of a process that took more than a decade, drew on responses from over 14,000 patients and health professionals across every world region, and was backed by more than 50 patient and professional organisations, including the Endocrine Society [1]. When a name change takes that much scrutiny, it's worth understanding why.

Why "polycystic ovary syndrome" was retired

The old name has three real problems, and I see the fallout from all three in clinic regularly.

• It centres on ovarian cysts, which aren't actually required for diagnosis. Plenty of people with PCOS don't have ovarian cysts at all, and plenty of people with ovarian cysts don't have PCOS. The name promises something the diagnosis doesn't require - which is confusing for patients and imprecise for clinicians.

• It obscures what's actually driving the condition. "Polycystic ovary syndrome" points you toward the ovaries. But the condition is now understood to be a multisystem one - endocrine, metabolic, reproductive, dermatological, and even psychological... and the ovaries are only one part of that picture [1].

• It contributes to underdiagnosis and misdiagnosis. Up to 70% of people with the condition go undiagnosed, and a misleading name is part of why [1]. If you're not showing the "textbook" ovarian symptoms the name implies, it's easy for both patients and clinicians to look past the diagnosis entirely, even while the metabolic and endocrine features are very much present. The confusion cuts the other way too: hypothalamic amenorrhea (HA), a completely different condition covered in detail below, can produce the same missing or irregular periods as PMOS. A name built around ovaries and cysts doesn't leave much room for that distinction, so it's easy for HA to be mistaken for PMOS, or the reverse and getting it wrong means starting treatment in the wrong direction entirely.

How PMOS is diagnosed

The name has changed, but the diagnostic approach hasn't (at least not yet). The Rotterdam criteria remain the most widely used framework, and diagnosis still requires at least two of the following three [2]:

• Irregular or absent periods (a sign of ovulation dysfunction)

• Elevated androgens - either on a blood test or physical signs such as acne, excess hair growth, or hair loss

• Polycystic ovaries visible on ultrasound

Notice that ovarian cysts are only one of three criteria, and you don't need them to be diagnosed - which is exactly the mismatch the old name created. It's also essential to rule out other causes of irregular periods before landing on a PMOS diagnosis, HA being the main one — more on HA, and why it's so easily confused with PMOS, below.

An irregular cycle is a clue. It isn't a diagnosis.

What PMOS actually is

Here's the piece I think matters most: insulin resistance is present in the large majority of people with PMOS, including in around 75% of lean women (BMI ≤25) [1]. That's a detail that surprises a lot of clients. The assumption is often that insulin resistance is a "bigger body" issue, but it isn't. It's a core feature of the condition, and it's the metabolic driver, not a side effect. Insulin resistance pushes the ovaries to produce more androgens, which is what shows up as the more visible symptoms (irregular cycles, acne, hirsutism). The androgen excess is downstream of the metabolic issue, not the other way around.

This is exactly what the new name is trying to capture - "polyendocrine" and "metabolic" come before "ovarian" for a reason.

Worth flagging too: research is increasingly mapping PMOS into distinct subtypes with different underlying drivers [3], and this matches what I see in clinic - two people can both meet the diagnostic criteria and still need quite different care, depending on what's actually driving it. Broadly, the patterns we work with are:

• insulin-resistant PMOS

• post-pill PMOS

• inflammatory PMOS

• and adrenal PMOS.

We're not going to unpack each one here (that's a post of its own), but it's the reason a blanket "one-size-fits-all" approach to PMOS nutrition has never quite made sense, and why identifying which pattern (or combination) is present matters more than the label alone.

Not every irregular or absent period is PMOS.

Hypothalamic amenorrhea (HA) can produce the exact same presentation: missing or unpredictable cycles - but for the opposite underlying reason. HA happens when your body senses an energy deficit, usually from a combination of overtraining, high stress, or undereating (whether intentional or not), and responds by shutting down reproductive hormone signalling to conserve energy [4]. It's a protective mechanism, not a malfunction - but it needs addressing all the same.

Where this gets clinically important is that PMOS and HA need opposite nutrition approaches. PMOS care generally focuses on improving insulin sensitivity (which may mean tightening up your carbohydrate frequency, increasing your fibre, adequate protein and regular movement). HA care focuses on restoring energy availability - which often means more food, less exercise and stress management.

Get this backwards, and you can genuinely make things worse. Someone with HA who's told to "eat less and move more" because their symptoms look PMOS-like can deepen the very energy deficit driving their missing periods. Someone with PMOS who's told to simply "eat more to bring their period back" may see their metabolic picture worsen instead of improve. This is why working out which condition is actually present matters... not just noting that periods are irregular. That's the importance of understanding the whole picture!

The symptom can look identical. The physiology is often completely different.

Why this is a job for a dietitian, not a diet

This isn't a "clean eating" problem, and it was never going to be solved by a generic wellness plan. Telling PMOS and HA apart means reading the whole clinical picture together. This includes your cycle history, your training and stress load, your labs, your relationship with food - and matching the nutrition approach to the condition that's actually present, not the one that looks most familiar from the outside.

That's what a dietitian is trained to do: not guess from symptoms alone, but get clear on the root cause and build a tailored approach to address your needs.

Maitri Health

References:

1. Teede HJ, Bahri Khomami M, Morman R, Laven JSE, Joham AE, Costello MF, et al. Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: a multistep global consensus process. Lancet. 2026;407:2329–2339.

2. Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod. 2004;19(1):41–47.

3. Gao X, Zhao S, Du Y, Yang Z, Tian Y, Zhao J, et al. Data-driven subtypes of polycystic ovary syndrome and their association with clinical outcomes. Nat Med. 2025;31(12):4214–4224.

4. Gordon CM, Ackerman KE, Berga SL, Kaplan JR, Mastorakos G, Misra M, et al. Functional hypothalamic amenorrhea: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2017;102(5):1413–1439.