PCOS Is Being Renamed PMOS — What This Means for Patients

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For decades, millions of women have been diagnosed with Polycystic Ovary Syndrome — a name that carries with it a set of deeply misleading implications. The word "cysts" causes immediate alarm when there are no cysts involved. The word "ovary" implies the problem is confined to the reproductive organs when it is, in fact, a whole-body metabolic disorder. And the word "syndrome" has long obscured the condition's complexity, severity, and lifelong consequences. A landmark 2023 international consensus process led by the European Society of Human Reproduction and Embryology (ESHRE) has formally proposed renaming the condition to PMOS — Polycystic Morphology Ovary Syndrome. This article explains what the name change means, why it matters, how the diagnostic criteria have been updated, and what it changes about clinical management and patient experience.

Why the Old Name Was Always a Problem

The term "Polycystic Ovary Syndrome" has been in use since 1935, when Stein and Leventhal described a group of women with enlarged, cystic-appearing ovaries, irregular periods, and signs of androgen excess. The name stuck. For 90 years, clinicians and patients alike have used it — even as the medical understanding of the condition evolved far beyond what the original name suggested.

The fundamental problem is that PCOS is not a disease of cysts. What appears on ultrasound as polycystic morphology is not the presence of true ovarian cysts — fluid-filled sacs with a wall and contents. Instead, what is seen is an unusually large number of small antral follicles, each containing a developing egg that has failed to reach full maturity and ovulate. These follicles are the result of a disrupted hormonal environment, not cyst formation. They are a consequence of the condition, not its cause.

Furthermore, the ovaries are not even the primary site of pathology. The condition is rooted in insulin resistance and androgen excess — metabolic abnormalities that affect the liver, adipose tissue, skeletal muscle, the adrenal glands, and the hypothalamic-pituitary axis. Calling it an ovarian syndrome is akin to calling type 2 diabetes a "pancreatic syndrome" — technically touching on one organ involved, while missing the systemic nature of the disorder entirely.

The ESHRE 2023 Consensus: What Actually Changed

In 2023, ESHRE published an updated international evidence-based guideline on PCOS/PMOS, representing the work of over 80 international experts across endocrinology, reproductive medicine, general practice, psychology, and patient advocacy. This was the most comprehensive update to PCOS guidelines in over a decade, and it proposed several significant changes.

The Name: PMOS vs PCOS

The consensus favoured renaming the condition to Polycystic Morphology Ovary Syndrome (PMOS). The key word substitution — from "cystic" to "morphology" — is deliberate and meaningful. "Morphology" describes the appearance or form of the ovaries on ultrasound, without implying pathological cyst formation. It accurately reflects that the ovarian appearance is a feature of the condition, not its underlying cause. The word "syndrome" is retained because the condition remains a cluster of features rather than a single disease with a single aetiology.

It is important to note that at the time of writing, "PMOS" remains a proposed nomenclature within the specialist community. Clinical guidelines in Ireland and the UK continue to use "PCOS" in their official documentation, and healthcare providers are transitioning the language gradually. Patients should not be alarmed if their GP or a different specialist still uses "PCOS" — the underlying condition, its management, and its implications remain the same.

Updated Ultrasound Diagnostic Threshold: The Single Most Important Change

The ESHRE 2023 guideline introduced a critical change to the ultrasound criterion for diagnosing polycystic ovarian morphology. The old threshold, established in the 2003 Rotterdam consensus, defined PCOM as ≥12 follicles (2–9 mm diameter) per ovary, or ovarian volume ≥10 ml. This threshold was set in an era of lower-resolution ultrasound technology.

Modern high-frequency transvaginal probes can now identify significantly more follicles than earlier equipment. Using the old threshold of ≥12 follicles with a contemporary probe would lead to massive over-diagnosis — many women with normal ovarian morphology would be labelled as having PCOM. The 2023 guideline therefore updated the follicle count threshold to:

This update means that some women who were previously diagnosed with PCOS based on polycystic morphology alone — using older equipment and the ≥12 follicle threshold — may no longer meet the revised ultrasound criterion. However, the diagnosis of PMOS requires only 2 of the 3 Rotterdam criteria; polycystic ovarian morphology on ultrasound is just one element. Women with clinical or biochemical hyperandrogenism and irregular cycles retain their diagnosis regardless of the updated ultrasound threshold.

The Three Diagnostic Criteria: Rotterdam Retained

The 2023 guideline retains the foundational Rotterdam 2-of-3 diagnostic framework but refines how each criterion is applied. A diagnosis of PMOS requires the presence of at least two of the following three features, after exclusion of other causes:

Criterion	How It Is Assessed (2023 Update)
Oligo/anovulation (irregular or absent ovulation)	Menstrual cycles <21 days or >35 days, or fewer than 8 cycles per year. In the first year following menarche, cycle irregularity is normal and should not be used diagnostically. In perimenopause, cycle variability alone is insufficient.
Clinical or biochemical hyperandrogenism	Clinical: hirsutism (modified Ferriman-Gallwey score ≥4–6 depending on ethnicity), acne (moderate-severe), or androgenic alopecia. Biochemical: elevated total or free testosterone; DHEAS; androstenedione. LC-MS/MS is the preferred assay. SHBG should be measured to calculate free androgen index (FAI = total T × 100 / SHBG).
Polycystic ovarian morphology (PCOM)	≥20 follicles per ovary (high-resolution probe ≥8 MHz) or ovarian volume ≥10 ml per ovary. AMH (anti-Müllerian hormone) may support PCOM diagnosis but is not yet a standalone criterion.

Conditions that must be excluded before diagnosing PMOS include: congenital adrenal hyperplasia (17-OHP), thyroid dysfunction (TSH), hyperprolactinaemia (prolactin), Cushing's syndrome (if clinically suspected), and androgen-secreting tumours (if testosterone is markedly elevated, typically >5 nmol/L).

The Four Phenotypes: Not All PMOS Is the Same

One of the most clinically important but commonly overlooked aspects of PMOS is that it is phenotypically heterogeneous. Based on which of the three Rotterdam criteria are present, four distinct phenotypes are recognised. The phenotype significantly influences metabolic risk and guides the intensity of screening and intervention.

Phenotype	Features Present	Metabolic Risk
A (Classic)	Hyperandrogenism + Anovulation + PCOM	Highest. Insulin resistance, dyslipidaemia, elevated cardiovascular risk.
B	Hyperandrogenism + Anovulation (no PCOM)	High. Similar metabolic profile to Phenotype A.
C	Hyperandrogenism + PCOM (regular cycles)	Intermediate. Androgen excess is present but ovulatory function maintained.
D (Non-androgenic)	Anovulation + PCOM (no hyperandrogenism)	Lower but not absent. Important: metabolic screening still warranted.

This phenotypic classification has direct implications for management. A woman with Phenotype A should be screened more aggressively for insulin resistance, prediabetes, dyslipidaemia, and cardiovascular risk factors than a woman with Phenotype D. Treating all PMOS patients identically is a clinical error.

The Metabolic Reality of PMOS

One of the most important shifts in the 2023 guidelines is the explicit recognition that PMOS is primarily a metabolic condition, not simply a reproductive one. This reframing has profound implications for how the condition is managed across a patient's lifetime — well beyond the reproductive years.

Insulin Resistance: The Central Pathology

Insulin resistance is present in approximately 70–80% of women with PMOS, irrespective of BMI. In the hyperinsulinaemic state that follows, the ovaries — uniquely sensitive to insulin — produce excess androgens. The liver responds by reducing its production of sex hormone-binding globulin (SHBG), which further increases free androgen bioavailability. The pituitary, under the influence of elevated androgens and disrupted negative feedback, increases LH pulse frequency, which stimulates further ovarian androgen production. This creates a self-reinforcing cycle of androgen excess, follicular arrest, and anovulation.

The key clinical implication: treating insulin resistance is treating the root of PMOS. Lifestyle interventions, metformin, and — increasingly — GLP-1 receptor agonists all work in part by improving insulin sensitivity.

Long-Term Metabolic Risks

Women with PMOS face substantially elevated lifetime risks across several domains:

• Type 2 diabetes: Risk 5–10× higher than age-matched controls. Approximately 10% of women with PMOS have impaired glucose tolerance at the time of diagnosis, even if BMI is normal. ESHRE 2023 recommends an oral glucose tolerance test (OGTT) or HbA1c at diagnosis, with repeat testing every 1–3 years.
• Gestational diabetes: Risk 2–3× higher during pregnancy, with implications for both maternal and foetal outcomes.
• Cardiovascular disease: Risk of hypertension, dyslipidaemia, and non-alcoholic fatty liver disease (NAFLD) is elevated. Atherosclerotic cardiovascular events may be increased, though the independent contribution of PMOS beyond classical risk factors remains under investigation.
• Endometrial cancer: Chronic anovulation leads to unopposed oestrogen stimulation of the endometrium. Women with fewer than 4 periods per year should receive progestogen exposure (either via cyclical progesterone, the combined oral contraceptive pill, or the levonorgestrel-releasing IUS) to reduce endometrial cancer risk.
• Obstructive sleep apnoea: Prevalence is 5–10× higher than in women without PMOS, driven by central adiposity, insulin resistance, and androgen excess effects on upper airway musculature. Sleep symptoms should be actively enquired about.
• Non-alcoholic fatty liver disease (NAFLD/MASLD): Insulin resistance and androgen excess independently promote hepatic lipid accumulation. Liver function tests and, in high-risk patients, hepatic ultrasound assessment should be considered.

Mental Health: The Under-Recognised Burden

The 2023 guideline places unprecedented emphasis on mental health screening as a mandatory component of PMOS assessment. Women with PMOS have a 3–4× increased risk of depression and anxiety compared to women without the condition. This excess is driven by multiple factors: the symptom burden (hirsutism, acne, weight gain, irregular periods), the impact of infertility concerns, the history of delayed or incorrect diagnoses, and possibly neurobiological effects of androgen excess and insulin resistance on the central nervous system.

Body dysmorphia, disordered eating, and binge eating disorder are also over-represented in PMOS and can be profoundly worsened by clinical approaches that focus exclusively on weight loss without addressing psychological wellbeing.

Treatment in the PMOS Era

The ESHRE 2023 guideline provides an updated evidence hierarchy for treatment. The key shift is from a reproductive-centric model ("manage the periods and help with fertility") to a comprehensive metabolic management model that addresses weight, insulin resistance, cardiovascular risk, and mental health as primary treatment targets — not secondary afterthoughts.

Lifestyle Intervention: Still First-Line

A sustained weight loss of 5–10% of body weight in women with overweight or obesity reduces androgen levels, restores ovulatory function in a significant proportion, improves insulin sensitivity, and reduces cardiovascular risk. This degree of weight loss is the single most effective intervention available for PMOS in women with excess weight, yet it is also the most difficult to achieve and maintain without clinical support.

The 2023 guideline emphasises that lifestyle advice must be delivered in a non-stigmatising, individualised way that acknowledges the physiological barriers to weight loss in PMOS. Women with PMOS have intrinsically higher appetite-driving signals, lower basal metabolic rates relative to fat mass, and greater difficulty with weight maintenance compared to women without the condition — even at equivalent caloric intake. Telling a patient simply to "eat less and exercise more" is both clinically insufficient and psychologically harmful.

Strength and resistance training is particularly beneficial in PMOS: it builds metabolically active muscle mass, improves insulin sensitivity at the muscular level, and reduces visceral adiposity without the hormonal consequences of extreme caloric restriction.

Metformin: Broader Indications

Metformin is recommended by ESHRE 2023 for metabolic and reproductive benefits in PMOS regardless of BMI. Its primary mechanism is reducing hepatic glucose output and improving peripheral insulin sensitivity. In PMOS specifically:

• Improves menstrual regularity in 40–50% of patients
• Reduces free androgen levels by increasing SHBG
• Reduces progression from impaired glucose tolerance to type 2 diabetes
• Improves ovulation rates (augments response to letrozole for ovulation induction)
• Reduces miscarriage rates in women with PMOS who conceive (meta-analysis data)
• Reduces gestational diabetes risk when continued into pregnancy in high-risk women

Standard dosing begins at 500 mg once daily with evening meal, increasing weekly to a target of 1500–2000 mg daily in divided doses. Gastrointestinal side effects (nausea, diarrhoea) are common at initiation and largely resolve with gradual dose escalation and food co-administration. The slow-release (XR) formulation is significantly better tolerated and is preferred in patients with gastrointestinal sensitivity. Metformin requires normal renal function (eGFR >45 ml/min/1.73m²) and annual monitoring of B12, as prolonged use can deplete B12 stores.

GLP-1 Receptor Agonists: Emerging Evidence in PMOS

GLP-1 receptor agonists — semaglutide (Ozempic/Wegovy) and liraglutide (Victoza/Saxenda) — are generating significant interest in PMOS management. Their role is not yet established in formal guidelines as a first-line PMOS treatment, but the evidence base is rapidly expanding.

In women with PMOS and overweight or obesity, GLP-1 RAs produce substantially greater weight loss than lifestyle intervention or metformin alone. The SELECT trial (2023) demonstrated 17.4% mean weight loss with semaglutide 2.4 mg weekly versus placebo over 68 weeks in non-diabetic individuals with overweight and cardiovascular disease — a degree of weight loss not previously achievable without bariatric surgery. Early PMOS-specific trials show improvements in menstrual regularity, androgen levels, and markers of insulin resistance with GLP-1 RA treatment, though larger randomised controlled trials specifically in PMOS populations are ongoing. SURMOUNT-1, 2023

In clinical practice, GLP-1 RAs should be considered in women with PMOS and:

• BMI ≥30 kg/m² (or ≥27 with metabolic complications) when lifestyle intervention and metformin have been insufficient
• Type 2 diabetes or prediabetes — particularly when glycaemic control is suboptimal
• Established cardiovascular disease or high cardiovascular risk
• Persistent anovulation and desire for pregnancy (though cessation 2 months before conception is recommended given limited safety data in the first trimester)

Inositol: An Evidence-Based Supplement

Inositol — specifically the combination of myo-inositol and D-chiro-inositol in a 40:1 ratio — has a growing evidence base in PMOS. Inositols are insulin second-messengers; reduced inositol signalling contributes to insulin resistance and impaired follicular development in PMOS. Supplementation at doses of 2–4 g myo-inositol daily has been shown in multiple randomised controlled trials to:

• Improve insulin sensitivity comparably to metformin in some studies
• Reduce free testosterone and increase SHBG
• Improve menstrual regularity
• Improve oocyte quality in women undergoing IVF
• Reduce gestational diabetes risk in high-risk pregnancies

Inositol is not a licensed medication and is classified as a food supplement in Ireland and the UK. It is not yet included in ESHRE 2023 as a formal treatment recommendation, but is acknowledged as having a favourable safety profile and may be considered as an adjunct to lifestyle intervention, particularly in women who do not tolerate metformin or who prefer not to take prescription medications initially.

Combined Oral Contraceptive Pill (COCP): Updated Guidance

The COCP remains a first-line pharmacological option for women with PMOS who require contraception, menstrual cycle regulation, or management of androgenic symptoms (hirsutism, acne). It acts by:

• Suppressing LH-driven ovarian androgen production
• Increasing hepatic SHBG synthesis (reducing free androgen availability)
• Providing regular withdrawal bleeds (protecting endometrial lining)
• Providing reliable contraception

The ESHRE 2023 guideline emphasises that COCP choice matters in PMOS. Pills containing anti-androgenic progestogens — drospirenone (Yasmin, Eloine), cyproterone acetate (co-cyprindiol/Dianette), or dienogest — are preferable to pills with androgenic progestogens such as levonorgestrel or norethisterone, which can partially negate the androgen-lowering benefit and may worsen acne and hirsutism. Drospirenone-containing pills offer the additional benefit of anti-mineralocorticoid activity, which may reduce bloating and fluid retention.

Women should understand that the COCP manages symptoms but does not treat the underlying metabolic pathology. It masks menstrual irregularity and androgen excess, but insulin resistance and its consequences persist and require independent metabolic management.

Ovulation Induction: Letrozole as Preferred Agent

For women with PMOS who wish to conceive and are anovulatory, ovulation induction is required. The 2023 guideline unambiguously positions letrozole (an aromatase inhibitor) as the first-line agent for ovulation induction in PMOS, superseding clomiphene citrate (clomifene). This represents a significant change from older practice.

Letrozole produces higher ovulation rates, higher live birth rates, and a lower rate of multiple pregnancy compared to clomiphene in PMOS — as demonstrated in the landmark ESPART trial and confirmed in multiple subsequent meta-analyses. Legro RS, NEJM 2014 Letrozole is administered for 5 days in the early follicular phase, with ultrasound monitoring to confirm follicular development and timing of intercourse or insemination.

Clomiphene may still be used where letrozole is unavailable or not tolerated, but it is no longer the preferred first step. Women who fail to ovulate on letrozole alone may benefit from the addition of metformin, which enhances ovulation induction response.

What Does the Rename Mean Practically for Current Patients?

If you have been diagnosed with PCOS, you do not need to do anything differently. Your diagnosis is not being invalidated; the underlying condition remains the same. The name change is a medical community process that will filter into clinical practice progressively over the coming years. What you should understand is that this rename reflects a more accurate, less stigmatising understanding of your condition — one that acknowledges:

• You do not have cysts — you have a pattern of follicle development that reflects a hormonal imbalance
• Your ovaries are not the source of the problem — they are responding to insulin resistance and androgen excess that originates in your metabolic physiology
• PMOS is a lifelong condition requiring lifelong monitoring — not a diagnosis that disappears when your periods regularise or your fertility concerns resolve
• Your mental health is as much a part of PMOS as your metabolic health — and deserves equal clinical attention
• There are effective, evidence-based treatments available that go beyond "lose weight and come back"

A Note on the Ongoing Name Debate

It is worth acknowledging that not all clinicians support "PMOS" as the correct replacement term. Some experts have advocated for entirely different names — including "Metabolic Reproductive Syndrome," "Functional Female Hyperandrogenism," or "Ovarian Androgen Excess Syndrome" — each emphasising different aspects of the condition's pathophysiology. The debate reflects genuine scientific uncertainty about which feature of the condition should define it: the ultrasound morphology, the hormonal excess, the metabolic consequence, or the reproductive impact.

What the 2023 process achieved, regardless of which name ultimately prevails, is a consensus that the term "Polycystic Ovary Syndrome" is no longer adequate — and that patients deserve a name that reflects their lived experience of a systemic, metabolic condition rather than a localised ovarian disease. That shift in clinical thinking is, in itself, clinically significant.