🔔 Official Name Change · The Lancet · May 2026

Polyendocrine Metabolic
Ovarian Syndrome

Formerly known as Polycystic Ovary Syndrome (PCOS) · New acronym: PMOS
1 in 8
women affected worldwide
Neven et al., Hum Reprod Update 2026
170M+
individuals during reproductive years
Teede et al., The Lancet 2026
~70%
remain undiagnosed globally
March et al., Hum Reprod 2010
14,360
survey responses driving this consensus
Teede et al., The Lancet 2026
Published May 12, 2026 in The Lancet: Following a rigorous, multi-step global consensus process involving 14,360 survey respondents from all world regions and 56 organizations, the condition previously named polycystic ovary syndrome (PCOS) has been officially renamed polyendocrine metabolic ovarian syndrome (PMOS). A 3-year transition period is now under way.
What Changed — and Why It Matters
❌ Old Name (retiring)
PCOS
Polycystic Ovary Syndrome
Implies pathological ovarian cysts — which are not a feature. Ovarian-centric framing obscures multisystem endocrine and metabolic pathophysiology. Contributes to delayed diagnosis and stigma.
✅ New Name (2026)
PMOS
Polyendocrine Metabolic Ovarian Syndrome
Accurately reflects: multiple interacting endocrine abnormalities (polyendocrine), insulin resistance and cardiometabolic burden (metabolic), and ovarian dysfunction in folliculogenesis and steroidogenesis (ovarian).
For clinical practice now: During the 3-year transition period, both PCOS and PMOS are acceptable. ICD coding changes and guideline updates are in progress. The 2028 update of the International Guidelines (used in 195 countries) will formally incorporate the new name.
Why Previous Renaming Efforts Failed

Prior attempts to rename PCOS stalled due to lack of inclusive global leadership, absence of coordinated international consensus, misalignment between patient advocacy groups, no agreed alternative, and no implementation strategy. This 2026 process was the first to address all five barriers simultaneously — securing dedicated funding, governance across 56 organizations, iterative Delphi methods, nominal group technique workshops across world regions, and a co-designed implementation roadmap.

Big news in women's health: The medical condition called "polycystic ovary syndrome" or PCOS has been officially renamed. Its new name is polyendocrine metabolic ovarian syndrome, or PMOS. Doctors around the world agreed to make this change in 2026.
Why was the name changed?

The old name "polycystic ovary syndrome" was misleading. The word "polycystic" makes it sound like you have cysts on your ovaries — but most women with this condition do not have harmful cysts. The old name made it seem like only the ovaries were affected, when in fact this condition affects the whole body — including hormones, metabolism, heart health, and mental wellbeing.

The new name — PMOS — is more accurate. It describes a condition involving many hormones (polyendocrine), the way your body processes energy (metabolic), and how your ovaries work (ovarian).

Does my diagnosis change?

No. If you were diagnosed with PCOS, you now have PMOS. Same condition, better name. Your treatment plan, medications, and care do not change because of the renaming. Talk to your doctor if you have questions about what this means for you specifically.

Did you know? Up to 70% of people with PMOS are never diagnosed. If you have irregular periods, unwanted hair growth, acne, difficulty losing weight, or difficulty getting pregnant — ask your doctor about being tested.
The Global Consensus Process 56 organizations · 14,360 survey respondents · All world regions
2012
US National Institutes of Health Evidence-based Methodology Workshop first formally highlighted inaccuracy of the PCOS name and recommended a change. Prior advocacy efforts had repeatedly stalled.
2017 & 2023
Serial longitudinal surveys conducted by Teede et al. (EClinicalMedicine 2025). Overall 84% of respondents endorsed a global consensus process to identify and implement a new name. Accompanying impact assessment found benefits of renaming outweighed risks.
September 2024
Funding secured. Australian National Health and Medical Research Council awarded resources to the Centre for Research Excellence in Women's Health in Reproductive Life. Leadership also provided by the Androgen Excess and PCOS Society and Verity (UK patient charity).
December 2024
Governance established. International steering group formed. 56 academic, clinical, and patient organizations engaged across all world regions. International PCOS Guideline Network recruited as foundation.
April – October 2025
Survey A launched. 9,358 people with PCOS and 3,656 health professionals responded. Available in English, Chinese, German, Persian, and Malay via Qualtrics, Google Forms, and WeChat. Principles, naming approaches, and key terms identified. 86% of patients and 71% of health professionals favored adopting a new accurate symptom-based name.
November 2025
Workshop A. 90 attendees from all world regions. Modified nominal group technique. Breakout groups preassigned for balanced representation. Preferred terms: endocrine, metabolic. "Ovulatory" preferred over "reproductive" (less stigmatizing). "Endocrine metabolic ovulatory syndrome" initially top-ranked but rejected due to cultural overlap with "emo" subculture; acronym EMOS problematic.
December 2025
Marketing analysis. Pro bono assessment from global marketing agency using AI tools. Recommendation: evolutionary rebranding (continuity with existing acronym) rather than revolutionary (implies new condition). "Polyendocrine" selected in part because it shares first letter with PCOS.
January 20–31, 2026
Survey B. 1,346 responses (49% response rate). Polyendocrine metabolic ovarian syndrome ranked first at 66% (patients 69%, health professionals 57%). "Ovarian" supported by 62% of patients and 67% of health professionals on prior surveys.
February 2026
Workshop B consensus. Workshop B revised top survey name to polyendocrine metabolic ovarian syndrome. All participants supported the new name (2 dissenting, same 2 who opposed any name change). Final consensus achieved.
May 12, 2026
Published in The Lancet. Health Policy article by Teede, Bahri Khomami, Morman et al. Implementation strategy now active. 3-year transition period begins.
Guiding Principles (per panel 3 of the source publication): Scientific/medical accuracy · Ease of communication · Avoidance of stigma (especially fertility-linked terms in culturally sensitive regions) · Cultural and linguistic appropriateness · Feasibility of implementation
How was the new name chosen?

This wasn't a decision made by a small group of doctors. It was a worldwide effort that started years ago and involved over 14,000 people — including women living with the condition and doctors from dozens of countries.

People answered surveys about what the name should communicate, what stigma they wanted to avoid, and what would be most helpful. They held workshops across the world. They consulted branding experts. They tested dozens of possible names. The goal was a name that was scientifically accurate, easy to understand, and didn't cause additional shame or confusion.

What does the new name mean?

Poly-endocrine: "Many hormones." This condition involves several hormones that are out of balance — not just one.

Metabolic: Affects how your body processes energy, blood sugar, and fat. Insulin resistance is central.

Ovarian: The ovaries are still involved — but the word "cysts" has been removed because most people don't actually have harmful cysts.

Women helped lead this change. Patient organizations — including Verity, a UK advocacy group — were involved at every step: from designing the surveys to sitting on the international steering committee.
Diagnostic Criteria for PMOS Based on 2023 International Evidence-Based Guidelines — Rotterdam-derived framework
Diagnosis requires exclusion of other disorders first, then the presence of at least 2 of 3 criteria in adults (age ≥20 years). Adolescents (age 10–19 years) require criteria 1 AND 2 (both must be present).
1
Oligo-Anovulation

Irregular or absent menstrual cycles reflecting disordered ovulation. In clinical practice: cycles <21 days or >35 days, or fewer than 8 cycles per year. In adolescents, irregular cycles are normative in the first 2 years post-menarche — caution required.

2
Clinical or Biochemical Hyperandrogenism

Clinical: Hirsutism (modified Ferriman-Gallwey score), acne, androgenic alopecia.

Biochemical: Elevated calculated free testosterone or total testosterone (mass spectrometry preferred). DHEAS and androstenedione may supplement. Note ethnic variation in hirsutism cut-offs (Bizuneh et al., 2025).

3
Polycystic Ovarian Morphology or Elevated AMH

Ultrasound: ≥20 follicles per ovary (2–9mm) on transvaginal US (updated threshold from 2023 guidelines), or ovarian volume >10 mL in at least one ovary, excluding dominant follicle/cyst.

AMH: Now included in adult diagnostic criteria per 2023 guidelines. Threshold varies by assay and age. (van der Ham et al., Fertil Steril 2024)

Exclusion First

Before diagnosis, exclude: thyroid dysfunction (TSH), hyperprolactinemia (prolactin), congenital adrenal hyperplasia (17-OHP), Cushing syndrome, androgen-secreting neoplasm. Consider premature ovarian insufficiency if relevant.

Adolescent Diagnosis — Different Standard

In adolescents (age 10–19 years), both criteria 1 and 2 must be present. Polycystic ovarian morphology alone is not sufficient for diagnosis in this age group, as multi-follicular ovaries are common in adolescence and AMH data in this population is less definitive. The 2023 International Guidelines provide specific thresholds for adolescent assessment. (Peña et al., BMC Med 2025)

The "Polycystic" Misnomer — Now Formally Corrected

Multiple studies have confirmed that pathological ovarian cysts are not increased in PMOS compared to controls. (Piltonen et al., JAMA Intern Med 2026; Pea et al., Hum Reprod Update 2024). The classic ultrasonographic appearance reflects arrested follicular development (small antral follicles, 2–9mm), not true cysts. This distinction is clinically important in patient counseling and has been a primary driver of the name change.

How Is PMOS Diagnosed?
Your doctor will first rule out other conditions that can cause similar symptoms. Then they look for at least 2 of these 3 signs.
Sign 1: Irregular Periods

Periods that come less than every 21 days, more than every 35 days, or fewer than 8 times a year. This happens because the ovaries aren't releasing eggs regularly.

Sign 2: High Androgen Hormones

Androgens are often called "male hormones," but women produce them too — just in smaller amounts. With PMOS, these levels are higher than normal. This can cause: extra hair growth on the face, chest, or back; acne; or hair thinning on the scalp. Your doctor can also measure this with a blood test.

Sign 3: Ovary Appearance or AMH Level

An ultrasound may show many small follicles in your ovaries. Note: these are not dangerous cysts — they are small fluid-filled sacs that are part of the normal process but aren't developing fully. Alternatively, a blood test called AMH (anti-Müllerian hormone) can show elevated levels.

Important for teenagers: In girls under 20, doctors need to be more careful. Irregular periods and some ovarian changes are normal in the first couple of years after your first period. A diagnosis in adolescence requires irregular periods and signs of high androgens together.
Multisystem Features of PMOS Source: Teede et al., The Lancet 2026; 2023 International Guidelines; cited studies below
Metabolic
  • Insulin resistance (85% of all PMOS; 75% of lean individuals)
  • Impaired glucose tolerance / type 2 diabetes
  • Gestational diabetes
  • Dyslipidemia
  • Hypertension
  • Metabolic dysfunction-associated steatotic liver disease (MASLD)
  • Central adiposity (Mendelian randomization: causal relationship)
  • Sleep apnea
🌸
Reproductive
  • Ovulatory dysfunction
  • Irregular menstrual cycles
  • Subfertility / infertility
  • Pregnancy complications (preeclampsia, GDM, preterm birth)
  • Endometrial cancer (unopposed estrogen from anovulation)
  • Elevated AMH (disordered folliculogenesis)
🧠
Psychological
  • Depression
  • Anxiety
  • Eating disorders
  • Reduced quality of life
  • Distress linked to condition name itself
  • Stigma, particularly in fertility-focused cultures
Dermatological
  • Hirsutism (androgen-driven terminal hair growth)
  • Acne (often adult-onset)
  • Androgenic alopecia
  • Ethnic variation in hirsutism expression
Cardiovascular Disease Risk in PMOS

Source: Tay et al., J Am Heart Assoc 2024 — predominantly premenopausal women. Odds ratios vs. controls without PMOS.

OR 1.68
Composite cardiovascular disease
Tay et al., J Am Heart Assoc 2024;13:e033572
OR 2.50
Myocardial infarction
Tay et al., J Am Heart Assoc 2024;13:e033572
OR 1.71
Stroke
Tay et al., J Am Heart Assoc 2024;13:e033572
These odds ratios apply to predominantly premenopausal women. Cardiometabolic surveillance should begin at diagnosis, not deferred until perimenopause.
What this means for you: PMOS is not just about periods or fertility. It affects your whole body. Regular checkups for blood sugar, blood pressure, and cholesterol are an important part of your care — even if you feel well right now. Ask your doctor which screenings are right for you.
Pathophysiology — Why "Polyendocrine"? Justification for the new name from the biological evidence base
PMOS involves multiple interacting endocrine systems — not an isolated ovarian disorder. This is the scientific rationale for "polyendocrine" in the new name.
Hyperandrogenism is the central diagnostic and pathological endocrine feature. Elevated ovarian androgens — and often adrenal androgens — contribute to hirsutism, acne, alopecia, and metabolic dysfunction. Hyperandrogenemia arises from both theca cell overproduction and impaired sex hormone-binding globulin (SHBG) production due to insulin resistance. (Azziz et al., Nat Rev Dis Primers 2016; Stener-Victorin et al., Nat Rev Dis Primers 2024)
Increased GnRH pulsatility leads to elevated LH relative to FSH. This drives excessive ovarian androgen secretion from theca cells while impairing follicle-stimulating hormone-dependent follicular maturation — producing the classic arrested folliculogenesis pattern. This is a central (hypothalamic) as well as ovarian abnormality.
Insulin resistance is present in ~85% of individuals with PMOS (75% of lean women with BMI ≤25 kg/m²), confirmed by euglycaemic-hyperinsulinaemic clamp studies (Cassar et al., Hum Reprod 2016; Stepto et al., Hum Reprod 2013). Compensatory hyperinsulinaemia amplifies ovarian androgen secretion by acting synergistically with LH on theca cells, suppressing hepatic SHBG production, and disrupting steroidogenesis. This metabolic–endocrine interplay is central to PMOS pathophysiology and justifies the "metabolic" component of the new name.
Ovarian dysfunction in PMOS involves intrinsic abnormalities in granulosa and theca cell function, exacerbated by hyperinsulinaemia-driven dysregulation. These disrupt folliculogenesis, causing accumulation of small antral follicles (the classic ultrasound appearance). Elevated AMH — produced by antral follicles — reflects disordered follicular maturation and is now included in adult diagnostic criteria (van der Ham et al., Fertil Steril 2024). These disturbances manifest clinically as ovulatory dysfunction, menstrual irregularity, and subfertility.
Meta-analyses of large-scale genomic analyses confirm that PMOS has polygenic origins spanning neuroendocrine, metabolic, and reproductive pathways (Hiam et al., J Clin Med 2019; Zhao et al., Nat Genet 2025). This polygenic, multi-system architecture is further evidence against reducing the condition to an ovarian disorder. Genetic susceptibility loci include regions implicated in insulin signaling, LH receptor function, and androgen biosynthesis.
Altered adipokine signaling (adiponectin, leptin), gut-hormone interactions, and sympathetic nervous system dysfunction contribute to the metabolic and reproductive manifestations of PMOS (Shorakae et al., Clin Endocrinol 2018). Low-grade chronic inflammation amplifies insulin resistance and androgen excess. These additional hormonal and metabolic interactions reinforce the "polyendocrine" framing — no single endocrine axis explains the full phenotype.
Bottom line: PMOS is a condition of interacting endocrine, metabolic, and ovarian dysfunction with polygenic origins. Psychological and dermatological features are largely downstream of the endocrine disturbances. The new name — polyendocrine metabolic ovarian syndrome — accurately encodes this multi-system biology.
Understanding PMOS in Your Body
It starts with hormones — many of them

PMOS involves several hormones that are out of balance at the same time. Your brain sends too many signals to your ovaries, causing them to produce too many androgens ("male-type" hormones). Your body also has trouble using insulin properly (called insulin resistance), which makes the hormone imbalance worse.

What does insulin resistance mean for me?

Insulin is the hormone that helps your body use sugar for energy. In PMOS, your cells don't respond to insulin as well as they should, so your body produces extra insulin to compensate. This extra insulin makes your ovaries produce even more androgens — so the two problems feed each other. It also raises your long-term risk for type 2 diabetes.

Insulin resistance is present in about 8 out of 10 people with PMOS — including many lean people. It is not caused by lack of willpower or poor lifestyle choices.

Can PMOS be treated? Yes. Diet, exercise, medications (like metformin), and in some cases weight management interventions can significantly improve symptoms and reduce health risks. Ask your doctor which approach is right for you.
Global Implementation Strategy 8-stage roadmap · 3-year transition period · 2028 Guideline update
During the transition period (2026–2029): Both PCOS and PMOS are acceptable terminology. ICD code changes are in progress via engagement with WHO. The 2028 International Guidelines update (used in 195 countries) will formally incorporate the new name. Electronic health record vendors are being engaged for SNOMED-CT updates.
01
Publication & Academic Dissemination
This Health Policy paper in The Lancet (May 2026), supported by accompanying editorials, clinical reviews, and textbook/educational material updates.
02
Resource Development
Co-design of multilingual patient and clinician resources across platforms and delivery modes.
03
Global Communication
Society toolkits, multimedia dissemination, professional education programs, coordinated events worldwide.
04
Health System Integration
SNOMED-CT integration, EHR vendor engagement, university and textbook publisher education.
05
Policy & Research Alignment
Governments, research funders, journal editors, regulators, and pharmaceutical industry engaged to update research classifications and funding systems.
06
ICD / WHO Classification
Formal WHO engagement for ICD code update. Global classification alignment across health systems.
07
3-Year Transition
Managed transition 2026–2029 with monitoring and evaluation. Consideration of emerging evidence on phenotypic subtypes. Refinement as understanding evolves.
08
International Guidelines 2028
Integration into the International Guideline used in 195 countries — next update scheduled 2028. Full formal adoption at that point.
What Should Clinicians Do Now?
  • Begin introducing PMOS alongside PCOS in patient conversations and documentation
  • Use the transition period to update patient education materials
  • Be prepared to explain the name change — many patients will encounter it from media before their clinician does
  • Diagnostic criteria are unchanged; clinical management is unchanged
  • Cardiovascular risk assessment and metabolic surveillance remain critical at diagnosis
  • Watch for ICD-10/11 code transition guidance from your health system
What happens now?

The name change is official as of May 2026. But it will take up to 3 years for everything to catch up — medical records, drug labels, insurance codes, and textbooks all need updating. During this time, doctors may still use "PCOS" — both names are correct for now.

What should I tell my doctor?

You can simply say: "I've been diagnosed with PCOS, which is now also called PMOS." Your medical history, diagnosis, and treatment remain the same. Nothing about your care changes because of the name.

Your voice matters. More than 10,000 people with PCOS/PMOS were part of the surveys that led to this name change. This is one of the first times patients drove a major shift in how a medical condition is classified worldwide.
Source Publications Vancouver format · All citations verified against published sources
1. Teede HJ, Bahri Khomami M, Morman R, et al. Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: a multistep global consensus process. Lancet. 2026; Published online May 12. doi:10.1016/S0140-6736(26)00717-8 The LancetMay 2026Primary
Full consensus process, survey data (n=14,360), workshop methodology, and implementation strategy. Basis for name change content throughout this tool.
2. Teede HJ, Tay CT, Laven JJE, et al; International PCOS Network. Recommendations from the 2023 international evidence-based guideline for the assessment and management of polycystic ovary syndrome. Eur J Endocrinol. 2023;189:G43–64.
International diagnostic criteria and management framework; basis for Diagnosis tab content.
3. Neven ACH, Forslund M, Ranasinha S, et al. Prevalence of polycystic ovary syndrome: a global and regional systematic review and meta-analysis. Hum Reprod Update. 2026; published online Jan 13. doi:10.1093/humupd/dmaf030
Source for "1 in 8 women" global prevalence figure.
4. Tay CT, Mousa A, Vyas A, Pattuwage L, Tehrani FR, Teede H. 2023 international evidence-based polycystic ovary syndrome guideline update: insights from a systematic review and meta-analysis on elevated clinical cardiovascular disease in polycystic ovary syndrome. J Am Heart Assoc. 2024;13:e033572.
CVD odds ratios (composite CVD OR 1.68; MI OR 2.50; stroke OR 1.71) cited in Clinical Features tab.
5. Peña AS, Witchel SF, Boivin J, et al. International evidence-based recommendations for polycystic ovary syndrome in adolescents. BMC Med. 2025;23:151.
Adolescent-specific diagnostic criteria referenced in Diagnosis tab.
6. Stener-Victorin E, Teede H, Norman RJ, et al. Polycystic ovary syndrome. Nat Rev Dis Primers. 2024;10:27.
Comprehensive pathophysiology review; basis for Pathophysiology tab content.
7. van der Ham K, Laven JSE, Tay CT, Mousa A, Teede H, Louwers YV. Anti-Müllerian hormone as a diagnostic biomarker for polycystic ovary syndrome and polycystic ovarian morphology: a systematic review and meta-analysis. Fertil Steril. 2024;122:727–39.
AMH as diagnostic criterion; referenced in Diagnosis tab.
8. Cassar S, Misso ML, Hopkins WG, Shaw CS, Teede HJ, Stepto NK. Insulin resistance in polycystic ovary syndrome: a systematic review and meta-analysis of euglycaemic-hyperinsulinaemic clamp studies. Hum Reprod. 2016;31:2619–31.
Insulin resistance prevalence data (85% overall, 75% lean) cited in Pathophysiology tab.
9. Piltonen T, Kuusiniemi E, Teede HJ. Ovarian cysts in polycystic ovary syndrome. JAMA Intern Med. 2026; published online May 11. doi:10.1001/jamainternmed.2026.1370
Confirms pathological ovarian cysts are not increased in PMOS; basis for the "polycystic misnomer" discussion.
10. March WA, Moore VM, Willson KJ, Phillips DI, Norman RJ, Davies MJ. The prevalence of polycystic ovary syndrome in a community sample assessed under contrasting diagnostic criteria. Hum Reprod. 2010;25:544–51.
Source for ~70% undiagnosed statistic cited in hero section.
11. Teede HJ, Moran LJ, Morman R, et al. Polycystic ovary syndrome perspectives from patients and health professionals on clinical features, current name, and renaming: a longitudinal international online survey. EClinicalMedicine. 2025;84:103287.
Prior longitudinal survey showing 84% support for global consensus renaming process.
12. Zhao H, Xu Y, Xue B, et al. Multi-ancestry genome-wide association analyses of polycystic ovary syndrome. Nat Genet. 2025;57:2669–81.
Polygenic architecture of PMOS; referenced in Pathophysiology tab.
All data displayed in this tool are sourced from the publications above. No values have been extrapolated beyond published findings. See footer for abbreviated citation. This tool does not replace clinical judgment.