Dr. Jaclyn Smeaton, ND

 

A clinical review of the landmark renaming of PCOS to PMOS and why this shift reframes the condition as a whole-body endocrine and metabolic disorder requiring broader assessment and long-term care.

This article explores the recent reclassification of polycystic ovary syndrome (PCOS) to polyendocrine metabolic ovarian syndrome (PMOS) and the clinical implications of this paradigm shift. It examines the condition’s broader endocrine, metabolic, cardiovascular, and reproductive impacts while outlining how clinicians can adapt screening, counseling, and treatment strategies to better support long-term patient outcomes.

 

Introduction

On May 12, 2026, The Lancet published what may be the most consequential nomenclature shift in women’s endocrinology in decades. Polycystic ovary syndrome — PCOS — is now officially renamed polyendocrine metabolic ovarian syndrome, or PMOS.¹ For clinicians (and patients) who have spent years navigating the limitations of the old name, this is not merely a rebrand- it is a formal, evidence-backed acknowledgment that we have been undermanaging this condition.

 

What Has Changed

This renaming came out of a global consensus process led by the Monash Centre for Health Research and Implementation, in collaboration with Verity (a UK patient charity), the Androgen Excess and PCOS Society, and 56 additional academic, clinical, and patient organizations worldwide.¹ Over 14,360 survey responses were collected from patients and multidisciplinary clinicians across all world regions, with additional inputs from group workshops and marketing analysis.¹

Most clinicians will agree that the scientific case against the old name has been building for over a decade. A 2012 NIH workshop had already flagged its inaccuracy.¹ The specific problems were clear: 

• “Polycystic ovary” implies pathological cysts, which are not actually a required feature of the condition.¹ What appear on ultrasound as cysts are actually immature follicles, arrested in development — a consequence of disrupted folliculogenesis- not primary ovarian pathology.² 
• The old name compressed a complex polyendocrine, cardiometabolic, neuroendocrine, and reproductive disorder into a single, simplified and misleading target. The downstream consequences were tangible: up to 70% of affected individuals remain undiagnosed and patient dissatisfaction with information and care has been consistently documented.¹

The new name, polyendocrine metabolic ovarian syndrome, was chosen with a focus on prioritizing scientific accuracy, stigma reduction, and cultural appropriateness. The three preferred terms, polyendocrine, metabolic, and ovarian, each carry specific clinical weight that the old name entirely ignored or at least abscured.¹ A three-year managed transition is underway, with formal integration into the 2028 International Guidelines update and eventual ICD reclassification.¹

Let’s break this down in the key changes and clinical implications:

 

The Importance of “Polyendocrine”

The “poly” in polyendocrine is the most exciting part of this change. PMOS physiology involves multiple interacting endocrine systems and communication axes, including the hypothalamic-pituitary-ovarian axis (HPO),  adrenal androgen production, the pancreatic insulin-signaling pathway, adipokine signaling from adipose tissue, and gut-hormone interactions.¹ Genome-wide association studies confirm polygenic origins spanning neuroendocrine, metabolic, and reproductive pathways.⁴  In summary, the pathophysiology and genetic predispositions center around multiple endocrine systems, not only one.  (In fact, interestingly, subtypes of PMOS (PCOS in studies) in biological males are also being explored in literature, further separating the condition from female reproductive physiology2.)

The neuroendocrine picture is particularly underappreciated in clinical practice. Increased frequency of gonadotropin-releasing hormone (GnRH) pulsation elevates LH relative to FSH, driving excess ovarian androgen production.²   Hyperandrogenism is the defining diagnostic and clinical feature, contributing not only to hirsutism, acne, and alopecia, but directly fueling metabolic dysfunction through its effects on fat distribution and insulin signaling.¹⁵.  And so, while the impact is related to the ovaries through reproductive hormonal changes, the dysregulation is not ovarian – it is actually upstream, beginning in the hypothalamus. 

For clinicians, this polyendocrine framing demands a broader assessment than the condition has historically received. Evaluating PMOS through an ovarian-only lens, ordering a pelvic ultrasound and free testosterone and calling it complete, is no longer adequate.  While integrative providers may have looked through this lens for many years, the majority of patients do not have providers who do so.

 

The Metabolic Focus

This is where the name change carries the greatest clinical urgency and practice changes. The word metabolic in the new name is not incidental. It is a formal acknowledgement that the reproductive-first framing that has dominated “PCOS” management is flawed. Medical care for PCOS was typically focused on fertility and reproduction, at the expense of its other effects. Yet the metabolic burden is staggering and begins early.  The change from PCOS to PMOS puts this front and center, where it cannot be ignored.

Insulin resistance is present in up to 85% of individuals with PMOS — including 75% of lean women.¹ It is the central metabolic driver: hyperinsulinemia amplifies ovarian androgen secretion, suppresses sex hormone-binding globulin (SHBG), drives fat redistribution toward central adiposity, and perpetuates a cycle that worsens every axis of the condition simultaneously.⁶ Hyperinsulinemia also promotes lipogenesis and dyslipidemia, establishing a vicious cycle linking insulin resistance, androgen excess, and metabolic dysfunction.

The long-term cardiovascular impact and risks have been described in literature.   A 2024 systematic review and meta-analysis found that the odds ratios for composite cardiovascular disease (1.68), myocardial infarction (2.50), and stroke (1.71) are significantly elevated in women with PMOS compared to those without.⁷ Despite this, PMOS remains largely overlooked within the realm of cardiology.

The liver is another underrecognized target organ. A 2023 meta-analysis found a pooled prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD) of 43% in patients with PCOS.⁸ Women with PMOS have three times risk of MASLD, and serum androgens are independent predictors, with highest risk in the classic hyperandrogenic phenotype. Obstructive sleep apnea is present in an estimated 30–40% of women with PMOS, driven by a combination of androgen excess, obesity, and insulin resistance — yet it is rarely screened for outside of pulmonology.⁹

The clinical imperative is direct: every patient with PMOS should receive a complete cardiometabolic workup as standard of care, and earlier in life than many women are currently receiving screening. 

A panel for screening should include:

• Fasting insulin and glucose with HOMA-IR calculation
• Full lipid panel
• Liver function tests, particularly when patients concurrently have obesity or androgen excess
• Blood pressure assessment at every visit
• Sleep apnea screening in appropriate patients
• 2-hour glucose tolerance test for impaired fasting glucose or elevated HOMA-IR, with annual screening thereafter¹⁰

 

Ovarian Changes in PMOS

Ovarian dysfunction remains central to PMOS, but how we discuss and describe it to patients matters. The follicular arrest seen in PMOS is the downstream result of hormone dysregulation and hyperinsulinemia — not a primary ovarian defect.²  To restate this, the ovary is the victim, not the villain.

Elevated anti-Müllerian hormone (AMH), now included in adult diagnostic criteria as an alternative to ultrasound, reflects disordered folliculogenesis and granulosa-cell dysregulation driven by the broader endocrine environment.¹¹

Clinically, this reframing matters for fertility counseling. Ovulatory dysfunction and irregular cycles in PMOS are not simply “irregular periods” — they are downstream manifestations of a whole-system endocrine disorder. Treating them with ovulation induction alone – typically with metformin in the fertility world – without addressing the underlying metabolic root cause, is addressing the symptom while ignoring the disease process.

There is also an elevated endometrial cancer risk in PMOS, which is directly tied to chronic anovulation and unopposed estrogen — another reason metabolic and ovulatory health must be addressed together, not sequentially.⁹

 

What This Means for Your Practice

The renaming of PCOS to PMOS is not asking clinicians to learn new pathophysiology. It is asking them to act on what was already very clear in the literature. We know that patients with “PCOS” faced problems such as delayed diagnoses, fragmented care, and general stigma.   Most important clinically is that we missed opportunities for early intervention to address metabolic and cardiovascular risks.

With PMOS renaming, we pull critical clinical priorities out of the forgotten shadows and push them into the spotlight:

1. Metabolic assessment at time of diagnosis, regardless of BMI or reproductive goals. Insulin resistance is present in lean and obese phenotypes alike. A thin woman with PMOS is not a lower metabolic risk.¹² All women need evaluation
2. Longitudinal cardiometabolic follow-up. PMOS does not resolve at menopause. The metabolic and cardiovascular risk burden persists — and in some respects intensifies — beyond reproductive years.¹³ These patients require monitoring for type 2 diabetes, dyslipidemia, hypertension, and cardiovascular events throughout their lifespan.
3. Androgen assessment that includes both ovarian and adrenal sources. Functional ovarian hyperandrogenism accounts for approximately 87% of cases, but adrenal-predominant patterns exist and respond to different treatment strategies.¹⁴ DHEA-S, free and total testosterone, and androgen metabolite evaluation in urine provide meaningful clinical differentiation which allows you to treat the unique pattern of androgen production in each patient.
4. Updated patient communication. Patients who have been told they have “cysts on their ovaries” and managed exclusively with oral contraceptives deserve to understand the full metabolic scope of their condition — including what is at stake if it is left unaddressed.
5. Expanded referral. Assessment and management should address reproductive, metabolic, cardiovascular, dermatologic, sleep, and psychological features. For many patients, this means coordinated care across endocrinology, cardiology, nutrition, and mental health, and ensuring that a naturopathic root-cause approach to care addresses the spectrum of concerns as needed.  
6. Expanded treatment options: The focus on metabolic health as an addressable root cause for downstream clinical sequelae can’t be overstated.  In addition to lifestyle changes, which should always be considered a critical part of any treatment plan for PMOS, expect to see additional pharmaceutical options open up for diagnosed patients, such as GLP-1s in addition to the standard metformin.

 

Conclusion

The renaming of PCOS to PMOS is a landmark moment. It is also a straightforward clinical mandate that really resonates with naturopathic physicians: treat the whole person. The endocrine, metabolic, and ovarian axes of PMOS are inseparable. The follicular arrest we see on ultrasound is not where the story starts, it starts with insulin resistance, androgen excess, hormone dysregulation, and metabolic inflammation that often begin decades before a patient ever presents for a consultation.  If we are to truly support patients with PMOS, we need to address those root causes effectively and apply a preventive medicine framework for long-term success.

 

References

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. Published online May 12, 2026. doi:10.1016/S0140-6736(26)00717-8
2. Jafarabady K, Mohammadi I, Firouzabadi SR, Mohammadifard F, Soltani SM, Paksaz A, Noroozzadeh M, Ramezani Tehrani F. Male polycystic ovarian syndrome phenotype: a meta-analysis of endocrine-metabolic dysregulation in fathers and brothers of PCOS-affected women. Basic Clin Androl. 2025 Nov 16;35(1):44. doi: 10.1186/s12610-025-00290-1. PMID: 41243102; PMCID: PMC12621411.

2. Stener-Victorin E, Teede H, Norman RJ, et al. Polycystic ovary syndrome. Nat Rev Dis Primers. 2024;10:27.
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4. Zhao H, Xu Y, Xue B, et al. Multi-ancestry genome-wide association analyses of polycystic ovary syndrome. Nat Genet. 2025;57:2669–2681.
5. Joham AE, Norman RJ, Stener-Victorin E, et al. Polycystic ovary syndrome. Lancet Diabetes Endocrinol. 2022;10:668–680.
6. 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(11):2619–2631.
7. 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.
8. Manzano-Nunez R, Santana-Dominguez M, Rivera-Esteban J, et al. Non-alcoholic fatty liver disease in patients with polycystic ovary syndrome: a systematic review, meta-analysis, and meta-regression. J Clin Med. 2023;12(3):856.
9. Joham AE, Teede HJ. PCOS — a metabolic condition with health impacts on women and men. Nat Rev Endocrinol. 2022;18:197–198.
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11. 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: a systematic review and meta-analysis. Fertil Steril. 2024;122:727–739.
12. Stepto NK, Cassar S, Joham AE, et al. Women with polycystic ovary syndrome have intrinsic insulin resistance on euglycaemic–hyperinsulinaemic clamp. Hum Reprod. 2013;28(3):777–784.
13. Thong EP, Codner E, Laven JSE, Teede H. Diabetes: a metabolic and reproductive disorder in women. Lancet Diabetes Endocrinol. 2020;8:134–149.
14. Azziz R, Carmina E, Chen Z, et al. Polycystic ovary syndrome. Nat Rev Dis Primers. 2016;2:16057.
15. Shorakae S, Ranasinha S, Abell S, et al. Inter-related effects of insulin resistance, hyperandrogenism, sympathetic dysfunction and chronic inflammation in PCOS. Clin Endocrinol (Oxf). 2018;89:628–633.
16. Bahri Khomami M, Shorakae S, Hashemi S, et al. Systematic review and meta-analysis of pregnancy outcomes in women with polycystic ovary syndrome. Nat Commun. 2024;15:5591.
17. Norman RJ, Morman R, Teede HJ. “Tis but thy name that is my enemy” — the problem with the naming of polycystic ovary syndrome. Fertil Steril. 2023;120:249–250.
18. Su P, Chen C, Sun Y. Physiopathology of polycystic ovary syndrome in endocrinology, metabolism and inflammation. J Ovarian Res. 2025;18:34.
19. Dobbie LJ, Pittam B, Zhao SS, et al. Childhood, adolescent, and adulthood adiposity are associated with risk of PCOS: a Mendelian randomization study with meta-analysis. Hum Reprod. 2023;38:1168–1182.
20. Samarasinghe SNS, Leca B, Alabdulkader S, et al. Bariatric surgery for spontaneous ovulation in women living with polycystic ovary syndrome: the BAMBINI multicentre, open-label, randomised controlled trial. Lancet. 2024;403:2489–2503.

 

Bio:

Dr. Jaclyn Smeaton, N.D. is a licensed naturopathic physician who has dedicated her life to serving women from an integrative perspective. For over 15 years, she has been the nation’s leading expert on integrative approaches to infertility, reproductive, and genitourinary health. In her practice, Hello Fertility, she has helped hundreds of couples conceive when they thought there was no hope, and has taught thousands of doctors her successful methods. In 2025, she completed a Certification in Women’s Health and Menopause through Harvard Medical School.

In addition to reproductive medicine, Dr. Smeaton has a diverse career spanning clinical laboratory work, dietary supplements, health technology and innovation, and strategic leadership and commercial strategy in the integrative medicine industry. She currently serves as the Chief Medical Officer for Precision Analytical, creators of the DUTCH Test.

She has served as adjunct faculty for Bastyr University, as President for both the New Hampshire Association of Naturopathic Doctors and the American Association of Naturopathic Physicians, as an Ambassador for the Academy of Integrative Health and Medicine, and a board member of the Integrative Health Policy Consortium, the American Herbal Products Association, and several others.