By Dr Gautam V. DaftaryDirector, Aksigen IVF
Last reviewed June 202618-minute read4,500 words
If you have ever sat across from a doctor and been told you have polycystic ovary syndrome, the first thing you should know is that the name has changed.
In May 2026, after a fourteen-year global consensus process led by Monash University and involving fifty-six leading academic, clinical, and patient organisations, the condition formerly called polycystic ovary syndrome — PCOS — was formally renamed polyendocrine metabolic ovarian syndrome, or PMOS1.
The decision was published in The Lancet and has been endorsed by the American Society for Reproductive Medicine, the Endocrine Society, and the International Androgen Excess and Polycystic Ovary Syndrome Society. Over the next three years, the new name will be reflected in international clinical guidelines, in medical school curricula, and in the diagnostic codes used across 195 countries.
This is not merely a change of label.
The old name focused attention on a single feature — small fluid-filled sacs visible on an ovarian ultrasound — that is neither the cause of the condition nor present in every woman who has it. The cysts, in fact, are not cysts in the medical sense at all. They are immature follicles, and they are a downstream consequence of the underlying problem, not the problem itself.
For decades, the name created confusion. Women without cysts were told they could not possibly have PCOS. Women with cysts but no other features were told they did. The metabolic, hormonal, and psychological dimensions of the condition — which are often more clinically important than the ovarian features — were systematically underweighted in diagnosis, in treatment, and in patient understanding.
The new name corrects this. Polyendocrine acknowledges that multiple hormonal systems are involved — insulin, androgens, gonadotropins, neuroendocrine signals from the brain. Metabolic names the dimension that matters most to long-term health: insulin resistance, weight regulation, lipid metabolism, glucose tolerance, and the cardiovascular consequences of all of these. Ovarian retains the connection to ovulatory disturbance, which remains a defining feature and the reason most women come to a specialist.
If you have been diagnosed with PCOS, you have PMOS. The condition is the same. The treatment principles are the same. What changes is the framing — and the framing changes what gets diagnosed early, what gets treated, and what gets followed through life.
This article is a comprehensive introduction to PMOS for women, partners, and families. It covers what the condition is, how it shows up, how it is diagnosed and treated, what it means for fertility and pregnancy, what the long-term health considerations are, and what is particular to PMOS in the Indian context. It is written to be read in full at first, then returned to in sections as questions arise.
1. What is PMOS?
Polyendocrine metabolic ovarian syndrome is the most common endocrine condition affecting women of reproductive age. Globally, it affects approximately one in eight women — more than 170 million people1.
In India, the most authoritative epidemiological data, from the Indian Council of Medical Research's PCOS National Task Force, places the prevalence at 19.6 percent of Indian women aged 18 to 40 when assessed against Rotterdam criteria, and 13.6 percent when assessed against the more conservative Androgen Excess and Polycystic Ovary Syndrome Society criteria22. That higher Indian figure translates to roughly 44 million women across the country — a public-health burden of a different order from what most clinical conversations acknowledge.
PMOS is not a single disease. It is a syndrome — a recognisable cluster of clinical features that share an underlying biological pattern but present differently in different women. Three core features define it:
Ovulatory dysfunction. Periods that are irregular, infrequent, or absent, reflecting cycles in which ovulation either fails or occurs inconsistently.
Clinical or biochemical hyperandrogenism. Visible signs of elevated androgen activity (acne, hirsutism, hair thinning) or blood tests showing elevated androgen levels.
Polycystic ovarian morphology. The ultrasound finding of multiple small follicles arranged in a characteristic pattern on the ovary, or an elevated anti-Müllerian hormone (AMH) level reflecting the same underlying biology.
Under the most widely used diagnostic system — the Rotterdam criteria as updated in the 2023 International Evidence-Based Guideline — the diagnosis is made when any two of these three features are present and other causes have been excluded3. This is the framework currently in operation; the 2026 PMOS-branded guideline update, expected in late 2026 or 2027, is expected to retain this three-feature structure.
Around the core features sits a much broader cluster of associated conditions: insulin resistance, weight regulation difficulties, dyslipidaemia, sleep disturbance, depression, anxiety, infertility, and elevated risks of gestational diabetes, hypertension during pregnancy, type 2 diabetes, and cardiovascular disease across the lifespan.
Not every woman with PMOS has all of these. Most have several. The combination differs from woman to woman, and the constellation can change over time within the same woman — which is one of the reasons PMOS is best thought of as a long-term endocrine condition rather than a one-off reproductive diagnosis.
2. Why the Name Changed
The change from PCOS to PMOS was not undertaken lightly. The renaming consortium spent fourteen years on it, ran iterative global surveys involving more than 22,000 respondents, and held workshops with patients and clinicians from six continents. Eighty-six percent of patients and 71 percent of clinicians ultimately supported the change1.
Three reasons drove the decision.
The first is accuracy. The ovarian appearance the old name described is neither universal nor causal. Some women diagnosed with PCOS have no detectable cysts on ultrasound; some women with cysts have no underlying syndrome. Naming a condition after its least specific feature is a structural error in disease nomenclature.
The second is clinical reframing. The metabolic and cardiometabolic dimensions of the syndrome — insulin resistance, glucose intolerance, cardiovascular risk — are often more consequential for long-term health than the reproductive features. A name that focuses attention exclusively on the ovaries delays the metabolic conversation that should happen at diagnosis. Women are routinely diagnosed with PCOS, treated for fertility, and then surprised to be told a decade later that they have developed type 2 diabetes or hypertension at unusually young ages. The new name builds the metabolic conversation into the diagnosis itself.
The third reason is patient experience. Surveys conducted as part of the renaming process documented widespread dissatisfaction with the previous name. Patients reported feeling that PCOS framed them as having a fertility problem when they were also living with a long-term metabolic and mood-related condition. They reported delayed diagnosis — often by years — because their non-reproductive symptoms were not connected to the diagnosis. They reported a sense that the name itself trivialised what they were experiencing.
For practical purposes, what changes with the rename is what gets attended to. Under PCOS, the typical clinical encounter has been organised around fertility. Under PMOS, the encounter is organised around the whole picture — metabolic, hormonal, reproductive, and psychological — from the start.
3. How PMOS Shows Up
PMOS does not present the same way in every woman. The condition is heterogeneous by design. Some women present in adolescence with irregular periods and acne; some present in their late twenties with infertility; some present in their thirties with weight gain and central adiposity that has resisted reasonable lifestyle change.
Some present with pronounced hirsutism; others have none. Some carry significant excess weight; others are lean. The diversity of presentation is not a diagnostic obstacle — it is a defining feature.
The most common signs and symptoms, in approximate order of how often they bring women to a doctor:
Menstrual irregularity. Cycles longer than 35 days, fewer than nine periods a year, or completely absent periods are the most common reason women seek evaluation. Some women have apparently regular cycles but are not ovulating consistently; this is harder to detect without specific assessment.
Hirsutism, acne, and hair thinning. These are the visible signs of hyperandrogenism. Hirsutism in PMOS typically affects the face (chin, upper lip, sideburn area), neck, chest, and lower abdomen. Acne tends to be persistent into adulthood and often cystic in distribution. Hair thinning, when it occurs, tends to be along the central scalp parting in a pattern that is different from male-pattern baldness.
Weight changes and central adiposity. Weight gain in PMOS is often disproportionately central — around the waist — and resistant to ordinary diet and exercise interventions. This pattern reflects insulin resistance, not lifestyle, and is one of the markers that most clearly separates PMOS-driven weight change from other causes.
Acanthosis nigricans. Dark, velvety patches of skin, typically at the back of the neck, in the armpits, or in skin folds — a visible marker of significant insulin resistance.
Depression and anxiety are substantially more common in women with PMOS than in the general population. The most-cited meta-analysis on this question, by Cooney and colleagues in Human Reproduction, found that women with PCOS / PMOS have significantly elevated odds of moderate to severe depressive and anxiety symptoms, independent of body weight4. The link is biological, not just situational — although the situational dimensions (dealing with infertility, weight, skin manifestations, delayed diagnosis) compound the underlying biology.
Many women first encounter the diagnosis when trying to conceive. PMOS is the most common cause of anovulatory infertility worldwide. Sleep disturbance, fatigue, and obstructive sleep apnoea are also more common than in age-matched controls.
The pattern matters more than any single feature. A woman with irregular cycles, acne that has persisted past her teens, and a tendency to gain weight around her midsection despite a reasonably active lifestyle is showing a recognisable PMOS pattern, even if no individual symptom is dramatic.
4. How PMOS is Diagnosed
The diagnostic framework is laid out in the 2023 International Evidence-Based Guideline for the Assessment and Management of Polycystic Ovary Syndrome — the most authoritative current document3. The 2026 PMOS update will build on the same structure.
Diagnosis in adults requires two of three features:
Oligo-anovulation or anovulation. Infrequent or absent ovulation, demonstrated by cycle history or biochemistry.
Hyperandrogenism. Clinical (hirsutism, acne, hair thinning) or biochemical (elevated total testosterone, free androgen index, or DHEAS).
Polycystic ovarian morphology on ultrasound. Typically defined as twenty or more follicles per ovary in at least one ovary, or an elevated AMH used as a surrogate marker.
These features must be present in the absence of other identifiable causes. Congenital adrenal hyperplasia, androgen-secreting tumours, thyroid dysfunction, hyperprolactinaemia, and Cushing's syndrome must be excluded, which is what the standard workup is designed to do.
In adolescents, the criteria are more conservative. Polycystic ovarian morphology should not be used to make the diagnosis in adolescents because immature follicles are common in adolescent ovaries even without PMOS. Diagnosis in adolescents typically requires both ovulatory dysfunction and hyperandrogenism, and the diagnosis may be deferred pending follow-up.
The workup that establishes the diagnosis typically includes:
A detailed clinical history. Menstrual pattern, pubertal development, weight trajectory, family history, and current symptoms.
A physical examination. Body composition, hirsutism scoring (typically the modified Ferriman-Gallwey scale), and signs of insulin resistance.
Hormonal blood tests. Total and free testosterone, sex hormone-binding globulin, DHEAS, 17-hydroxyprogesterone, prolactin, TSH, and AMH.
Metabolic blood tests. Fasting glucose and insulin, a 75-gram oral glucose tolerance test (recommended in the 2023 Guideline for almost all women with PMOS at diagnosis), HbA1c, and a fasting lipid profile.
Imaging. A transvaginal ultrasound (or transabdominal in adolescents and unmarried women) to assess ovarian morphology and exclude other pelvic pathology.
Four phenotypes are commonly described, defined by which combination of features is present:
Phenotype A. All three features — anovulation, hyperandrogenism, and polycystic ovarian morphology.
Phenotype B. Anovulation plus hyperandrogenism, without polycystic ovarian morphology.
Phenotype C. Hyperandrogenism plus polycystic ovarian morphology, with regular cycles.
Phenotype D. Anovulation plus polycystic ovarian morphology, without hyperandrogenism.
In the Indian context, the ICMR national data shows phenotype C as the most common at 40.8 percent — women with regular cycles, hyperandrogenism, and polycystic ovarian morphology2. This is clinically important. Many Indian women with PMOS have apparently normal cycles and are not picked up unless the workup looks beyond menstrual history.
5. What's Behind PMOS
PMOS is fundamentally a disorder of how the body regulates hormones — specifically the interaction between insulin, the androgens, and the reproductive hormones produced by the brain and ovaries. The full mechanism is not entirely understood and varies between phenotypes, but the central pattern is recognisable.
The hypothalamus, the part of the brain that coordinates reproductive hormone signals, releases gonadotropin-releasing hormone in a pulsatile pattern. In PMOS, this pulse pattern is altered — pulses occur more rapidly than normal, which biases the pituitary toward releasing more luteinising hormone (LH) than follicle-stimulating hormone (FSH). The altered LH-to-FSH ratio drives the ovary to produce more androgens — testosterone and androstenedione — than it normally would.
Simultaneously, insulin resistance is present in a majority of women with PMOS. Insulin resistance means the body's cells require more insulin to do the same job — the muscle cells, the fat cells, the liver. To compensate, the pancreas produces more insulin. The elevated insulin then has two effects relevant to PMOS. First, it directly stimulates the ovaries to produce more androgens. Second, it lowers sex hormone-binding globulin in the bloodstream, which increases the proportion of testosterone that is biologically active.
The result is a self-reinforcing loop: insulin resistance drives elevated insulin, elevated insulin drives elevated androgens, elevated androgens contribute to ovulatory dysfunction and to the central adiposity that further worsens insulin resistance.
This is why PMOS is called polyendocrine — multiple hormonal axes are involved. It is also why it is called metabolic — the insulin and glucose-handling dimension is central to the pathophysiology, not incidental to it. And it is why treatment that addresses only the reproductive features without addressing the metabolic dimension typically delivers short-term cycle regulation without the long-term health benefits that matter.
6. How PMOS is Treated
PMOS treatment in 2026 is organised around what we call ametabolic-first framework. The principle is straightforward: address the underlying metabolic biology, and many of the downstream features improve in parallel. Treat only the downstream features — cycles, hirsutism, acne — without attending to the metabolism, and short-term improvement is followed by recurrence and by accumulating long-term risk.
This is not a single treatment. It is a coordinated set of interventions matched to each woman's specific phenotype, symptoms, and goals.
Lifestyle and metabolic management. A combined dietary and exercise intervention with a modest sustained weight loss target — typically 5 to 10 percent of body weight, where weight loss is appropriate — produces measurable improvements in cycle regularity, ovulation, androgen levels, insulin sensitivity, and pregnancy outcomes. The Cochrane synthesis on lifestyle interventions confirms this, and the 2023 International Guideline recommends combined diet and exercise as first-line.
What matters more than any particular diet is the metabolic-load characteristics of the food pattern — moderate carbohydrate quantity, low glycaemic index, adequate protein, and consistent timing5. Regular structured exercise, ideally combining aerobic and resistance work, contributes independently of weight change.
Metformin. An insulin-sensitising drug, the most evidence-based pharmacological agent for the metabolic dimension of PMOS. Used for insulin resistance, prediabetes, and as an adjunct to ovulation induction. The Cochrane synthesis on insulin sensitisers confirms its central role.
Combined oral contraceptive pills. For women not currently trying to conceive who want regulation of cycles, reduction of androgen-driven symptoms, and protection against the endometrial-thickening risk that accompanies long-term anovulation. The choice of pill matters; some are more anti-androgenic than others.
Anti-androgens. Spironolactone is the most widely used, prescribed for hirsutism and androgen-driven hair loss when oral contraceptives alone are not sufficient. Generally combined with a contraceptive because of teratogenic potential.
Inositol supplementation — myo-inositol, often combined with D-chiro-inositol — is widely used in India and internationally. The most recent meta-analysis informing the 2023 International Guideline concluded that the evidence supporting inositol is, in their words, limited and inconclusive — it may improve some metabolic measures and ovulation, but the certainty is low6.
This is worth knowing as a patient. Inositol is generally safe and inexpensive, and many clinicians use it as an adjunct, but the strong claims sometimes made for it are not supported by current evidence.
Acne and hirsutism are often treated alongside hormonal management — topical retinoids, hormonal acne therapy, laser hair reduction. These are not cosmetic luxuries; the psychological burden of these features is real and contributes to the depression and anxiety load of PMOS.
The 2023 International Guideline recommends screening for depression and anxiety at diagnosis. Where present, both pharmacological treatment and psychological support are appropriate. Treating PMOS without attending to the mental-health dimension is treating half the condition.
Treatment in PMOS is therefore not a single decision. It is an evolving plan, revisited as goals change — particularly when a woman moves into or out of a phase of trying to conceive.
8. Pregnancy and Beyond
PMOS does not end at conception. Women with PMOS carry elevated risks of several pregnancy complications, and these risks should be discussed at the start of pregnancy — ideally before it begins — and managed actively across the antenatal period.
The most robust meta-analyses on this question, by Bahri Khomami and colleagues, have established the following10:
Gestational diabetes. The risk is approximately two to three times higher than in women without PMOS. Most centres now screen women with PMOS earlier in pregnancy — a 75-gram OGTT in the first or early second trimester rather than waiting until 24 to 28 weeks.
Hypertensive disorders of pregnancy. The odds of gestational hypertension are approximately 2.6 times higher; the odds of preeclampsia approximately 1.9 times higher.
Preterm birth. Modestly elevated risk.
These elevated risks are independent of obesity. Lean women with PMOS also carry elevated risk. The condition itself, not body weight alone, drives the risk profile. A population-scale study of 9.1 million pregnancies confirmed PMOS as an independent risk factor.
This does not mean every PMOS pregnancy is high-risk11. The majority of women with PMOS have uncomplicated pregnancies and healthy babies. What it does mean is that PMOS pregnancies benefit from informed monitoring — early screening for gestational diabetes, blood pressure surveillance, and an obstetric team who knows the diagnosis is relevant.
Beyond pregnancy, PMOS continues to matter across the lifespan. The Wekker 2020 meta-analysis quantified the long-term cardiometabolic risk profile — elevated odds of type 2 diabetes, hypertension, dyslipidaemia, and non-fatal stroke12.
A 2024 update by Tay and colleagues, supplementing the 2023 International Guideline, confirmed elevated clinical cardiovascular disease risk in PMOS13. Newer cohort data from the UK Biobank suggests that long-term risk may differ between phenotypes — normoandrogenic PMOS associated more with cardiovascular outcomes, hyperandrogenic PMOS more with hepatic steatosis.
PMOS does not go away at menopause. The metabolic, cardiovascular, and endometrial dimensions persist. Postmenopausal care for women with PMOS should include continuing attention to metabolic health, cardiovascular risk, and endometrial protection.
9. PMOS in India
A patient-facing guide written from a clinical centre in Mumbai would be incomplete without specific attention to what PMOS looks like in the Indian context.
Three things are particular to PMOS in India.
Prevalence is substantially higher. The ICMR national data places Indian prevalence at 19.6 percent of women aged 18 to 40 under Rotterdam criteria, compared with the global figure of 10 to 13 percent2. This is not a measurement artefact. It appears to reflect a combination of genetic predisposition, dietary patterns, and metabolic background. Whatever the cause, the practical consequence is that PMOS in India is more common than most clinicians and patients recognise.
The phenotype distribution is different. Phenotype C — hyperandrogenism plus polycystic ovarian morphology in a woman with apparently regular cycles — is the most common phenotype in India at 40.8 percent. This is a different distribution from many Western cohorts where phenotype A predominates. The clinical implication is that many Indian women with PMOS will not be picked up by a workup that begins and ends with cycle history. The workup must look at androgens and imaging from the outset.
The mental-health burden is higher. A 2024 systematic review of PMOS-related depression and anxiety in low- and middle-income countries found pooled prevalence of depression at 51 percent and anxiety at 45 percent, with India-specific pooled estimates of 55 percent and 51 percent respectively — substantially higher than the global Cooney 2017 figures14. The reasons include delayed diagnosis, restricted access to mental-health care, and the particular sociocultural pressure around fertility and appearance that operates in Indian settings.
What this means in practice is that PMOS care in India needs to look like Indian PMOS care. It needs to incorporate the dietary and lifestyle context that Indian patients actually live in — rice- and pulse-based meals, joint family eating patterns, regional dietary diversity. It needs to incorporate the cultural framing around fertility and around menstrual symptoms. It needs to take the mental-health dimension seriously, particularly given the limited mental-health infrastructure in many parts of the country.
A patient diagnosed with PMOS in India deserves care that has been adapted to her context, not transplanted from elsewhere.
References
- 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. The Lancet. Published online May 12, 2026. DOI: 10.1016/S0140-6736(26)00717-8.
- Ganie MA, Chowdhury S, Suri V, Joshi B, Bhattacharya PK, Agrawal S, et al. Prevalence, phenotypes, and comorbidities of polycystic ovary syndrome among Indian women. JAMA Network Open. ICMR-PCOS National Task Force, n = 9,824.
- Teede HJ, Tay CT, Laven J, Dokras A, Moran LJ, Piltonen TT, et al., on behalf of the International PCOS Network. Recommendations from the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome. Human Reproduction. 2023;38(9):1655–1679. DOI: 10.1093/humrep/dead156.
- Cooney LG, Lee I, Sammel MD, Dokras A. High prevalence of moderate and severe depressive and anxiety symptoms in polycystic ovary syndrome: a systematic review and meta-analysis. Human Reproduction. 2017;32(5):1075–1091.
- Lim SS, Hutchison SK, Van Ryswyk E, Norman RJ, Teede HJ, Moran LJ. Lifestyle changes in women with polycystic ovary syndrome. Cochrane Database of Systematic Reviews. CD007506.
- Fitz V, Graca S, Mahalingaiah S, et al. Inositol for polycystic ovary syndrome: a systematic review and meta-analysis to inform the 2023 update of the International Evidence-based PCOS Guidelines. Journal of Clinical Endocrinology & Metabolism. 2024;109(6):1630–1655.
- Legro RS, Brzyski RG, Diamond MP, et al. Letrozole versus clomiphene for infertility in the polycystic ovary syndrome. New England Journal of Medicine. 2014;371(2):119–129.
- Lin H, Li Y, Li L, Wang W, Yang D, Zhang Q. Is a GnRH antagonist protocol better in PCOS patients? A meta-analysis of RCTs. PLoS ONE. 9(3):e91796.
- Chen ZJ, Shi Y, Sun Y, Zhang B, Liang X, Cao Y, et al. Fresh versus frozen embryos for infertility in the polycystic ovary syndrome. New England Journal of Medicine. 2016;375:523–533.
- Bahri Khomami M, Joham AE, Boyle JA, et al. Increased maternal pregnancy complications in polycystic ovary syndrome appear to be independent of obesity. Obesity Reviews. 2019;20(5):659–674.
- Mills G, Badeghiesh A, Suarthana E, Baghlaf H, Dahan MH. Polycystic ovary syndrome as an independent risk factor for gestational diabetes and hypertensive disorders of pregnancy: a population-based study on 9.1 million pregnancies. Human Reproduction. 2020;35(7):1666–1674.
- Wekker V, van Dammen L, Koning A, et al. Long-term cardiometabolic disease risk in women with PCOS: a systematic review and meta-analysis. Human Reproduction Update. 2020;26(6):942–960.
- 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 PCOS. Journal of the American Heart Association. 2024;13:e033572.
- Depression and anxiety among women with polycystic ovarian syndrome in low- and middle-income countries: a systematic review and meta-analysis. 2024.
Aksigen IVF•Bharat Daftary Knowledge Centre•Understanding PMOS, v1.0•June 2026
+91 86556 78747
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