Recoining polycystic ovarian syndrome: a new era of polyendocrine metabolic ovarian syndrome and what dietitians can do

The name that has defined millions may no longer fit. Polycystic ovary syndrome (PCOS) has long been the defining label for one of the most common endocrine conditions affecting women of reproductive age, estimated to affect 8–13% of women globally.[1] Yet the name itself has been a persistent source of confusion and misrepresentation, as well as a barrier to diagnosis and appropriate care.

Not all women with PCOS have polycystic ovaries on ultrasound. Not all have a syndrome in the traditional sense. The name points to a structural finding that is neither necessary nor sufficient for diagnosis, and says nothing about the hormonal, metabolic and reproductive complexity beneath the surface.

A landmark international consensus recommended renaming the condition to polycystic metabolic ovarian syndrome (PMOS), reflecting a more accurate understanding of what this condition truly is: a complex metabolic and endocrine disorder with far-reaching consequences beyond the ovaries.[2]

This is not merely semantic. It is a clinical milestone with profound implications for how we diagnose, treat and support women with this condition. And dietitians are uniquely positioned to lead the conversation.

Why the rename is important

PCOS (or PMOS) is fundamentally a disorder of:

  • Insulin resistance, which is present in up to 70% of women regardless of body weight, driving excess androgen production.[3]

  • Androgen excess, manifesting as hirsutism, acne and menstrual irregularity.

  • Hypothalamic-pituitary dysregulation, altering hormone pulsatility. Normal pulsatility means hormones are released in a rhythmic, pulsing pattern throughout the day and cycle. Think of it like a regular heartbeat for your hormones.

  • Chronic low-grade inflammation, perpetuating insulin resistance and increasing cardiovascular risk.

  • Metabolic dysfunction, including dyslipidaemia, impaired glucose tolerance and a 5–10-fold increased risk of T2D.[4]

The new name, PMOS, places the metabolic dimension at the centre of clinical understanding. It acknowledges that this condition affects the liver, pancreas, cardiovascular system, skin, gut microbiome and long-term cardiometabolic health, not just the ovaries.

What PMOS means for our nutrition practice

The rename reframes the entire therapeutic target. If PMOS is fundamentally a metabolic syndrome with reproductive consequences, then metabolic intervention through nutrition is not a complementary afterthought, but it is central to management.

1. Prioritise insulin sensitivity

Insulin resistance is the metabolic engine driving PMOS. The Mediterranean dietary pattern has the strongest evidence base for improving insulin sensitivity, reducing androgens and improving menstrual regularity.[5] Its emphasis on monounsaturated fats, oily fish, legumes, wholegrains and polyphenol-rich foods creates an anti-inflammatory, insulin-sensitising pattern that is sustainable long-term. Low glycaemic index approaches further reduce postprandial insulin secretion and downstream androgen excess.

2. Address chronic inflammation

The chronic low-grade inflammatory state in PMOS is both driver and consequence of insulin resistance. Key anti-inflammatory dietary components include omega-3 fatty acids from oily fish (sardines, mackerel, salmon) and walnuts, polyphenols from berries and leafy greens, fibre from vegetables and legumes and avoidance of ultra-processed foods that promote inflammation.

3. Support the gut microbiome

Women with PMOS show reduced microbial diversity and altered bile acid metabolism.[6] Diet is the most powerful modifiable factor influencing the microbiome. Dietitians can support diversity through high fibre intake from diverse plant sources (aiming for 30 different plant foods weekly), fermented foods (tofu, kefir, miso, pickles, sauerkraut, parmesan cheese) where tolerated, prebiotic foods and reducing ultra-processed food intake.

4. Target key nutritional deficiencies

Several micronutrient deficiencies consistently reported in PMOS require clinical attention:

  • Vitamin D: Deficiency is highly prevalent and associated with greater insulin resistance and higher androgen levels. Correction improves insulin sensitivity and menstrual regularity.[7]

  • Magnesium: Involved in over 300 enzymatic reactions including insulin signalling. Dietary sources include dark leafy greens, nuts, seeds and wholegrains.[8]

  • Zinc: Supports insulin receptor function and reduces androgen activity. Supplementation has been shown to reduce testosterone and improve menstrual regularity.[9]

  • Myo-inositol: The most robustly evidenced supplement in PMOS. At 4000mg daily, it improves ovulation rates, menstrual regularity and insulin sensitivity.[10]

  • Methylfolate: Elevated homocysteine is common in PMOS and linked to cardiovascular risk. Women with MTHFR gene variants require active methylfolate rather than standard folic acid.[11]

5. Reframe the weight conversation

One of the most damaging legacies of the old PCOS framework has been its conflation with weight and obesity. Women with PMOS are frequently told to lose weight without acknowledging that the insulin resistance driving PMOS makes weight management physiologically more difficult and that PMOS exists across all body sizes.

The new guidelines emphasise that even modest 5–10% weight loss can improve metabolic outcomes in women with overweight, but lean women with PMOS require the same metabolic attention. A non-diet, health-at-every-size approach that prioritises metabolic health markers over weight is increasingly supported by evidence and ethical frameworks.

6. Support mental health through nutrition

PMOS carries a significantly elevated burden of anxiety, depression and disordered eating.[12] Avoid highly restrictive approaches that risk triggering disordered eating, by de-centring food as reward. Optimise gut health for downstream mood effects, ensure adequate omega-3 intake and screen for disordered eating before implementing dietary change.

The dietitian's role in the new PMOS era

The renaming of PCOS to PMOS is an invitation to think more broadly, accurately and compassionately about this condition. For dietitians, it is a call to step confidently into a leadership role, not as adjuncts to medical care, but as primary therapeutic partners. The metabolic nature of PMOS places nutrition at the very centre of evidence-based treatment. The dietitian's ability to translate complex nutritional science into practical, personalised, sustainable guidance is precisely what women with PMOS need most.

As the name changes, so too must our clinical ambition. PMOS is a metabolic condition. Nutrition is metabolic medicine. Dietitians are the experts in this space.

Ines Jabir RD is a Clinical Specialist Dietitian who works within the NHS and at My Nutrition Balance, a nutrition service to support health and lifestyle changes, free from diet culture.

Ines Jabir RD

References:

  1. Salari N, Nankali A, Ghanbari A, Jafarpour S, Ghasemi H, Dokaneheifard S, Mohammadi M. Global prevalence of polycystic ovary syndrome in women worldwide: a comprehensive systematic review and meta-analysis. Arch Gynecol Obstet. 2024. 310:1303-1314. doi:10.1007/s00404-024-07607-x

  2. Teede HJ, Khomami MB, 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

  3. Unluhizarci K, Karaca Z, Kelestimur F. Role of insulin and insulin resistance in androgen excess disorders. World J Diabetes. 2021. 12:616-629. doi:10.4239/wjd.v12.i5.616

  4. Agrawal A 4th, Dave A, Jaiswal A. Type 2 Diabetes Mellitus in Patients With Polycystic Ovary Syndrome. Cureus. 2023. 15:e46859. doi:10.7759/cureus.46859

  5. Barrea L, Arnone A, Annunziata G, et al. Adherence to the Mediterranean Diet, Dietary Patterns and Body Composition in Women with Polycystic Ovary Syndrome (PCOS). Nutrients. 2019.11:2278. doi:10.3390/nu11102278

  6. Li C, Cheng D, Ren H, Zhang T. Unraveling the gut microbiota's role in PCOS: a new frontier in metabolic health. Front Endocrinol (Lausanne). 2025. 16:1529703. doi:10.3389/fendo.2025.1529703

  7. Argano C, Mirarchi L, Amodeo S, Orlando V, Torres A, Corrao S. The Role of Vitamin D and Its Molecular Bases in Insulin Resistance, Diabetes, Metabolic Syndrome, and Cardiovascular Disease: State of the Art. Int J Mol Sci. 2023.24:15485. doi:10.3390/ijms242015485

  8. Hamilton KP, Zelig R, Parker AR, Haggag A. Insulin Resistance and Serum Magnesium Concentrations among Women with Polycystic Ovary Syndrome. Curr Dev Nutr. 2019.3:nzz108. doi:10.1093/cdn/nzz108

  9. Fazel Torshizi F, Chamani M, Khodaei HR, Sadeghi AA, Hejazi SH, Majidzadeh Heravi R. Therapeutic effects of organic zinc on reproductive hormones, insulin resistance and mTOR expression, as a novel component, in a rat model of Polycystic ovary syndrome. Iran J Basic Med Sci. 2020.23:36-45. doi:10.22038/IJBMS.2019.36004.8586

  10. DiNicolantonio JJ, H O'Keefe J. Myo-inositol for insulin resistance, metabolic syndrome, polycystic ovary syndrome and gestational diabetes. Open Heart. 2022. 9:e001989. doi:10.1136/openhrt-2022-001989

  11. Xiong Y, Bian C, Lin X, Wang X, Xu K, Zhao X. Methylenetetrahydrofolate reductase gene polymorphisms in the risk of polycystic ovary syndrome and ovarian cancer. Biosci Rep. 2020. 40 doi:10.1042/BSR20200995

  12. Lalonde-Bester S, Malik M, Masoumi R, et al. Prevalence and Etiology of Eating Disorders in Polycystic Ovary Syndrome: A Scoping Review. Adv Nutr. 2024.15:100193 doi:10.1016/j.advnut.2024.100193

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