For those who are confused…
In May 2026, after a decade-long global consensus process involving around 14,000 people and endorsed by more than 50 medical and patient organisations, polycystic ovary syndrome (PCOS) was formally renamed polyendocrine metabolic ovarian syndrome, or PMOS (1). The old name pointed at "cysts" that are not really cysts (they are arrested follicles), and it fixed attention on the ovaries when the disorder reaches far beyond them. PMOS is in fact a multisystem lifelong disorder that affects metabolic processes alongside reproductive health.
This article will look into everything there is to know, broadly, about PMOS. If you, or someone you care about is affected by PMOS, let this be the article that helps take the first step to understanding, and perhaps plants the seeds for curiosity into the complexity that is PMOS. Remember, knowledge is power!
What actually is PMOS?
PMOS affects up to 1 in 8 women worldwide (1). It is characterised by androgen (e.g. testosterone) excess known as hyperandrogenism, ovulatory dysfunction, and metabolic/insulin dysregulation, with knock-on effects on menstrual cycles, weight, metabolic and mental health. It leads to a 3x increased chance of experiencing obesity and 4x higher risk of developing type 2 diabetes (2). It is also linked to higher risk of psychological disorders and cardiovascular disease, showing that it truly is a lifelong metabolic and endocrine disorder that carries real personal and societal costs.
With the current diagnostic criteria, you need at least two of these three features:
1. Irregular or absent ovulation - cycles longer than 35 days, or fewer than 9 periods a year.
2. Clinical or biochemical signs of excess androgens - visible signs like acne, excess facial or body hair (hirsutism), or scalp hair thinning, or elevated testosterone on a blood test.
3. Polycystic ovarian morphology - 12 or more small follicles (2–9mm) in an ovary on ultrasound, an ovarian volume over 10cm³, or, more recently, an elevated anti-Müllerian hormone (AMH) level, which the 2023 guideline update now accepts as a substitute for ultrasound
Because only two of the three are needed, two people can both carry a PMOS diagnosis while sharing almost no features. Someone with irregular cycles and high testosterone but normal-looking ovaries qualifies. So does someone with polycystic-looking ovaries and irregular cycles but no signs of excess androgens.
The basic biology: what’s actually going wrong, and where
Before getting into insulin and the subtypes, here's the general pattern behind PMOS. Researchers are upfront that the starting point of this pathway is hard to decipher - several processes are going on at once in PMOS, and they reinforce each other, which makes them difficult to untangle.
Normally, your brain and your ovaries send hormone signals back and forth to keep things balanced, including two hormones (LH and FSH) that together mature an egg each month and trigger its release- and the brain cells behind this signal are also listening for cues like insulin, tying reproduction to metabolism from the start.
In PMOS, this back-and-forth gets thrown off. For many people, that means the ovaries (and sometimes the adrenal glands) end up making more androgens - testosterone and related hormones - than usual, and ovulation becomes irregular or stops. When androgens are elevated, eggs often can't finish developing: they start to grow, then stall. A cluster of these stalled eggs is what shows up as "cysts" (actually arrested follicles) on an ultrasound - a sign of the imbalance, not the cause of it.
Because those same brain cells are listening for metabolic signals, too, insulin resistance in PMOS doesn't just tag along quietly - it plugs straight into this wiring and tends to make everything else worse. More on that next.
Once these processes are running, insulin resistance and hyperandrogenism drive each other in both directions - insulin stimulates androgen production, and androgens worsen insulin resistance in fat and muscle - so it becomes a self-sustaining loop rather than a one-way chain.
That same hormonal and metabolic disruption also reaches other parts of the brain. Excess androgens and insulin resistance are both linked to lower levels of mood-regulating neurotransmitters (serotonin, dopamine, GABA) and to more background inflammation - a plausible biological reason, on top of the day-to-day burden of symptoms, why PMOS carries a higher risk of anxiety and depression.
Insulin resistance is the engine of PMOS
Insulin resistance affects 65-95% of women with the disorder (3). Normally, insulin helps to regulate glucose and nutrient supply. In PMOS, high insulin levels act directly on various organs to fuel the disorder
Increase testosterone levels: Insulin directly stimulates testosterone production from the ovaries, it can suppress the levels of SHBG, so less testosterone is mopped up, and it can increase the adrenal glands’ sensitivity to adrenocorticotropic hormone (ACTH), which stimulates the adrenal gland to produce more androgens.
Impair ovulation and follicular development: Insulin can make the egg cell mature too early, leading to an inability to release the egg and the halting of ovulation.
A vicious cycle in fat tissue:: High levels of androgens act on fat tissue and reduce the presence of a transporter protein that mops up free glucose, leading to insulin resistance. Fat tissue that is insulin resistance releases more inflammatory chemicals, which worsens insulin resistance further, creating a vicious cycle.
Disruptions in the brain: High insulin levels act directly on the hypothalamic-pituitary system - leading to excessive secretion of LH, which further drives the ovaries to overproduce androgens and prevents normal ovulation.
Why the classic ‘subtypes’ are contested
Online, you’ve probably seen four main ‘subtypes’ of PMOS being circulated, namely: “insulin resistant”, “inflammatory”, “adrenal” and “post-pill”. They’re everywhere, and they get one thing right: no two people with PMOS look the same. But these subtypes don’t exactly follow the current available evidence.
A recent study published in Nature Medicine looked at a cohort of almost 12,000 women, and clustered them according to their core clinical measures (4). Here are the subtypes that they found:
1. Hyperandrogenic subtype (25%): Marked by high testosterone levels alongside metabolic disorders. It carries the highest risk of second trimester pregnancy loss.
2. Obesity related subtype (26%): Characterised by higher BMI and higher glucose and insulin levels in a fasted state. The highest prevalence of type 2 diabetes and hypertension is seen in this subtype.
3. High sex hormone binding globulin (SHBG) subtype (26%): Takes its name from sex hormone binding globulin, the protein that controls how much of your hormones stay active. It has the most favourable reproductive outcomes and the lowest incidence of diabetes and high blood pressure.
4. High LH-AMH subtype (23%): This subtype is characterised by high levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and aniti-Mullerian hormone (AMH). It carries the greatest risk of ovarian hyperstimulation during IVF.
What is means for fertility
As PMOS results in altered insulin and hormonal signalling, fertility is altered in many ways (5). It’s the most common cause of infertility linked to absent or infrequent ovulation. It can cause egg quality to decrease. When there is a viable fertilized egg, implantation difficulties can follow along with pregnancy complications.
Prescribed treatment: Metformin and GLP-1s
For a long time, first-line treatment was centred on the combined oral contraceptive pill. It suppresses ovulation and produces a predictable withdrawal bleed which can help manage (or “mask””) symptoms, but it doesn’t restore ovulation and does nothing for the metabolic root of the disorder or its long-term risks.
More recently, two medications first developed for diabetes have changed the conversation.
Metformin, in a 2023 systematic review, resulted in greater reductions in BMI and insulin resistance than placebo (6). It shortened menstrual cycle length, lowered total testosterone, and reduced inflammatory markers linked to cardiovascular risk.
GLP-1 receptor agonists, the class that includes semaglutide, are now being studied for PMOS too (7,8). Studies have shown:
◉ 62% of women on GLP-1s had more regular menstrual cycles, compared to 28% on placebo.
◉ Compared to metformin, GLP-1s resulted in a significantly greater reduction in BMI and body weight and showed a greater capacity to reduce overall insulin resistance.
◉ 86% ovulated on GLP-1plus metformin, vs, 29% on metformin alone (that’s 3x higher)
Where Nutrition Fits
Medication is only part of the picture, and this is where nutritional interventions may be the key to adjunctive treatment for PMOS. Some studies are beginning to show promising results.
Vitamin D
In a systematic review and meta analysis, daily, low dose vitamin D supplementation of less than 4000IU per day resulted in significantly decreased HOMA-IR, which shows improved overall insulin sensitivity (9). Vitamin D was also seen to improve menstrual periods, increase folliculogenesis (maturation of ovarian follicles) and decrease blood testosterone levels (11). When combined with other nutrients like calcium, magnesium, zinc or vitamin K, there was a significant reduction in both fasting glucose levels and improvements in how well your body uses insulin.
Magnesium
After 2 months of 250mg/day supplementation of magnesium oxide, women with PMOS showed significant decreases in serum insulin levels and improved insulin sensitivity (10). This makes sense, as magnesium is a co-factor for enzymes involved in glucose metabolism and insulin function.
Omega-3 fatty acids
A systematic review and meta analysis shows that omega 3 supplementation can improve PMOS symptoms (12):
◉ Significantly improves insulin sensitivity
◉ Reduced lipid levels which are key cardiovascular risk factors
Inositol (The 40:1 ratio)
One nutrient that has been getting a lot of attention online is inositol, which is a carbohydrate. In PMOS, the ratio between Myo-inositol and D-chiro-inositol is disrupted, which creates poor egg quality and irregular cycles. Research points to a 40:1 ratio of myo to D-chiro supplementation as the sweet spot - mirroring healthy physiology.
At that ratio, trials show reduced testosterone, more regular cycles and improved insulin sensitivity (13).
The takeaway
PMOS is not a problem with your ovaries that happens to affect the rest of you. It is a whole-body condition with metabolism at its centre, and the new name finally reflects that.And that’s why the medications like metformin and GLP-1s that primarily act on metabolic pathways, are what’s working. If you have spent years being told your symptoms were separate, minor or in your head, the science says otherwise. You deserve treatment that addresses the whole disorder, not only the parts that are easiest to see.
References
1. Teede H, Khomami M, Morman R et al. Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: a multistep global consensus process. The Lancet, 2026; 407, 2329-2339
2. Helena J Teede, Chau Thien Tay, Joop J E Laven, Anuja Dokras, Lisa J Moran, Terhi T Piltonen, Michael F Costello, Jacky Boivin, Leanne M Redman, Jacqueline A Boyle, Robert J Norman, Aya Mousa, Anju E Joham, on behalf of the International PCOS Network, Recommendations From the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome, The Journal of Clinical Endocrinology & Metabolism, Volume 108, Issue 10, October 2023, Pages 2447–2469, https://doi.org/10.1210/clinem/dgad463
3. Zhao, H., Zhang, J., Cheng, X., Nie, X., & He, B. (2023). Insulin resistance in polycystic ovary syndrome across various tissues: an updated review of pathogenesis, evaluation, and treatment. Journal of ovarian research, 16(1), 9. https://doi.org/10.1186/s13048-022-01091-0
4. Gao, X., Zhao, S., Du, Y. et al. Data-driven subtypes of polycystic ovary syndrome and their association with clinical outcomes. Nat Med 31, 4214–4224 (2025). https://doi.org/10.1038/s41591-025-03984-1
5. Zhuang, S., Jing, C., Yu, L., Ji, L., Liu, W., & Hu, X. (2022). The relationship between polycystic ovary syndrome and infertility: a bibliometric analysis. Annals of translational medicine, 10(6), 318. https://doi.org/10.21037/atm-22-714
6. Johanna Melin, Maria Forslund, Simon Alesi, Terhi Piltonen, Daniela Romualdi, Poli Mara Spritzer, Chau Thien Tay, Alexia Pena, Selma Feldman Witchel, Aya Mousa, Helena Teede, The impact of metformin with or without lifestyle modification versus placebo on polycystic ovary syndrome: a systematic review and meta-analysis of randomized controlled trials, European Journal of Endocrinology, Volume 189, Issue 2, August 2023, Pages S38–S64, https://doi.org/10.1093/ejendo/lvad098
7. Lin, S., Deng, Y., Huang, J. et al. Efficacy and safety of GLP-1 receptor agonists on weight management and metabolic parameters in PCOS women: a meta-analysis of randomized controlled trials. Sci Rep 15, 16512 (2025). https://doi.org/10.1038/s41598-025-99622-4
8.Hoteit et al. The dual impact of GLP-1 receptor agonists on metabolic and reproductive health in polycystic ovary syndrome: insights from human and animal trials. Ther Adv Endocrinol Metab. 2025;7;16:20420188251383064.
9. Łagowska, K., Bajerska, J., & Jamka, M. (2018). The Role of Vitamin D Oral Supplementation in Insulin Resistance in Women with Polycystic Ovary Syndrome: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Nutrients, 10(11), 1637. https://doi.org/10.3390/nu10111637
10. Mohan A, Haider R, Fakhor H, Hina F, Kumar V, Jawed A, Majumder K, Ayaz A, Lal PM, Tejwaney U, Ram N, Kazeem S. Vitamin D and polycystic ovary syndrome (PCOS): a review. Ann Med Surg (Lond). 2023 Jun 5;85(7):3506-3511. doi: 10.1097/MS9.0000000000000879. PMID: 37427232; PMCID: PMC10328709.
11. Shahmoradi, S., Chiti, H., Tavakolizadeh, M. et al. The Effect of Magnesium Supplementation on Insulin Resistance and Metabolic Profiles in Women with Polycystic Ovary Syndrome: a Randomized Clinical Trial. Biol Trace Elem Res 202, 941–946 (2024). https://doi.org/10.1007/s12011-023-03744-7
12. Yang, K., Zeng, L., Bao, T. et al. Effectiveness of Omega-3 fatty acid for polycystic ovary syndrome: a systematic review and meta-analysis. Reprod Biol Endocrinol 16, 27 (2018). https://doi.org/10.1186/s12958-018-0346-x
13. Olga Pustotina, Samuel H. Myers, Vittorio Unfer, Irina Rasulova; The Effects of Myo-Inositol and D-Chiro-Inositol in a Ratio 40:1 on Hormonal and Metabolic Profile in Women with Polycystic Ovary Syndrome Classified as Phenotype A by the Rotterdam Criteria and EMS-Type 1 by the EGOI Criteria. Gynecol Obstet Invest 11 April 2024; 89 (2): 131–139.
