Understanding the Shift from PCOS to PMOS

As of May 2026, the name of the most common endocrine condition in reproductive females, polycystic ovary syndrome (PCOS), has been changed to polyendocrine metabolic ovarian syndrome (PMOS). Let’s talk about what this condition is, why this name change was necessary, and how this changes the game for those diagnosed with PMOS.

What is PMOS?

PMOS, previously known as PCOS, is the most common endocrine disorder among females of reproductive age worldwide, with about 5% to 26% of females affected and more than 170 million females affected globally (Shukla et al., 2025; Teede et al., 2026). With features of metabolic, reproductive, psychological, and dermatological abnormalities, PMOS is a complex disorder with multiple likely causes. 

Some of the most commonly proposed causes include altered signalling of important endocrine hormones, such as follicle-stimulating hormone and luteinizing hormone, which result in abnormal androgen (male sex hormones) levels and contribute to excess fat around organs and the abdomen (Shukla et al., 2025). Insulin resistance is also a major contributor to PMOS, as it is present in approximately 85% of PMOS patients and can lead to increased androgen levels (Cassar et al., 2016; Stepto et al., 2013). There have also been strong findings suggesting that there is a genetic component to PMOS, where environmental exposures can influence genes and contribute to the development of PMOS (Escobar-Morreale, 2018). With that being said, there have been many other causes speculated to contribute to PMOS, including chronic low-grade inflammation and changes in the gut microbiome (Aboeldalyl et al., 2021; Zhu et al., 2026).

Several common symptoms present with PMOS, including worsening acne, hirsutism which is coarse hair growth in patterns typical of males but seen in females, hair loss, abnormal menstruation, higher body mass index, and fertility problems (Shukla et al., 2025). 

Typically, diagnosis of PMOS consisted of patients meeting 2 out of 3 criteria from the Rotterdam criteria (Dason et al., 2024): 

• Irregular menstrual cycles

• Increased amounts of androgens, which are seen either clinically or biochemically

• Polycystic ovaries or elevated levels of anti-Müllerian hormone, which is produced by ovarian follicles in females

Why is this name change necessary?

After a global deliberation that engaged with 10,411 patients, 3,949 healthcare professionals from various healthcare fields, expert groups, and organizations representing disciplines ranging from gynecology, endocrinology, primary care, psychology, dermatology, imaging, and nutritional science, 84% of respondents agreed that PMOS is a more fitting term than PCOS (Teede et al., 2025). PCOS can be misleading as it focuses on the presence of ovarian cysts, which implies that they are present in every patient diagnosed with the condition. However, PMOS places greater emphasis on the polyfollicular and metabolic nature of the condition. With less emphasis on cyst formation in the ovaries (which not all patients present with), and more emphasis on its multisystem features, PMOS shifts the focus of this condition towards its potential metabolic roots rather than solely on the symptoms that may or may not be present.

What can we expect from this change?

This name change should lead to a greater understanding of the condition and improve the accuracy of future diagnostic criteria, quality of care, policy, and research. By rethinking what the syndrome is, this may result in changes to the diagnostic criteria, potentially incorporating metabolic criteria such as insulin resistance, abnormal blood sugar levels, or abnormal blood lipid levels. This name change may also encourage physicians to screen for other health concerns aside from the characteristic PMOS symptoms as certain metabolic abnormalities may be present even in patients who fall within the normal BMI range. 

Overall, PMOS allows the condition to be viewed as more complex than it was previously understood. By doing so, patients can be assessed more comprehensively, and future PMOS research focusing on metabolic causes may receive greater attention and funding. Additionally, policies can potentially be developed to improve the lives of patients exposed to relevant risk factors.

References

Aboeldalyl, S., James, C., Seyam, E., Ibrahim, E. M., Shawki, H. E., & Amer, S. (2021). The role of chronic inflammation in polycystic ovarian syndrome-A systematic review and meta-analysis. International Journal of Molecular Sciences, 22(5), 2734. https://doi.org/10.3390/ijms22052734

Cassar, S., Misso, M. L., Hopkins, W. G., Shaw, C. S., Teede, H. J., & Stepto, N. K. (2016). Insulin resistance in polycystic ovary syndrome: a systematic review and meta-analysis of euglycaemic-hyperinsulinaemic clamp studies. Human Reproduction, 31(11), 2619–2631. https://doi.org/10.1093/humrep/dew243 

Dason, E. S., Koshkina, O., Chan, C., & Sobel, M. (2024). Diagnosis and management of polycystic ovarian syndrome. Canadian Medical Association Journal, 196(3), E85–E94. https://doi.org/10.1503/cmaj.231251 

Escobar-Morreale H. F. (2018). Polycystic ovary syndrome: definition, aetiology, diagnosis and treatment. Nature Reviews Endocrinology, 14(5), 270–284. https://doi.org/10.1038/nrendo.2018.24

Shukla, A., Rasquin, L. I., & Anastasopoulou, C. (2025). Polyendocrine metabolic ovarian syndrome. StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK459251/ 

Stepto, N. K., Cassar, S., Joham, A. E., Hutchison, S. K., Harrison, C. L., Goldstein, R. F., & Teede, H. J. (2013). Women with polycystic ovary syndrome have intrinsic insulin resistance on euglycaemic-hyperinsulaemic clamp. Human Reproduction, 28(3), 777–784. https://doi.org/10.1093/humrep/des463

Teede, H. J., Khomami, M. B., Morman, R., Laven, J. S. E., Joham, A. E., Costello, M. F., Patil, M., Rees, D. A., Berry, L., Cree, M. G., Zhao, H., Norman, R. J., Dokras, A., Piltonen, T., & Global Name Change Consortium. (2026). Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: A multistep global consensus process. The Lancet, 407(10545), 2329–2339. https://doi.org/10.1016/S0140-6736(26)00717-8 

Teede, H. J., Moran, L. J., Morman, R., Gibson, M., Dokras, A., Berry, L., Laven, J. S. E., Joham, A., Piltonen, T. T., Costello, M. F., Norman, R. J., & Bahri Khomami, M. (2025). Polycystic ovary syndrome perspectives from patients and health professionals on clinical features, current name, and renaming: A longitudinal international online survey. eClinicalMedicine, 84, 103287. https://doi.org/10.1016/j.eclinm.2025.103287

Zhu, T., Sha, Y., Wang, Q., Yang, H., & Liu, T. (2026). Gut microbiota and polycystic ovary syndrome: Pathogenesis and novel therapeutic approaches. Microbiological Research, 312, 128643. https://doi.org/10.1016/j.micres.2026.128643