Polycystic Ovarian Syndrome (PCOS) as a Metabolic Disorder

by

Introduction

If PCOS is primarily a hormone and reproductive disorder, then the approach to treatment would be different than if high levels of male hormones and chronic failure to ovulate were symptoms. This article looks at PCOS as primarily a metabolic disorder, similar to other metabolic disorders that often accompany it. It is driven by insulin resistance and hyperinsulinemia, and the symptoms can be controlled and can be put into remission by targeting these underlying drivers. 

What is PCOS

PCOS
Polycystic Ovarian Syndrome (PCOS) is the most common hormone-related disorder among females. Depending on the diagnostic criteria used, its prevalence ranges from 5-26%. Diagnosis is usually made based on having 2 out of 3 symptoms.

  • chronic failure to ovulate (often resulting in irregular periods
  • excess production of male hormones (androgens), such as testosterone, characterized by hirsutism (excessive body/facial hair), and male pattern hair loss.
  • polycystic ovaries – which may or may not be present

Several other conditions are commonly associated with PCOS, including

  • metabolic syndrome [2]
  • obesity [3]
  • impaired glucose tolerance [4]
  • type 2 diabetes [5]
  • hypertension [6]
  • non-alcoholic fatty liver disease (NAFLD) – recently renamed “metabolic dysfunction-associated steatotic liver disease (MASLD). [7]

Understanding PCOS as a metabolic disorder that results in hormone disruption, rather than hormonal failure that leads to metabolic disease, reframes both the underlying cause and treatment. It shifts the focus from high testosterone and irregular cycles as the root cause of PCOS to understanding these as the downstream symptoms of metabolic disruption. 

Current research points to the underlying cause of PCOS as a combination of insulin resistance and hyperinsulinemia [8].

  • After we eat, the breakdown of food results in glucose rising in the blood.
  • Since the body requires blood sugar (glucose) to be kept in a very narrow range, insulin is released from the beta cells of the Pancreas to lower blood sugar.
  • Insulin binds to an insulin receptor on the surface of the cell. This acts like a “key,” sending a signal to the cell to open up “glucose doors” (GLUT4 transporters).
  • Once these doors are open, glucose can move from the blood into the cell

Insulin resistance is a state where the body becomes “deaf” (resistant) to insulin’s signal.

  • Instead of what occurs when a person is not insulin resistant, the “glucose doors” of the cell no longer open in response to insulin. They don’t “hear” the knock at the door.
  • Blood glucose keeps rising, so the pancreas pumps out more and more insulin to try to force the “doors” of the muscle and liver open, to move the excess glucose out of the blood.
  • Insulin resistance results in the liver ignoring the insulin signal, which normally would cause it to stop producing sugar (a process called gluconeogenesis). This insulin resistance results in the liver pumping out even more glucose into the blood while simultaneously converting the excess into fat—leading to the fatty liver so common in PCOS.

This creates a state of hyperinsulinemia (too much insulin in the blood).

While the muscles and liver have become “deaf” to insulin’s signal (i.e., insulin resistance), the ovaries remain sensitive to insulin and “hear” insulin’s signal just fine.

  • The huge amounts of insulin released by the pancreas in an attempt to lower blood glucose (i.e., hyperinsulinemia) result in the ovaries misinterpreting this signal, and instead of maturing an egg, the excess insulin results in them producing testosterone instead. This sets off a hormonal domino effect.
  • Normally, after ovulation, the empty follicle left after the egg has been released becomes the corpus luteum, which produces progesterone. Progesterone is the “calming” hormone that balances estrogen.
  • Without ovulation, there is no progesterone. This leaves estrogen unopposed, which can lead to heavier periods, mood swings, and further metabolic disruption.
  • High insulin increases androgens (such as testosterone); high androgens stall ovulation; stalled ovulation leads to low progesterone; low progesterone makes the body even more sensitive to stress and insulin, and the vicious cycle continues.

In PCOS, the ovaries are caught in a form of metabolic “cross-talk”. They respond to a signal that was never meant for them, resulting in the androgen excess and stalling ovulation, which are hallmarks of PCOS [8].

Treating PCOS as a Metabolic Disorder

Years ago, I thought PCOS was a gynaecological disorder outside my scope of practice, but approximately 10 years ago, I came to understand it as primarily a metabolic disorder — driven by insulin resistance and hyperinsulinemia. I already had almost a decade of experience teaching a lower-carbohydrate diet to those with other disorders driven by the same two factors, including pre-diabetes and type 2 diabetes, and approaching it similarly enabled women with PCOS to significantly lower their symptoms. This is the same approach I use today.

A 2025 meta-analysis found that both low-carbohydrate and ketogenic diets have been successfully used in 12 studies in women with PCOS [9].

Another approach that enables insulin levels to fall is to avoid between-meal snacks, and this is readily embraced once the person has a Meal Plan designed for their needs that keeps them from feeling hungry between meals. In addition, teaching a person to time their meals around their body’s normal day-night cycle (circadian rhythm) enables their insulin levels to fall significantly overnight.

Something as simple as encouraging women to engage in some form of resistance training enables them reduce insulin resistance in the muscle.

The best part is that these dietary and lifestyle changes are easy to adopt and are sustainable long-term. 

Understanding PCOS as a metabolic disorder is key to understanding why a lower carbohydrate dietary and specific lifestyle changes help reduce its symptoms.

More Info

To learn about me here, and about the Polycystic Ovarian Syndrome (PCOS) Package that I offer.

To your good health.

Joy

You can follow me on:

Twitter: https://twitter.com/jyerdile
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

Support for PCOS

I can design a Meal Plan for you to address the underlying
insulin resistance and high insulin levels of PCOS,
which will enable you to lose weight,
without being hungry all the time.

Book an Appointment

 

References

  1. Bozdag G, Mumusoglu S, Zengin D, Karabulut E, Yildiz BO. The prevalence and phenotypic features of polycystic ovary syndrome: a systematic review and meta-analysis. Hum Reprod. 2016 Dec;31(12):2841-2855.
  2. Prosperi S, Chiarelli F. “Insulin resistance, metabolic syndrome and polycystic ovaries.” Frontiers in Endocrinology, Front. Endocrinol., 30 September 2025, Sec. Pediatric Endocrinology
  3. Volume 16 – 2025 | https://doi.org/10.3389/fendo.2025.1669716
  4. Amiri M, Hatoum S, Hopkins D, Buyalos RP, Ezeh U, Pace LA, Bril F, Sheidaei A, Azziz R. The Association Between Obesity and Polycystic Ovary Syndrome: An Epidemiologic Study of Observational Data. J Clin Endocrinol Metab. 2024 Sep 16;109(10):2640-2657. doi: 10.1210/clinem/dgae488. PMID: 39078989.
  5. Sulu C, Pervaz I, Gurer T et al, The frequency of polycystic ovary syndrome in women with prediabetes compared with normoglycemic women, Frontiers in Endocrinology, Front. Endocrinol., 25 November 2025, Sec. Reproduction, Volume 16 – 2025 | https://doi.org/10.3389/fendo.2025.1722978
  6. Dokras, A, Polycystic ovary syndrome in 2025—insights and innovations, Fertility and Sterility,
    Volume 124, Issue 5, Part 2, 2025, Pages 907-909, ISSN 0015-0282,
    https://doi.org/10.1016/j.fertnstert.2025.09.025.(https://www.sciencedirect.com/science/article/pii/S0015028225019223)
  7. Romero DG, Abdelhameed AM, Eissa MA, Yanes Cardozo LL. Hypertension and Obesity in Women with PCOS: Now Is the Time to Improve Women’s Care. Journal of Women’s Health. 2025;34(12):1435-1437. doi:10.1177/15409996251380342
  8. Spremović Rađenović, S., Pupovac, M., Andjić, M., Bila, J., Srećković, S., Gudović, A., Dragaš, B., & Radunović, N. (2022). Prevalence, Risk Factors, and Pathophysiology of Nonalcoholic Fatty Liver Disease (NAFLD) in Women with Polycystic Ovary Syndrome (PCOS). Biomedicines, 10(1), 131. https://doi.org/10.3390/biomedicines10010131
  9. Houston EJ, Templeman NM. Reappraising the relationship between hyperinsulinemia and insulin resistance in PCOS. J Endocrinol. 2025 Mar 12;265(2):e240269. doi: 10.1530/JOE-24-0269. PMID: 40013621; PMCID: PMC11906131.
  10. Tosatti JAG, Magalhães FMV, Gomes KB. Effects of the very low-carbohydrate ketogenic diet in women with polycystic ovary syndrome: a systematic review with meta-analysis of clinical trials. British Journal of Nutrition. Published online 2025:1-16. doi:10.1017/S0007114525105692
LEGAL NOTICE: The contents of this blog, including text, images, and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this content.