Polycystic Ovarian Syndrome (PCOS) as a Metabolic Disorder

This article was originally posted on January 27, 2026, and was updated on April 19, 2026.

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 put into remission by targeting these underlying drivers. 

Practitioner’s Preface

In my almost 18 years of private clinical practice and my licensure in British Columbia, Alberta, and Ontario, I have provided care to scores of women with PCOS. Most have thought of it primarily as a reproductive disorder, rather than a metabolic disorder. While PCOS does affect menstrual cycles and thus, reproduction, that is an effect, rather than an underlying cause.  PCOS is primarily a metabolic disorder driven by high levels of insulin and resulting insulin resistance.

What is 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

In my experience, some women are told they don’t have PCOS because an ultrasound doesn’t show that they have polycystic ovaries, yet they are struggling with hirsutism, or male pattern hair loss, and often have some of the other conditions 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 ~10 years ago, I came to understand it as primarily a metabolic disorder — driven by insulin resistance and hyperinsulinemia. At the time, I already had almost a decade of experience teaching a carbohydrate-controlled diet to those with other disorders driven by the same two factors, including pre-diabetes and type 2 diabetes. Applying this approach to PCOS was a natural progression and one that is supported by a 2025 meta-analysis that found that low-carbohydrate and ketogenic diets have been successfully used in 12 studies in women with PCOS [9].

• While the overall dietary approach I take in PCOS is similar to that of other metabolic disorders, I also include specific modifications that are tailored to the needs of women with PCOS. 
• One example is encouraging women to avoid between-meal snacks because this supports insulin levels falling; however, an important consideration is that this will only be sustainable if she also doesn’t feel hungry between meals. This is where a Meal Plan developed specifically for her comes in.
• I also teach women with PCOS to time their meals around their body’s normal day-night cycle (circadian rhythm), which further supports insulin levels falling overnight.
• Even something as simple as encouraging women to engage in simple forms of resistance training that can be incorporated into daily life enables them to reduce insulin resistance in the muscles.

These dietary and lifestyle changes are easy to adopt and to sustain long-term, and it starts with understanding PCOS as primarily a metabolic disorder.

Clinical Application

To effectively treat a condition, we first need to understand what drives it. Helping women understand that PCOS is primarily a metabolic disorder that affects their reproductive system helps them understand why dietary and lifestyle changes focus on high levels of circulating insulin and insulin resistance.

More Info

Learn about me and the Polycystic Ovarian Syndrome (PCOS) Package that I offer. 

To your good health.

Joy

You can follow me on:

Twitter: https://twitter.com/jyerdile
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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