For nearly nine decades, clinicians have used the term "polycystic ovary syndrome" to describe one of the most common endocrine conditions affecting women of reproductive age. That name is now officially retired.

On May 12, 2026, a large consensus paper published in The Lancet formally announced the renaming of polycystic ovary syndrome (PCOS) to polyendocrine metabolic ovarian syndrome (PMOS). The name change was the result of a global consensus process involving 56 leading academic, clinical, and patient organizations and over 22,000 survey responses collected across more than a decade of advocacy. In the final survey, 85.6% of patients and 76.1% of health professionals agreed with the change.

This is not merely a semantic update. It is a long-overdue correction that has the potential to reshape how providers diagnose, treat, communicate about, and fund research for this condition.

Limitations of the Old Name (PCOS)

The term “polycystic ovary syndrome” was first introduced in 1935, born from the observation of follicular structures on imaging that, at the time, resembled pathological cysts. The structures observed were arrested antral follicles, a consequence of hormonal dysregulation. The ovaries were reflecting a symptom, not the source of the problem. 

That distinction quietly shaped how the condition was taught, recognized, and researched, and not always for the better:

• Diagnostic delays: Up to 70% of affected individuals have never received a formal diagnosis.
• Fragmented care: By centering the ovaries, the broader hormonal and metabolic picture was frequently missed.
• Stigma: Patients without prominent cysts on imaging were often told they didn’t qualify for the diagnosis. 

The new name addresses all of this directly.

Breaking Down the New Name

Poly-endocrine: The condition is not driven by a single hormonal disruption. It involves multiple interacting endocrine axes, including elevated androgens (e.g., testosterone), dysregulated insulin signaling, luteinizing hormone (LH) hypersecretion, and disruptions in neuroendocrine regulation. Recognizing this polyendocrine nature is critical to understanding why no single intervention addresses all phenotypes of the condition.

Metabolic: This is perhaps the most clinically significant addition. PMOS carries profound metabolic implications, including insulin resistance, impaired glucose tolerance, dyslipidemia, and elevated cardiometabolic risk. These are not secondary concerns but more central to the condition's pathophysiology and long-term health outcomes.

Ovarian: The ovaries still remain part of the picture. Reproductive features, including anovulation, menstrual irregularity, and polycystic ovarian morphology (PCOM) on ultrasound, are still recognized as part of the syndrome. But they are now correctly framed as downstream consequences of systemic hormonal dysregulation, not the origin of the problem.

Syndrome: PMOS remains a syndrome, acknowledging its complexity. Not all patients will present identically, and the diagnostic criteria will continue to require clinical judgment.

The Metabolic Core of PMOS

For practitioners working with women with PMOS, understanding the metabolic architecture of this condition is essential. The name change itself helps signal this priority.

Insulin resistance (IR) is present in an estimated 50% to 75% of women with PMOS overall, rising to 70% to 80% in those with obesity and 20% to 25% in lean phenotypes. Insulin resistance is widely regarded as a chief driving force in the pathogenesis of the condition.

Insulin is a hormone secreted by the pancreas in response to rising blood sugar. Its job is to signal cells, in muscle, fat, and the liver, to take up glucose from the bloodstream and use it for energy. When cells become resistant to insulin's signal, the pancreas compensates by producing more and more insulin to get the job done. This state of elevated circulating insulin, known as hyperinsulinemia, is where much of the downstream damage in PMOS begins.

Androgen Excess: Hyperinsulinemia directly stimulates the ovarian theca cells to overproduce androgens, particularly testosterone and DHEA. At the same time, hyperinsulinemia suppresses the liver's production of sex hormone-binding globulin (SHBG), the protein responsible for binding and inactivating circulating androgens. Less SHBG means more free, biologically active testosterone, which drives the hallmark symptoms of PMOS, including hirsutism (excess facial and body hair growth), acne, and hair thinning.

Disrupted Ovulation: Hyperinsulinemia also disrupts the hormonal signaling rhythm of gonadotropin-releasing hormone (GnRH), causing a shift that preferentially drives luteinizing hormone (LH) secretion over follicle-stimulating hormone (FSH). This LH/FSH imbalance further amplifies androgen production and prevents follicles from maturing properly, resulting in the arrested antral follicles seen on ultrasounds and the irregular or absent ovulation that characterizes the condition.

From Mechanism to Management

Managing PMOS starts with addressing its true metabolic drivers. Dietary changes, regular movement, muscle-building activities, and targeted lifestyle strategies all play a meaningful role in supporting the underlying dysfunction at the core of this condition. Nutritional supplementation can also be a valuable piece of that picture. Among the options with growing clinical support, two stand out for their direct impact on insulin signaling: inositol and berberine.

Inositol

Inositol is a naturally occurring compound that acts like an internal relay signal inside your cells. When insulin signals the cell to take in glucose, inositol helps carry that message forward, essentially helping the cell door open. Without enough inositol, or when the balance between its two key forms (myo-inositol and D-chiro-inositol) is disrupted, that relay breaks down, glucose stays in the bloodstream, and the body compensates by pumping out even more insulin.

In women with PMOS, where cells often respond poorly to insulin's signal, inositol steps in to support that process, helping restore the relay and reduce the compensatory hyperinsulinemia that fuels the condition's downstream effects. This matters in part because the body requires the two inositol forms in a specific ratio, roughly 40 parts myo-inositol to one part D-chiro-inositol, particularly in ovarian tissue. When hyperinsulinemia is present, it can alter that ratio, with downstream consequences extending beyond blood sugar regulation into fertility or reproductive concerns. Egg quality may suffer, and ovulation may become irregular or stop altogether. 

Inositol use in the management of PMOS is well-documented. The most comprehensive synthesis to date, a 2026 umbrella review of 13 meta-analyses, the largest of which included 4,668 participants across 35 randomized controlled trials, found that inositol supplementation consistently improved hormonal profiles, glucose metabolism, lipid levels, and reproductive outcomes in women with PMOS, with myo-inositol showing particular benefit for insulin sensitivity and menstrual regularity.

Berberine

Berberine is a plant-derived compound found in herbs like barberry and goldenseal. It works by activating a cellular pathway called AMP-activated protein kinase (AMPK), the same one targeted by commonly used diabetes medication, which makes cells more responsive to insulin and better at managing blood sugar. AMPK acts like a switch. When activated, it signals cells to absorb more glucose, burn fat for energy, and become more sensitive to insulin. In women with PMOS, where insulin resistance is a core driver of the condition, activating this pathway allows cells to respond to insulin more effectively, reducing the compensatory overproduction of insulin that worsens androgen production in the ovarian theca cells, a hallmark pattern in PMOS. 

The evidence behind berberine use in PMOS is also well-documented. In a pilot study of 12 women with PCOS, berberine supplementation produced statistically significant reductions in insulin resistance (HOMA), testosterone, triglycerides, BMI, visceral fat, and inflammatory markers (CRP and TNF-α), alongside a significant increase in SHBG. In a randomized controlled trial of 129 women with PCOS, berberine used alone as a standalone intervention produced statistically significant improvements in waist circumference, waist-to-hip ratio, fasting insulin, testosterone, SHBG, free androgen index, and lipid profile, outperforming both metformin and myo-inositol in body composition, hormonal, and lipid parameters.

A More Complete Picture 

The renaming of PCOS to PMOS reflects a structural reframing of how this condition is classified and clinically approached. By formally recognizing its metabolic and polyendocrine nature, the new name better reflects the underlying pathophysiology and creates a more accurate foundation for future diagnosis and treatment. Interventions like inositol and berberine align with that framework, targeting the insulin signaling pathways that drive many of the condition's downstream hormonal and reproductive consequences. As the evidence base for PMOS continues to develop, so too will the clinical tools available to support the women affected by it.

Learn more about PMOS, inositol, and berberine:

Investigating the Role of Inositol in PCOS 

Berberine – The Missing Link in Blood Glucose Management?

Getting Back to the Basics of PCOS

PCOS and Insulin – When Diet Is Not Enough

By Ally LaGrutta, MS, CNS, CSCS