For nearly nine decades, doctors have used the term “polycystic ovary syndrome” to describe one of the most common endocrine disorders affecting women of childbearing age. This name is now officially retired.
On May 12, 2026, a major consensus paper was published in The lancet officially announced the renaming of polycystic ovary syndrome (PCOS) to polyendocrine metabolic ovary syndrome (PMOS). The name change was the result of a global consensus process involving 56 leading academic, clinical and patient organizations, as well as over 22,000 survey responses collected over more than a decade of advocacy. In the final survey, 85.6% of patients and 76.1% of healthcare professionals agreed to the change.
This is not just a semantic update. It’s a long-overdue fix that has the potential to reshape the way providers diagnose, treat, communicate about, and fund research into this condition.
Old Name Limitations (PCOS)
The term “polycystic ovary syndrome” was first introduced in 1935 and arose from the observation of follicular structures on imaging that resembled pathological cysts at the time. The structures observed were blocked antral follicles, a consequence of hormonal dysregulation. The ovaries reflected a symptom, not the cause of the problem.
This distinction quietly shaped the way the condition was taught, recognized, and researched, and not always for the better:
- Diagnostic delays: Up to 70% of affected people never received a formal diagnosis.
- Fragmented care: Ovarian centering often overlooked the broader hormonal and metabolic picture.
- stigma: Patients without abnormal cysts on imaging were often told that they were not candidates for the diagnosis.
The new name speaks to all of this directly.
Breaking down the new name
Polyendocrine: The condition is not caused by a single hormonal disorder. It includes multiple interacting endocrine axesincluding increased androgens (e.g. testosterone), impaired insulin signaling, hypersecretion of luteinizing hormone (LH), and disturbances in neuroendocrine regulation. Recognizing this polyendocrine nature is critical to understanding why no single intervention addresses all disease phenotypes.
metabolism: This is perhaps the most clinically significant supplement. PMOS is profound Effects on metabolismincluding insulin resistance, impaired glucose tolerance, dyslipidemia and increased cardiometabolic risk. These are not secondary concerns, but rather more central to the pathophysiology and long-term health consequences of the disease.
ovary: The ovaries remain part of the picture. Reproductive characteristicsincluding anovulation, menstrual irregularities and polycystic ovarian morphology (PCOM) on ultrasound, are still recognized as part of the syndrome. But they are now correctly framed as downstream consequences systemic hormonal dysregulation, not the cause of the problem.
syndrome: Despite its complexity, PMOS remains a syndrome. Not all patients will present the same and the diagnostic criteria still require clinical judgment.
The metabolic core of PMOS
It is important for clinicians working with women with PMOS to understand the metabolic architecture of this condition. The name change itself helps signal this priority.
It is estimated that there is insulin resistance (IR). 50% to 75% of women with PMOS overall, increasing to 70% to 80% in individuals with obesity and to 20% to 25% in individuals with a lean phenotype. Insulin resistance is generally considered to be a major cause of the pathogenesis of the disease.
insulin is a hormone released by the pancreas in response to rising blood sugar. Its job is to signal the cells in muscles, fat and liver to absorb glucose from the bloodstream and use it for energy. When cells become resistant to the insulin signal, the pancreas compensates by producing more and more insulin to get the job done. This condition is known as increased circulating insulin HyperinsulinemiaThis is where much of the downstream damage in PMOS begins.
Androgen excess: Hyperinsulinemia directly stimulates the theca cells of the ovary to the overproduction of androgens, especially testosterone and DHEA. At the same time, hyperinsulinemia suppresses the production of sex hormone-binding globulin (SHBG) in the liver, the protein responsible for binding and inactivating circulating androgens. Less SHBG means more free, biologically active testosterone, which causes the hallmark symptoms of PMOS, including hirsutism (excessive hair growth on the face and body), acne and hair loss.
Impaired ovulation: Hyperinsulinemia also disrupts that hormonal signaling rhythm of gonadotropin-releasing hormone (GnRH)This results in a shift that favors luteinizing hormone (LH) secretion over follicle stimulating hormone (FSH) secretion. This LH/FSH imbalance further increases androgen production and prevents the proper maturation of the follicles, resulting in antral follicle capture on ultrasound and the irregular or absent ovulation that is characteristic of the condition.
From mechanism to management
Treating PMOS begins with addressing the true metabolic drivers. Dietary changes, regular exercise, muscle-building activities, and targeted lifestyle strategies all play an important role in alleviating the underlying dysfunction that underlies this condition. Nutritional supplements can also make a valuable contribution. 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 in your cells. When insulin signals the cell to take up glucose, inositol helps relay that message, essentially helping to open the cell door. Without sufficient inositol or when the balance between its two key forms (Myo-Inositol and D-Chiro-Inositol) is disrupted, this relay breaks down, the glucose remains in the bloodstream and the body compensates for this by releasing even more insulin.
In women with PMOS, where the cells often respond poorly to the insulin signal, inositol supports this process and helps restore the relay and reduce compensatory hyperinsulinemia This increases the downstream effects of the disease. This is important in part because the body requires the two forms of inositol in a certain ratio. about 40 parts myo-inositol to one part d-chiro-inositolespecially in ovarian tissue. If hyperinsulinemia is present, it can change this relationshipwith downstream consequences that extend beyond blood sugar regulation to fertility or reproductive problems. Egg quality can suffer as a resultAnd Ovulation may become irregular or stop altogether.
The use of inositol in the treatment of PMOS is well documented. The most comprehensive synthesis to date, an overview review of 13 meta-analyses from 2026The largest of these included 4,668 participants in 35 randomized controlled trials. They 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 on insulin sensitivity and menstrual regularity.
Berberine
Berberine is a plant compound found in herbs such as barberry and goldenseal. It works Activation of a cellular signaling pathway called AMP-activated protein kinase (AMPK), the same one it targets commonly used diabetes medicationThis makes the cells respond better to insulin and can better control 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 central driver of the disease, activation of this pathway allows cells to do this respond more effectively to insulin and thus reduce the compensatory overproduction of insulin This worsens androgen production in the theca cells of the ovary, a characteristic pattern in PMOS.
The evidence supporting the use of berberine for PMOS is also there well documented. In one Pilot study In 12 women with PCOS, berberine supplementation resulted in a statistically significant reduction in insulin resistance (HOMA), testosterone, triglycerides, BMI, visceral fat, and inflammatory markers (CRP and TNF-α), as well as a significant increase in SHBG. In one randomized controlled trial In 129 women with PCOS, berberine alone as a standalone intervention resulted in statistically significant improvements in waist circumference, waist-to-hip ratio, fasting insulin, testosterone, SHBG, free androgen index, and lipid profile, and outperformed 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 realignment in the way this condition is classified and clinically treated. By formally recognizing its metabolic and polyendocrine nature, the new name better reflects the underlying pathophysiology and provides a more accurate basis for future diagnosis and treatment. Interventions such as inositol and berberine follow this framework and target the insulin signaling pathways that trigger many of the disease’s subsequent hormonal and reproductive consequences. As the evidence base for PMOS continues to evolve, the clinical tools available to support women affected by it continue to evolve.
Learn more about PMOS, inositol and berberine:
Investigating the role of inositol in PCOS
Berberine – the missing link in blood sugar management?
Back to the basics of PCOS
PCOS and insulin – when the diet is not enough
By Ally LaGrutta, MS, CNS, CSCS