In May, one of medicine’s most common — and most misunderstood — hormonal conditions took on a new name. Polycystic ovary syndrome, long known as PCOS, is now being rebranded as polyendocrine metabolic ovarian syndrome, or PMOS. The change reflects decades of evidence showing that ovarian cysts are neither universal nor central to the condition, and brings its underlying endocrine and metabolic dysfunction into clearer focus. Advocates hope that this rebrand will improve diagnosis, shift clinical focus beyond reproduction, and catalyze research into disease-modifying therapies that have remained elusive for decades.
To understand why the name change was needed, it helps to understand how it came to be in the first place. One of the first documented cases of this condition was in 1844, when French physician Achille Chereau published Maladies des Ovaires, a book on ovarian disease. In it, Chereau described ovaries that were enlarged, smooth, and contained many small cysts. In reality, these were not true cysts, but immature, egg-containing follicles that had stopped developing. In the decades that followed, this phenotype was referred to by many names, such as polycystic ovaries, sclerocystic ovaries, microcystic ovaries, or follicular degeneration.
That ovarian focus was solidified in the 1930s, when gynecologists Irving Stein and Michael Leventhal formally described what they believed to be a distinct clinical syndrome. Presenting a series of women with irregular or absent periods, hirsutism (excessive hair growth), infertility, and enlarged ovaries, they proposed that abnormal ovarian structure lay at the heart of the condition.
That ovarian appearance would go on to dominate how the condition was understood, and misunderstood, for more than a century. As the name shifted from Stein-Leventhal syndrome in the 1930s to polycystic ovarian disease in the 1960s, and finally to polycystic ovary syndrome in the 1990s, each new label reflected progress — but continued to center the wrong thing.
The problem with the name was that it focused everything on reproduction — on what the ovaries looked like.
—Ricardo Azziz, University of Alabama
“The problem with the name was that it focused everything on reproduction — on what the ovaries looked like,” Ricardo Azziz, a professor of reproductive endocrinology and gynecology at the University of Alabama at Birmingham, told DDN. “But the truth is, the ovaries don’t always look like that in all patients. And it’s much more than an ovarian disorder. It’s a metabolic disorder. It’s an endocrine disorder.”
The consensus for the new name was reached through a multistep global process involving 56 academic, clinical, and patient organizations, and informed by survey responses from 14,360 individuals, including patients and health professionals.
A diagnosis problem
Despite being historically framed as a gynecological disorder, PMOS is now widely recognized as a multisystem condition that extends far beyond the ovaries. It encompasses endocrine, metabolic, reproductive, dermatological, and psychological features — many of which emerge long before reproductive concerns bring patients into clinical care, if they do at all.
People with PMOS commonly exhibit metabolic dysfunction, including insulin resistance, hyperinsulinemia, and low-grade chronic inflammation. While most patients are not obese, excess adiposity significantly increases both the risk and severity of the condition. Those affected face elevated risks of impaired glucose tolerance, type 2 diabetes, metabolic syndrome, hypertension, and cardiovascular disease. Women with PMOS are also up to five times more likely to develop endometrial cancer.
“The core metabolic dysfunction is insulin resistance, which results in hyperinsulinemia,” Andrea Dunaif, a professor of molecular medicine at the Icahn School of Medicine at Mount Sinai, told DDN. “This confers a fourfold increased risk of type 2 diabetes, with an earlier age of onset than in the general population.”
Additionally, patients with PMOS are at higher risk of mental health issues, including depression, anxiety, premenstrual dysphoric syndrome, bipolar disorder, obsessive-compulsive disorder, and eating disorders. This vulnerability is likely driven by a combination of biological and psychosocial factors, including hormonal dysregulation, metabolic stress, and the visible and deeply personal symptoms of the condition, such as obesity, infertility, acne, and hirsutism.
Yet PMOS remains profoundly underrecognized. The World Health Organization estimates that approximately 70 percent of cases remain undiagnosed globally. Analyses of electronic health records likewise reveal substantial underdiagnosis compared with population-based epidemiological estimates, suggesting that PMOS is routinely overlooked, delaying diagnosis, intervention, and long-term risk management.
By changing the name to reflect the systemic nature of the syndrome, advocates hope that clinicians will recognize PMOS earlier, screen more comprehensively, and treat patients for the full scope of the disease they are living with — not just the reproductive symptoms.
Not just women
Depending on diagnostic criteria, the prevalence of PMOS is between six and 20 percent of reproductive-aged women. But there is more and more evidence that this condition is not sex-specific.
Family studies indicate a strong genetic component, with an estimated heritability of 70 percent. A register-based study of nearly 30,000 daughters of women with or without PMOS showed that daughters of women with PMOS have a fivefold increased risk of being diagnosed with the syndrome.
Additionally, evidence of a male phenotype dates back more than two decades. As early as 2002, researchers reported that brothers of women with PMOS had significantly elevated levels of dehydroepiandrosterone sulfate, an androgen produced primarily by the adrenal glands. More recently, a 2018 meta-analysis of first-degree relatives found significantly increased rates of metabolic abnormalities, with fathers showing higher prevalence of metabolic syndrome, hypertension, and dyslipidemia.
Their male relatives often carry the same genes, but in men the effects tend to show up more on the metabolic and cardiometabolic side.
—Adam Balen, Leeds University
“Their male relatives often carry the same genes, but in men the effects tend to show up more on the metabolic and cardiometabolic side,” Adam Balen, a National Health Service consultant and professor of reproductive medicine at Leeds University, told DDN.
This might lead some to wonder if keeping ‘ovarian’ in the name was suitable. Genetic studies have shown that PMOS has a complex, multigenic basis, encompassing interactions among brain, metabolic, and gonadal function, and is also associated with adverse cardiometabolic outcomes in both women and men.
“The syndrome could easily have been defined first as a metabolic disorder, rather than a reproductive one,” Dunaif said. “That wouldn’t mean downplaying fertility issues or the impact of high androgen levels — those are absolutely not trivial. But, because these metabolic aspects are still not well recognized in the internal medicine community, many of these women receive their general medical care without this context.”
Not everyone agrees. “There was a lot of debate as to whether to keep ovarian or reproductive or anything else in the name,” Azziz explained. “But it is still an ovarian disorder. The ovary doesn’t function normally, it doesn’t ovulate as it should, and it overproduces androgens.”
This was echoed by Balen. “We kept ‘ovarian’ in the name because the ovary is a key component, and it’s something we should never forget. Reproductive problems — particularly anovulation or irregular ovulation — are a central feature of the condition and the most common reason people come to see me with anovulatory infertility.”
Dunaif emphasized that while surveys demonstrated broad agreement that a name change was needed, they did not establish consensus on the name itself. The final name was selected at a closed workshop under strict embargo. "Organizations endorsed the principle of renaming, but there was no independent review of the final name before publication," she said.
She also pointed to substantive scientific gaps in the process. According to Dunaif, participants were not presented with key evidence, including more than two decades of studies documenting a male phenotype in relatives of affected women, or data showing that PMOS comprises genetically distinct subtypes.
This raises questions about whether the new name will achieve lasting consensus. If PMOS is increasingly defined by shared genetic risk and cardiometabolic consequences across sexes, then anchoring the name to ovarian function may limit its clinical reach — and could prompt renewed calls to revisit the decision as the science continues to mature.
More research and funding are needed
Beyond its clinical implications, advocates believe the new name could also help to broaden research attention and funding. “Certainly, we think that by having a new name — one that’s more accurate about the disorder — individual funders, patients, and practitioners will better understand the broad implications of the condition,” said Azziz. “Many funding agencies, and even governmental agencies, tend to push back and say, ‘We’re not interested. This is just a reproductive disorder.’”
That framing has had tangible consequences. Despite affecting millions of women worldwide and carrying a substantial metabolic, psychological, and economic burden, PMOS has historically been underfunded. Analyses of US federal funding from 2006 to 2015 showed that PMOS research received significantly less support than conditions such as rheumatoid arthritis, systemic lupus erythematosus, and tuberculosis — even though these diseases have comparable prevalence and impact on quality of life.
Additionally, funding for PMOS research has been unusually concentrated. The majority of US support has come from a single institute, the National Institute of Child Health and Human Development, reflecting the condition’s longstanding classification as a reproductive health issue. By contrast, diseases like lupus and rheumatoid arthritis are funded across multiple institutes within the National Institutes of Health, enabling broader investigation of their systemic effects.
That imbalance has limited progress. While PMOS is now well recognized as a metabolic and endocrine disorder, relatively little funding has come from institutes whose missions align with those complications, such as the National Heart, Lung, and Blood Institute or the National Institute of Diabetes and Digestive and Kidney Diseases.
Funding discovery research in PMOS is essential to understanding the pathological causes and mechanisms of the syndrome and developing specific treatments. “We need deeper molecular-level studies to understand why the ovary overproduces androgens, why insulin resistance develops, why the pancreas secretes excess insulin, why the brain produces elevated levels of luteinizing hormone, and how inflammation arises in these patients. There are so many unanswered questions,” Azziz said.
From a drug discovery standpoint, insulin and insulin sensitivity are clear therapeutic targets. It’s been shown that drugs which improve insulin sensitivity can also improve the reproductive features of the condition.
—Andrea Dunaif, Icahn School of Medicine
For Dunaif, those unanswered questions point squarely toward endocrinology and metabolism as central to PMOS biology. “From a drug discovery standpoint, insulin and insulin sensitivity are clear therapeutic targets,” she said. “It’s been shown that drugs which improve insulin sensitivity can also improve the reproductive features of the condition.”
Consistent underfunding has led to a research landscape dominated by small, often underpowered studies and slow progress toward disease-modifying therapies. Advocates hope that by explicitly naming the condition’s endocrine and metabolic dimensions in PMOS, it will help reposition it as a multisystem disorder deserving of broader scientific investment.
