Medicines, and not just renaming, heals disease

Lean women constitute a substantial proportion of those diagnosed with PCOS, though the proportion varies considerably between populations. (Shutterstock)

When a medical condition is given a new name, it begins to cast a different sort of shadow over the people who live with it. Polycystic Ovarian Syndrome (PCOS), a disorder that affects 170 million women worldwide, has been rechristened. It’s now called Polyendocrine Metabolic Ovarian Syndrome (PMOS).

Lean women constitute a substantial proportion of those diagnosed with PCOS, though the proportion varies considerably between populations. (Shutterstock)
Lean women constitute a substantial proportion of those diagnosed with PCOS, though the proportion varies considerably between populations. (Shutterstock)

The proponents (global experts and patient advocates) of re-naming argue the change was necessary because the old name encouraged a narrow focus on ovaries, leaving other important health consequences insufficiently recognised and addressed.

PCOS indeed extends beyond reproduction, encompassing insulin resistance, hypertension, diabetes, dyslipidaemia, atherosclerosis, sleep apnoea, body-image concerns, anxiety and depression; together, these may substantially increase future cardiovascular and psychological risk.

The metabolic and psychological dimensions of PCOS have long been recognised by gynaecologists and reproductive endocrinologists. Guidelines for identifying and managing these features have existed for years, most recently updated in 2023. The hope is that renaming may encourage wider adherence.

The rebranding, however well intentioned, creates two problems — imposing uniformity on a condition defined by variation, and inviting unnecessary alarm. PCOS is so heterogeneous that no global consensus exists on its diagnosis. Japanese and Chinese criteria differ from the International Consensus Guidelines and, in many ways, from each other. These divergences reflect the influence of ethnicity, environment and population-specific risk profiles on how the syndrome presents. Since 2003, the internationally accepted Rotterdam criteria have defined PCOS by the presence of any two of three features: Irregular periods, typically delayed or unpredictable; excess facial or body hair and acne in a male-pattern distribution; and polycystic ovaries on ultrasound.

Neither the Rotterdam criteria nor any major international guideline requires metabolic syndrome, or even insulin resistance, for a PCOS diagnosis. Clinicians have long recognised that metabolic dysfunction characterises some, but by no means all, women with the condition. This makes the “M” in PMOS troubling, and possibly a distortion. By placing metabolism at the centre of the definition, the new name risks rendering metabolically healthy women with PCOS conceptually invisible. Depending on the population studied, women without significant metabolic impairment comprise 50-70% of diagnosed cases. Metabolic risk is strongly associated with obesity, though leanness offers no absolute protection.

Lean women constitute a substantial proportion of those diagnosed with PCOS, though the proportion varies considerably between populations. Using a BMI threshold of less than 25 kg/m², they account for nearly 70% of cases in Japan and China, around 50% in India, and about 40% in western populations. Yet, leanness is not a simple category. Indians have a tendency to accumulate visceral fat at lower body weights, meaning that even a BMI of 25 may conceal a degree of metabolic and cardiovascular risk.

This pattern is less common in western populations, where BMI correlates more closely with overall fat distribution. A waist-hip ratio is more informative than weight alone. Among lean women with PCOS, roughly half store fat predominantly around the hips and thighs, while the remainder accumulate it centrally around the abdominal organs. These tendencies arise from a complex interplay of genetic, intrauterine and environmental influences.

Women with the gynoid form (0.7-0.8 waist-hip ratio) of lean PCOS typically lack insulin resistance and are not at increased risk of diabetes, hypertension, cardiovascular disease or stroke. The gynoid pattern of fat distribution seen in multiple celebrities who have talked of living with PCOS means that the fat is away from the abdominal organs, thereby mitigating metabolic risk. They nevertheless have genuine PCOS, driven by reproductive hormonal imbalance causing ovulatory dysfunction and hyperandrogenic symptoms. The new name risks obscuring this important reality: A purely reproductive, metabolically-healthy variant of PCOS exists.

Modern abundance has superimposed a lifestyle disorder upon a reproductive hormonal one. The renaming, therefore, risks making PCOS appear broader and more intrinsically pathological than it is, implying disease mechanisms beyond hormonal disturbance and obesity.

Weight gain, visceral adiposity, sedentary living and chronic caloric excess are the real forces shaping metabolic risks across a lifetime. Many of the non-reproductive manifestations associated with PCOS are not unique expressions of the syndrome itself, but reflections of the wider obesity-inducing environment in which it occurs.

Traditionally, this variation has been acknowledged by distinguishing between lean and obese PCOS, and between those with and without the metabolic syndrome, because future risk is embedded in those differences. The new name risks implying that metabolic dysfunction arises directly from PCOS itself, locating disease risk within an immutable pathology rather than the influence of lifestyle. To transfer responsibility for metabolic syndrome from lifestyle to biology is a dangerous manoeuvre. It encourages the comforting belief that nothing much can be done, and thereby makes doing something far less likely.

Ruma Satwik is a Delhi-based gynaecologist. The views expressed are personal

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Posted in US

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