PCOS Is Now PMOS. The Criteria Still Were Not Built for Perimenopause or Menopause.

Written by: Meredith Paci | Functional Health Coach

If you have been following us for any length of time, none of this will shock you. But it should sharpen how you think about it.

On May 12th, 2026, PCOS was formally renamed to PMOS, Polyendocrine Metabolic Ovarian Syndrome. Published in The Lancet. Presented at the European Congress of Endocrinology in Prague. Eleven years in the making, with input from roughly 22,000 people across the globe.

The name beat out two other finalists: endocrine metabolic ovulatory syndrome and ovulatory metabolic endocrine syndrome. It was not close.

Here is what I will say and this is solely my opinion. They started off great. "Polyendocrine" recognizes that multiple hormonal systems are involved. Insulin, androgens, neuroendocrine signaling from the hypothalamus and pituitary. I was cheering. "Metabolic" puts insulin resistance, inflammation, and long term cardiometabolic risk front and center. Still cheering. Then they kept "ovarian" in the name and I thought, we were so close.

Because "ovarian" still frames this as primarily an ovarian condition. Which, in my humble opinion, still leaves out the subset of women who do not have their ovaries. It still narrows the lens in a way the rename was supposed to widen. Growing research has pointed out that retaining "ovarian" also closes the door on the possibility of a male form of the syndrome, which early research has begun to suggest exists.

But progress is progress. And the core principle holds: this is a metabolic and endocrine condition first. The ovarian features are one possible downstream expression. They are not the root cause. For decades, "polycystic ovarian syndrome" anchored an entire condition to a finding on an ultrasound. Cysts on the ovaries. Except they are not even cysts. They are arrested follicles. And for many women, the ovaries were never the problem. They were a downstream casualty of something metabolic happening upstream.

What We Told You in January

Back in January 2026, I sent a newsletter after sitting through roughly six hours of PCOS-focused education over a weekend. The very first takeaway was that PCOS needed a new name. The proposed name discussed in that course was FEMS, Female Endocrine Metabolic Spectrum. I wrote at the time that I loved the logic. "Spectrum" reflected the range of systems affected, symptom patterns, and severities we see clinically.

The name that ultimately landed was different. The thesis was the same. If you read that January newsletter, you understood the reasoning behind this rename months before social media caught up to it. The specific acronym changed. The reasoning did not.

The Question That Sparked This Conversation

A coach inside our mentorship program recently asked a series of questions that I think every practitioner working with women should be sitting with right now.

What would PMOS look like in a woman who is in menopause? If up to 70 percent of cases go undiagnosed during reproductive years, what are we actually seeing in those women now? What would LH and FSH even tell us at that stage? And can someone present with more than one "type" of PCOS at the same time?

These are the questions that expose exactly where the current framework falls short.

Let me work through them.

Diagnosing PMOS in Menopause: When the Traditional Markers Disappear

The diagnostic criteria for PMOS still follow the 2023 framework: meet 2 out of 3. Excess androgens, either by bloodwork or clinical signs. Irregular menstrual cycles. And either elevated AMH on bloodwork or polycystic ovarian morphology on ultrasound.

Here is the problem. These criteria were designed for women in their reproductive years. Or even more specifically, women within their reproductive years who have reproductive capacity via intact ovaries. And in menopause, two of those three criteria become either irrelevant or uninterpretable.

Menstrual cycle irregularity is meaningless when there is no cycle. Ovarian morphology is meaningless when the ovaries are no longer functioning or, in some cases, are literally gone. And LH and FSH, which in reproductive-age women can show that characteristic flip where LH runs two to three times higher than FSH, both rise dramatically in menopause. FSH especially. That is supposed to happen. The brain is calling down to the ovaries and the ovaries are not answering. Once FSH climbs above 25 or so, we know where she is in that transition. Both numbers end up elevated, often into the 50s, and that ratio that was once a useful clinical clue essentially normalizes. It becomes noise.

So you lose the cycle pattern. You lose the ovarian morphology. You lose the LH to FSH ratio. And what you are left with is androgens and the metabolic picture.

But even the androgen piece requires a pause. Because not all androgen elevation in perimenopause and menopause means PMOS.

Normal Menopausal Shift Versus Actual PMOS

This is a distinction I think a lot of people are missing, and it is a clinically important one.

During the menopausal transition, estrogen and progesterone decline. Testosterone can hold relatively steady while the counterbalance drops away. The result is a state of relative androgen excess. The SWAN study, one of the best longitudinal datasets we have on the menopausal transition, showed that the testosterone to estradiol ratio increased roughly 10 percent per year over five years of follow-up. And that increasing ratio was associated with incident metabolic syndrome.

So a perimenopausal woman showing up with new facial hair, central weight gain, or worsening insulin sensitivity is not automatically developing PMOS. She may be experiencing the expected hormonal ratio shift of menopause. The androgen did not go up. The counterbalance went away. That is a critical distinction.

Now think about the demographic of women who are in natural menopause right now in 2026. These are the women who were told they did not need hormone testing. That their hormones fluctuate so why bother running labs. That what they were experiencing was normal. How many of them were actually navigating an undiagnosed metabolic and endocrine condition for decades and nobody looked? We genuinely do not know. And that is the problem.

These are also, in many cases, the same women who had hysterectomies earlier in life because of heavy periods, painful cycles, or issues that were managed surgically instead of investigated upstream. When you think about that demographic and what they were and were not offered in terms of evaluation, the 70 percent undiagnosed statistic starts to feel conservative.

So how do you distinguish a normal menopausal shift from something that actually looks like PMOS?

There is no single clean line. But several things tilt the picture.

Clinical history is your strongest differentiator. A woman who had textbook regular cycles, no androgen symptoms, and no metabolic issues in her 20s and 30s, and now presents with some facial hair and worsening insulin sensitivity at 51, that is likely a menopausal ratio shift until proven otherwise. Compare that to a woman who had irregular cycles since menarche, struggled with fertility, carried weight centrally her whole life, maybe had acne or hirsutism that was brushed off as cosmetic, and now in perimenopause those features are amplifying. That history tells you something was operating upstream long before estrogen started declining.

Going back to her history and really asking the right questions is probably the most powerful tool you have here. Labs are a snapshot. Her story is the whole film.

Absolute versus relative androgen levels. In the normal menopausal shift, testosterone typically is not falling as fast as estrogen. So if you see total testosterone or free testosterone that is genuinely above the age-adjusted reference range, not just higher relative to her now-low estradiol, that changes the conversation. If she has free testosterone that is well above clinical range, that starts to look like a duck and quack like a duck. But a mild elevation? You may need to pump the brakes or at least pause.

Same applies to DHEA-S, which typically naturally declines with age. A 52-year-old with a DHEA-S level that would be high even for a 30-year-old is telling you something beyond normal menopausal shift.

SHBG adds metabolic context. In menopause, SHBG can actually rise or normalize. In the PMOS metabolic picture, SHBG tends to be suppressed because insulin resistance drives it down. Hyperinsulinemia suppresses hepatic SHBG production. Inflammation further disrupts that liver signaling. A low SHBG in a woman in menopause, when you might expect it to be normal or elevated, is a metabolic red flag.

And here is something we have been talking about inside mentorship for a while: SHBG can drop before overt androgen elevation shows up on labs. So the woman whose total testosterone looks unremarkable but whose SHBG is low? She has more unbound, bioavailable testosterone circulating than that total number suggests. Symptoms can absolutely exist even when someone has been told her hormones are fine.

Inflammatory markers. hs-CRP, ferritin trending up, elevated homocysteine. If chronic low-grade inflammation is layered on top of the androgen and metabolic picture, you are looking at something systemic, not a simple hormonal ratio shift.

Even with all of that, some women are going to sit in a gray zone. And I want to be super clear about that. The menopausal transition itself worsens insulin sensitivity. The ratio shift itself can nudge inflammatory markers. So the line between "normal transition with metabolic consequences" and "underlying PMOS that menopause is now unmasking" can get blurry. For those women, the question is not which side of the diagnostic line she falls on. The question is what is driving her picture and what do we do about it.

She does not need a label to start making progress towards improving her health. She needs someone willing to connect the dots.

A Note on Hirsutism and Cultural Context

I want to address something here that does not get talked about enough. When we list hirsutism as a clinical sign of androgen excess, we need to be thoughtful about what we are comparing to and who we are comparing.

Prevalence data does show variation across populations. Higher reported rates of PCOS (now PMOS) exist in women of Middle Eastern, South Asian, and Mediterranean descent. But there is an ongoing and legitimate debate about how much of that reflects true genetic prevalence versus detection bias, differences in diagnostic criteria applied, and body hair norms influencing who even gets evaluated for hirsutism in the first place.

A woman from a culture where more body hair is normal should not be flagged as having androgen excess simply because she does not match a narrow standard…and vice versa. And a woman from a culture where body hair is minimal should not be reassured that her androgens are fine just because her hirsutism is "mild." The criteria assume a baseline that does not account for every woman sitting in front of you. Context here is everything.

The "Types" of PCOS: Drivers, Not Diagnostic Categories

The mentee also asked about the four types of PCOS that circulate widely, especially online: insulin resistant, adrenal, post-pill, and inflammatory. She wanted to know if someone can fall into two.

First, some important context. Those four categories come from a functional and integrative framework, popularized by Lara Briden and widely adopted in naturopathic and integrative circles. Briden is phenomenal. Her books are valuable. And to her credit, she acknowledges overlap between these types.

But these are not diagnostic criteria. And this distinction is one that I think every coach needs to understand clearly, because it is one of those areas where coaches can inadvertently undermine their own credibility. If you are sitting across from a provider and presenting the Briden types as though they are established diagnostic categories, you are showing a gap in your foundational knowledge. Not because the mechanisms are wrong, but because you are conflating a clinical reasoning framework with formal diagnostic criteria. That is not the same thing. Understanding the difference is what allows you to have a meaningful, credible conversation with a medical provider about your client.

The formal diagnostic standard is the Rotterdam criteria, which has been in place since 2003. To receive a diagnosis, a woman needs to meet 2 out of 3 criteria: hyperandrogenism (elevated androgens by bloodwork or clinical signs like hirsutism, acne, or alopecia), ovulatory dysfunction (irregular or absent cycles), and polycystic ovarian morphology on ultrasound. That creates four possible phenotype combinations, labeled A through D. Phenotypes A, B, and C all include hyperandrogenism. Phenotype D is the outlier …ovulatory dysfunction and ovarian morphology without androgen excess and it is the most debated, with some researchers questioning whether it belongs under the same umbrella at all.

Now, back to the actual question. Can someone present with more than one driver? That is the norm, not the exception. The mechanisms are not siloed. Insulin resistance drives inflammation. Inflammation worsens insulin resistance. Both influence adrenal output. The HPA and HPO axes are in constant crosstalk. A woman presenting with insulin resistance and elevated testosterone simultaneously is not "two types." She is one person with overlapping mechanisms feeding each other.

I do not think a woman or a client needs to be slotted into a specific type to understand what is happening or to improve her situation. Identify the drivers. Address the drivers. Let the clinical response guide you. The category is not the point.

DHEA-S Deserves Its Own Conversation

This comes up constantly and it is frequently misread, so I want to give it space.

DHEA-S is produced in the adrenal cortex in response to ACTH, the same signaling cascade that drives cortisol. It is an HPA axis output. When coaches or practitioners see elevated DHEA-S, the instinct is often to jump to "adrenal PCOS" or now "adrenal PMOS." But elevated DHEA-S does not automatically equal endocrine dysfunction.

Chronic stress stimulates the adrenal cortex through the HPA axis. In acute stress, both DHEA-S and cortisol tend to rise together. In chronic sustained stress, DHEA can decline while cortisol stays elevated, creating an unbalanced ratio. And for women in perimenopause specifically, the adrenals can start to pick up some of the responsibility as ovarian signaling falls. So you might see DHEA bump up during the transition itself. It is probably not going to be prolonged, but it is something to consider before jumping to a diagnosis.

Even life stress, sleep deprivation, overtraining, trauma history all of these can drive DHEA-S up without any underlying endocrine pathology. So when you see that number elevated, the clinical question has to be broader than "does she have PMOS?" . Numbers alone do not tell you the story. The numbers inside the full picture can give dialogue and action wings though.

Where the Criteria Are Heading

The formal diagnostic criteria have not changed yet. The name is new. The criteria are still the same Rotterdam framework. That update is expected with the 2028 international guideline revision, at which point PMOS should also replace PCOS in the International Classification of Diseases.

The lead researchers have noted that even under the current criteria, 60 percent of women only need two of the three, androgens and cycle patterns, and never need the ovaries assessed at all, which is interesting.

The trajectory is clear. The ovaries are becoming less central to the diagnosis with each revision. The metabolic and endocrine picture is becoming more central. And the women who were missed… the ones who went through decades of dismissed symptoms, were told their labs looked fine, maybe had a hysterectomy that nobody questioned nor even counseled them on, and arrived at menopause with a worsening metabolic profile and no framework to explain it… those women might finally have a system that can see them.

If This Resonates

If you are a woman navigating PCOS, now PMOS, perimenopause, menopause, metabolic resistance, or symptoms that have been dismissed or minimized, our 1:1 strategy sessions are built to help you see the full picture and map a grounded, realistic path forward.

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If you are a coach who wants to sharpen your ability to assess metabolic health, hormonal patterns, and complex presentations through a systems lens, our mentorship program is where these conversations happen every single week. A coach asked a question on a call. It turned into this entire blog. That is how we operate.

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