PCOS Is Dead: Why PMOS Changes Everything for Midlife Women

The death of PCOS. So why science just renamed the lifelong metabolic condition that was known as PCOS, and what does that mean to you if you happen to be in midlife? So for decades, women have been told that PCOS, which is polycystic ovarian syndrome, was just an ovarian disease and that it was required to have cysts on the ovaries for diagnosis. And here's the reality. 1 out of every 7 women is assumed to have this problem, and at least 70% are unaware of it. And there's been a historic global shift that proves that it's actually a lifelong metabolic and brain-based crisis. It's a hormonal imbalance between the endocrine system and the metabolic system that doesn't even require ovarian cysts for diagnosis. Now, how did we get here? So on May 12th, 2026, the Lancet published a historic and paradigm-shifting consensus paper called "Polycystic Ovarian Syndrome is Officially Dead," and it has now been renamed as Polyendocrine Metabolic Ovarian Syndrome. That's a mouthful, otherwise known as PMOS. By the end of this episode, you're going to understand why this name change is very important. And it's not just cosmetic medical semantics. It's a massive victory for women. And even if you're in menopause, even if you're like me in your mid-50s and you've been in this room for a long time, this is still really important to you because the framework that was the diagnostic framework for PCOS for decades basically excluded, excluded women all across the board because we didn't fit this very narrow description. But the truth is, is that metabolic ovarian syndrome is still going on even when the ovaries peter out and run out of eggs. Diagnostic criteria even that we use today make it more difficult to figure out. So what we're gonna do today is go through this massive victory and help you understand what was going on and then also what to do about it if it sounds like you. So PCOS was considered a localized fertility ovarian disease affecting just young women, right? So if you've never heard of that before, it was the presence of cysts and in many cases would result in fertility issues in women because they were not ovulating regularly. And that was sort of the mindset of PCOS. And so if those two things were not present, you were automatically just declined. That can't be true. Now, the underlying problem is a profound neuroendocrine and insulin-driven deficit that continues to silently accelerate risks of things like insulin resistance, prediabetes and diabetes, cardiovascular disease, chronic inflammation, and metabolic dysfunction that often leads to abnormal weight gain, weight loss resistance, and a host of other problems. And this continues across your entire lifespan long into menopause. Now, this again is a multi-axis endocrine disorder, and I'm going to go through all of it, but it's heavily rooted in the brain and particularly the hypothalamus. So think of that as the director of your show. It is the one taking in information that informs the pituitary, which is your conductor of the show and your conductor of your orchestra, which are your endocrine organs, like your thyroid, your adrenal glands, your ovaries. And it even impacts things like metabolic function, like pancreatic function and insulin, and especially cortisol and adrenals. So here's why this matters now. And it's actually my, one of my clips went viral when this came out, because midlife women, many of us, and I'm gonna go through my own personal story, felt like there was some hormonal landscape that wasn't working quite properly. And we were often dismissed if we didn't fit this particular early, you know, sort of narrow diagnosis. And then when you get into midlife, because estrogen is fluctuating and declining, and therefore also you get changes in your androgens like DHEA and testosterone, progesterone is declining. And in this case, even more so than before, all these sort of ways that we might have been looking at it back then are now hard to find. And like I said, for the 1 in 7 to 8 women that are per— expected to have PMOS, perimenopause is not just a transition. It is a metabolic collision of many, many things. And we've always, especially if you're midlife, are left outta clinical trials. Across the board, but particularly when it came to looking at PCOS as the old diagnosis and what was really happening, women were excluded if they were past that fertility age. And again, it was almost always exclusively looked at in the context of fertility. So here's where we need to look at it. So the physiology— so let's do a deep dive in what's really happening. So let's look at the actual metabolism because you deserve this real science. And PMOS is a polyendocrine crisis, and it spans multiple hormone axes. So think of the axis as the director of the show and the orchestra leader, the conductor, talking directly to those organs. And that's really where the sort of malfunction starts. It's not that your body can't do something. It's that the instruction set coming all the way from the brain is mismatched. So first, it starts in the brain, the hypothalamus, which is a specialized cluster of neurons called kndy neurons. Which secrete a thing called kisspeptin, neurokinin B, and dynorphin. They act as master peacemakers over the reproductive system. So these three messengers sort of keep everything balanced. In PMOS, these neurons are fundamentally overactive, so they're yelling instead of whispering, and they fire way too fast, accelerating gonadotropin-releasing hormone and also pulse frequency by up to 40%. So what does this mean? This rapid firing hits the pituitary gland and scrambles it out, its output. So, think of it, this is a way to think of it, the director of the show has had way too much caffeine and they're jumping around and they're talking so fast that the conductor can't get the message right. And essentially, what happens is the overproduction of a thing called luteinizing hormone by the pituitary, which talks to the ovaries, and it starves the body of follicular stimulating hormone. So ultimately what happens here is you have an elevated, what they call LH, luteinizing hormone to FSH ratio. This tells the ovarian cells to pump out excess androgens. This is hormones like DHEA, testosterone, and DHT. At the same time, the lack of SF— FSH, which is follicular stimulating hormone, doesn't stop the follicle from maturing and it traps them in this arrested state where they overproduce AMH, which is anti-Müllerian hormone, which loops back to the brain and then makes those KNDY neurons fire even faster. All right. So we're gonna go back to the, the analogy so you can understand it. The conductor of the show, has overdone caffeine that day, they're talking 90 miles a minute, the conductor gets the message, but they just start screaming at the orchestra to go. The orchestra part that tells the ovaries what to do, luteinizing hormone goes too high, follicular stimulating hormone goes too low 'cause they get mismatched. And that ultimately what happens because the follicle is arrested in development, the egg doesn't pop out or doesn't pop out appropriately or doesn't get the right message,, and then there's an overproduction of anti-malarian hormone, AMH, which then loops back to the brain and is like giving more caffeine to the hypothalamus, right? So here's the midlife nuance, right? So again, if we were fertile and we were doing a bunch of testing, we would figure this out. But obesity, so having extra weight and extra adiposity, which is adipose tissues, completely masks the hormone signature. On your standard lab tests. So, even if you went to the doctor and like, "I think some of this is going on," if you struggle with excess weight, it may be masking some of these messenger system, right? So, this can— your extra body weight, your adiposity that can also drive this and also be driven because of this acts as a pituitary brake that can also blunt LH. So again, we can get sort of this amplitude. So, you can get LH is elevated, but it's not as volatile. So LH has to have this sort of massive peaking and dropping to get prime— primary appropriate ovarian function. So when it's elevated, but not fluctuating, we get a kind of a blunted message and a blunted amplitude. So your lab works might show completely normal LH, possibly a completely normal FSH, cuz they also move a lot during reproductive years over the course of your month. So you have to look at them relative to if you're cycling, where you're cycling. But even if you are in menopause, that blunting of some of that function causes it to be very difficult to diagnose. So the, to the untrained clinician that may be looking at those labs, they'll say, oh, you don't have PCOS or PMOS because underneath that you don't have the amplitude changes that we would see and the, the significant elevation of LH. But underneath that mask, the rapid— basically, gonadotropin stimulating hormone is at the heart of the condition— is still beating, right? So, something we don't test for is still running amok in the background. So, why is this? It's because women, when we have excess body weight, we have it especially around the abdomen in the middle where we gain it when we're in perimenopause and menopause, have a higher BMI, right? Height-weight ratio. We also have hyperinsulinemia, and that takes over as the primary bully in this message. So insulin becomes a bully, and when it bypasses brain signaling entirely, right, it stops listening to the hypothalamus. It's like, screw that, I'm not listening to you anymore. The pituitary, you can go over there and do your thing too. Insulin bypasses all of that brain signaling and directly stimulates the ovaries to dump testosterone into your system. Simultaneously while crashing your sex hormone binding globulin, SHBG. The sex hormone binding globulin is your taxi cab that drives androgens around, and it also drives estrogen around. But you need a balanced SHBG against testosterone. If you don't have enough, you get way too much free testosterone, which then further messes up the LH-FSH ratio, drives insulin resistance, and can also drive excessive IGF-1, which causes more weight gain. And we basically leave a lot of free excess in testosterone circulating that can wreak havoc on your metabolism, causes hair loss, chin hair growth, acne, and more visceral fat storage. So, fat storage around the middle. Now, most of us, and I've talked about this too, having too little testosterone can also be a problem. So, there's a significant portion of women, you know, of the 1 in 8 that might be PMOS, those other 7 probably suffer from lower androgen levels relative to estrogen as they go through perimenopause, and then also lower androgen levels like testosterone postmenopausally because it's automatically on its way down. But relative to its estrogen, and in, in a woman with normative sort of metabolic and ovarian function, their, their androgens with no hormone replacement will be higher than their estrogens cuz By the time you're in menopause, estrogen levels are below an 8, you know, 8-year-old boy, right? So here's where it's gotta be important, right? So if you see this play out, the reality is, is a normal LH to FSH in a woman that is expressing a lot of these symptoms doesn't mean that it's not there. It just means that when we're looking at it, we're looking at it too much. So what does this mean? So let's say you had a doctor that looked at your hormones and says, LH looks normal, FSH looks normal, your androgens might be a little bit high, but not too much, 'cause that's often what's said, and you're struggling with, you know, excess body weight. And let's say you go on a very low calorie diet, right? You're, let's say, doing keto, who knows, you're cutting carbs, whatever it is you're doing. So here's what's interesting. When you have PMOS and you go on this acute, very low calorie diet, your insulin drops, which releases the pituitary brake, right? Remember the pituitary brake because of hyperinsulinemia. Now, what's interesting is your luteinizing hormone will then paradoxically spike. So, all of a sudden, the thing that was breaking the luteinizing hormone causes it to spike. But the research shows is about 1 to 1.5-fold, right? So, your underlying neuroendocrine deficit is unmasked, right? So, all of a sudden, it's unmasked So what does that mean? So if your standard eating less, exercising more advice completely backfires in midlife, PMOS, your nervous system reads it as a survival crisis and locks down your metabolism. So I'm gonna give you my story. So if this sounds like you, some of this may be you. So I was put on birth control relatively young, you know, in high school. Now, some of it was because I had painful periods, other stuff. The other thing was, you know, acne. There's lots of reasons why we do this. And it's not abnormal to have abnormal period variation when you're just starting your period, right? It doesn't automatically get to 26 to 28 days normally. It's all over the place. But often, we put girls on birth control early to control periods, make them less painful, less acne, skin, all kinds of reasons. Well, what that does is falsely cover up what may possibly be going on. But one of the things that was really evident to me, especially looking back in hindsight, was I— anybody that knows me, I'm barely 5'3", right? I like to say I'm 5'3". I'm not really. And I have a badonkadonk butt, right? I am curvy. And I went from being this skinny, scrawny little kid to when puberty hit, it was like everything exploded in every direction pretty quickly, particularly my hips and thighs. You know, I was thankful JLo came along because no matter how much I've ever done anything, I've always had kind of a lot of junk in the trunk. And I remember thinking like, why did that occur when my period started, right? Like, it just seemed like everything exploded. Yes, I expect to grow breasts, but like, it was over the top, right? Now, when I got older, it was very hard for me to, you know, even in my teens, early 20s, it was like, weight was a fight with me. It was very much a fight with me. And so I was always like on a diet, eating, and I even was a bodybuilder for a while and I sustained myself on like 1,300 calories, but I lifted heavy 6 days a week and I did cardio. So, like overdoing it all the way. That was '90s kind of competition mindset that was really unhealthy, but that was like the only way I could keep that going. I was still on the pill. I stopped the pill and then got my tubes tied. When I stopped the pill and got my tubes tied, all kinds of havoc broke out. I broke out in acne all over my face, cystic acne. I started losing my hair, started, you know, losing some of my eyebrow. And so, everybody was telling me, "It's your adrenals because you've gone back to school while working full-time 100 hours a week. It's your thyroid," which I do have issues. However, that started a 10-year fight with my body because I went into early perimenopause because of the tubal. I've talked about that at length. But, the other side of it was everything I did that functional medicine told me to do. Oh, you're estrogen dominant. You— we have to make sure that you, you get less of that and we try and reduce any effort of that. Take progesterone. Fine. I took progesterone, didn't do anything. Took testosterone and I gained 10 extra pounds. What I was uncovering was some of this PMOS behind the background. I never had massive cysts on my ovaries. I never had abnormal periods. However, I never gave myself a chance to do it because I was pretty much on the pill or tubes tied. Right? Or you— for you, it might be that you were on the pill or on some sort of birth control, had a kid, delivered the kid, you know, breastfed the kid, and then either had another kid or went right back on birth control. You may not even be able to see it. But the reality is, is when you have that change and you go, "Oh, forget it. I'm just gonna keep reducing calories. I'm gonna go on this really low-calorie diet," when this is existing in the background, that feedback back to the brain when that luteinizing hormone finally goes back up because you've reduced all of the insulin because you basically went on, let's say, a ketogenic diet. When that happens, it backfires and it slows everything down anyway. Right? So this is where you feel damned if you do, damned if you don't. So if some of that feels true for you, and again, 1 in 7 to 8 women, it's true for them. You may very well have had this your entire life. Right? So here's the practical translation, right? What do we do tomorrow morning now that we're listening to this? So the first part is if you're in perimenopause to menopause, your luteinizing hormone and follicular stimulating hormone, which are not standard, but you can ask for them as part of a sex hormone panel, may not reflect the ratio that's expected and/or a clean, you know, ovarian ultrasound. Neither one of those are necessary to diagnose PMOS. Because the reality is, is you could be having things going on in the background and it's particularly if you got excess body fat around the middle, which many of us are fighting, you may have hyperinsulinemia sort of burying that diagnosis. So how can you get a little bit more? So demanding a fasting insulin and a hemoglobin A1C, getting a continuous glucose monitor and a full sex hormone panel so you can see your androgens and your other hormones. Also getting a full thyroid panel because because you've heard me, if you've listened to me before, talk about the hormone symphony. If this stuff is going on with your sex hormones and your metabolic hormones, other hormones can be impacted like cortisol and adrenal and the thyroid as well. Here's another thing that can be very helpful, right? The glucose monitor might be able to help you understand how even very healthy foods may react differently in you. Not so much that you get really crazy high glucose, but especially if you also have more of a reactive hypoglycemia where it might drop lower than expected. You could see abnormalities there too. It's gonna be informative. It's not necessarily diagnostic in somebody who is not diabetic, but what it does do is help inform you how food may be playing a role and where your hormones go in their variability for your, for your blood sugar. Now, here's the other thing when you're talking to your provider. All right. So we have already talked about the fact that most all medical providers have zero understanding of perimenopause and menopause. That includes endocrinology and gynecology, internal medicine and family practice. So here's what I can promise you is the vast majority of them that are menopause literate are not PMOS literate, right? So this is going to take us taking on an active role in educating the medical community because most of them probably didn't read the Lancet article that actually set the stage for a new diagnostic pattern and expectation. It is a consensus document. When consensus documents come out, that should become standard of care, but it takes a long time to do that. The average is almost 18 years. All right, here's what you want to say is, given the 2026 Lancet article consensus that PCOS get renamed to PMOS, and that research on things like GLP-1 agonists like semaglutide and tirzepatide can be helpful, but here's where we know that these drugs play a role, and they particularly are effective in a premenopausal, uh, or perimenopausal menopausal and menopausal woman when coupled with highly personalized hormone replacement therapy. These drugs are very, very effective in this particular condition. And here's the reason why. They don't just help with your peripheral insulin sensitivity like your muscles and everything else. The GLP-1 receptors are physically located in the gonadotropin hormone-releasing neurons in the brain, hypothalamus, right? They may actually help quiet that overactive neuroendocrine storm and that feedback loop that causes some of the malfunction between luteinizing hormone and, and FSH and insulin and obesity and all of that. So, the reality is, is if I'm a woman, even if I'm 57 right now and I still feel like I'm struggling with my metabolism, and maybe you've tried hormone, maybe do somebody's dialing in your that thyroid and they got your T3 at the perfect level, but you're still like, hey, nothing's moving on the scale. You know, the reality is, is sometimes there's so many mechanisms here that are, are, are really not doing what we want them to do. But in many cases, these are things that our body did to protect us, you know, thousands of years ago when our ancestors had large times of starvation, right? That's the other thing. We're not broken. We're just operating in an environment with rules that our body is different than some of the other ones. So, when we apply other people's rules, they don't work the same. So, the GLP-1 frontier, the triseptid, the retratid, the semaglutide when coupled with appropriate hormone replacement for women. Now, if a woman is in this scenario and they have excess androgens, don't let somebody talk you into more androgens, right? This is where testing becomes really important. Because it's a, you know, a lot of people use a blanket statement, oh, everybody could benefit from testosterone, everybody could benefit from estradiol. That's not necessarily true. And so, the reality is, is before hormone replacement therapy, you should have testing to see what your real numbers are. And during hormone therapy, you should be tested to make sure that they are adequate and ideal so they can also provide prevention between cardiovascular disease, you know, Alzheimer's risk, and even osteoporosis. And that androgens, because you may have excess, may not be necessary. And, and consider the fact that semaglutide or tirzepatide and one of these other medications can help reset what's happening in the hypothalamus. Now, if you've listened to me years ago, I was a little bit— what's the word I'm looking for? I was a little bit harsh about the use of semaglutide and tirzepatide early on, not because I didn't like what the drugs did, It was because practitioners were prescribing them to people who did not need them, should not be on them, and may very well be dangerous for them. And we see it. I mean, you can look all the way across all the people on the red carpets at the Oscars and recognize that people are abusing these drugs. And what the research shows is, number one, there's significant muscle loss, particularly in those who are not significantly overweight, and there's significant weight gain in that population. And I'm very concerned about like bone loss. However, what we now understand is these are not just anorexic drugs. Like you'll hear that being said. Yes, they do cause a blunting of hunger cravings. Like we're seeing improvements in, um, blood sugar control and cravings and things like alcohol consumption, drug consumption, because it has this feedback to the hypothalamus and all the different regulatory hormones that come out there. And and the reality is, is they have a very strong influence on hypothalamic control of these metabolic hormones. And so, you know, if you've been like, I need to muscle this out and get it done on my own, and I need to just eat less and work out more, this might be a time to understand that your body has unique chemistry that your 30-year-old trainer doesn't have, right? And that these medications may work very well. Now, the truth is, is Eli Lilly came out with an oral tirzepatide that they showed doesn't work as strongly as the injectables, but it's much cheaper too. It's like $149 a month cash pay. And then with PPO, they have a coupon situation. So in many cases, just having that regulatory hormone, not necessarily where it makes you nauseous and you don't want to eat, can also help. So it doesn't mean that people have to take really high doses of these things. And I think it's one of those things that when you're talking to your provider, you wanna look at the entire picture. And we don't wanna necessarily take off one of the strongest supports for this sort of hypothalamic control that's affecting the metabolism and PMOS. You know, so if you've been gaslit, right? If you've had doctors be really dismissive about your personal history of what your periods were like, you know, here's the thing. Many women had abnormal periods, and again, it was hidden because you were on birth control, so you didn't see it. That may have been signs something was going on, but it's not even necessary. You don't have to have a single ovarian cyst for it to be necessary. However, if you did have ovarian cysts, this is your wake-up call. This is true, right? But we've been gaslit in many cases. And if you felt like this weight loss resistance and weight gain just got worse during, during perimenopause and menopause, I want you to know it's not a personal failure. It's not it's not you, it's your physiology. And you've been fighting like a multi-access sort of hormonal issue that is, is very, very different, right? And that we can't, we can't just say what works for everybody works for everybody because it doesn't, right? So here's what I want you to think about, you know, how would your relationship with your body change if you viewed it differently and understood that it's not a lack of willpower and other things? How would you view your body if you understood that maybe these hormones that are hiding behind the scenes, that many of which we can't test for, we can't test you for kisspepsin, right? We can't. But, you know, how would you feel about it if you understood that it was a physiology and not a moral failing, right? Because we, we internalize that. I also want you to think about, you know, are you carrying, uh, you know, some sort of medical shame that somebody's put on you because a PCOS diagnosis was given to you forever ago, but there was no answer for it. Right? Because then it was never properly explained because that happens a lot too. And, you know, given your health situation and where you're at today, what things can you do for yourself to maybe, A, explore if this happens to be true, and B, take control and command so you can feel better at the same time? You know, because the reality is the era of reducing women's healthcare to bikini medicine, that it's all about our reproductive organs. You know, it's our ovaries, our uterus, and our breasts is over, right? It is absolutely over. And the renaming of PCOS to polyendocrine metabolic ovarian syndrome is a monumental boundary in medical history. And it proves that your body requires a deep, holistic, multi-system, multi-hormone strategy, especially as you pass through those gates of perimenopause and menopause. And you're your own best advocate. You know your body best and your intuition is likely right in most cases, but you can't advocate for yourself with out-of-date information. And you know, cause now the map has changed and it's completely different. And I want you to know that if you've had somebody say something otherwise, you're not crazy. You're just dealing with a polyendocrine shift and that the right information and the right laboratory testing and the right understanding, even in the face of labs that may not be clear. Can be done and you can feel better. You just are gonna have to find the right practitioners that understand not only the hormones, but also the metabolic and endocrine impact of what happens when our hormones are in this situation. All right. So I wanna thank you for listening, and I hope this was helpful, cuz I know that when I was making the comments on Instagram, so many women came forward and said, oh my God, it sounds like me. And it definitely sound like me. I, I asked a million times if I had PCOS cuz I happened to be educated enough. I was lucky enough to understand that diagnosis. And I kept getting told that if I didn't have a ton of ovarian cysts, it can't be that. But I was like, everything else from the endocrine side looks like it. And so, you know, here's your wake-up call. If this is you, don't just take the education and run away, right? Take the education and apply it. Find somebody that can help you. And if we can, we'd love to, right? We'd love to. And if you have a comment or a question that you've had based on this episode, especially on YouTube, you have the ability to subscribe and comment. So subscribe and comment, and I can come back and feed you in on more information about these metabolic changes that happen to be about PMOS or anything else for that matter. And then if you happen to be listening to me on your favorite podcast platform, Obviously, I'd love for you to leave a 5-star review, but definitely reach out because we'd like to help you understand your body better. You know, this is why I do what I do at Menopause Mastery, and it's why we do what we do at GetMinerva and gethormonesnow.com. It's so we can help women live their best lives through perimenopause and menopause and actually improve the women's entire research gap at the same time. So, I wanna thank you for listening. If you've been pissed at the medical system, I hear you and I understand, and I'll be back with you next week.