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- [00:01]
Podcast Host (Sponsor Reader)
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- [00:38]
Dr. Chapa
Podcast Family On March 29th, 2023, we released an episode titled The Four PCOS Phenotypes. Okay, the four PCOS phenotypes. Of course. We'll put the link to that episode in our show notes now. Now that was two years ago. Now, on the 29th of October 2025, which was just like a week ago from when we were recording this, there's a new publication out of the journal Nature Medicine. Now, researchers have published a new data driven 4 Subtypes of polycystic ovary syndrome and their association with clinical outcomes. Now, y' all get this. This was just a week ago in the journal Nature Medicine. Now remember, we actually covered the four PCOS phenotypes on March 2023.
- [01:33]
Michael (Producer)
I told you. I told you. I told you.
- [01:37]
Dr. Chapa
So once again, one of the main reasons I hope that you listen to this program, outside of our witty charm, of course, is that we give you stuff, man. I'm telling you, it's not just opinion. It's stuff that's in the literature and stuff that makes sense. But I love how things come out in print because today in ACOG's Office of Communications News brief and today's by point of reference is November 4, 2025. ACOG had this in the news release. Hey, new researchers have published something about four PCOS phenotypes. You don't say.
- [02:14]
Michael (Producer)
Told you. I told you. I told you.
- [02:18]
Dr. Chapa
So what has happened here once again, as I said many times before, guys, there is nothing. Nothing. Nada. That's for my Hispanic brothers and sisters. Nada. Under the sun. That is new. But behold, alas, yes, it's in the ACOG news update on what's in new in print on October 29, 2025 for four actual subtypes of PCOS. Yeah, don't say one more time, guys, I told you.
- [02:48]
Michael (Producer)
I told you. I told you.
- [02:51]
Dr. Chapa
All right, all right. So we're going to cover both very quickly, those four PCOS phenotypes that we covered two years ago. Thank you very much. And then this new article, because it's the exact Same thing with a new spin. Now we're going to cover these four PCOS phenotypes, but the main take home message is this. The days when we consider the PCOS patient as the infertile, obese, hirsute patient as the stereotypical poster child, poster woman for pcos, that's outdated. I mean sure that's one phenotype, but they're not all that phenotype. So back in 2023 we discussed the four letter phenotype classification A, B, C and D, which is nothing new. Other authors have published this before this new publication in Nature Medicine and it's actually nothing, nothing new.
- [03:47]
Michael (Producer)
I told you, I told you so.
- [03:51]
Dr. Chapa
Again, it's just interesting that, you know, things kind of get digged up again and they're like, oh, look what I have discovered. And it's good, this is a good article. It's really good. Just as a reminder of what we've already known is that PCOS is a, is a constellation of presentations. Yes, Rotterdam criteria is good. That I get that you can check. Mark that. But there are different presentations of that phenotypically. Please go back to the link in our show notes and listen to that previous episode again two years ago. So what is this new article saying? It did actually agree with what we said two years ago. And what's the new data here? Well, what is new is that they actually tracked outcomes of these four phenotypes for outcomes for IVF and for pregnancy outcomes. Spoiler. PCOS is related to some pregnancy outcomes. Anyone? Anyone? Not everybody speak at once. I can't hear you. One at a time. Of course PCOS is linked to things like gestational hypertension and all hypertensive disorders in pregnancy and gestational diabetes. And lo and behold, that's what they found. Again, nada nu under the sun. We'll briefly talk about the IVF outcomes. It is interesting, but the short of it is if you have obesity phenotype with pcos, you're going to have some decreased success with ivf. That's just part of overall the oxidative stress of the body with obesity. We've known that. And if you have certain endocrine abnormalities, it's going to be harder to have success with ivh. Ivh. What is ivh, ivf, ivf than somebody who doesn't. That just makes sense. So there's really nothing new in this. And something a little new because they take what I covered two years ago and made it a clinical phenotype A, B, C and D, which We'll briefly discuss again in this episode. And it kind of built on that now using more lab based criteria, the LH level, anti mullerian hormone level, what is total testosterone and all those are fine. It's just a slightly more lab driven way and in my opinion maybe a little bit more cumbersome way than then just calling it based on phenotype A, B, C and D. And we'll remind each each one of us what those letters mean in the four different phenotypes. Once again, as we wrapped up the intro March 29, 2023 recovered the four PCOS phenotypes. And then again just out today in ACOG's news release of here's what's in print. Quote Data driven 4 Subtypes of polycystic ovary syndrome and their association with with clinical outcome. So you don't say. And once again guys, thank you all for supporting the show. And once again, just in all humility, trust me, in all humility.
- [06:40]
Michael (Producer)
I told you. I told you.
- [06:43]
Dr. Chapa
I told you. All right, now that I've set it up enough, I have a good time with this. Just so you know, I'm not in person with Michael, our producer for this episode. We're doing this a remote. So he's on my split screen and he's shaking his head. You knew I was going to do this. You knew I was going to do this. Let's get out of the intro. I'll be right back.
- [07:04]
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- [07:32]
Dr. Chapa
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- [07:37]
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- [08:28]
Dr. Chapa
This is Dr. Chapa's OBGYN no Spin podcast. Well, before we get into the non nonsense and get into the real data, does anybody. Did anybody recall or, or that familiar that little clip that we played in the intro that Michael found? Anybody? Anybody? You know who that was? I told you. I told you. Anybody Remember that?
- [09:13]
Michael (Producer)
Told you. I told you. I told you.
- [09:17]
Dr. Chapa
That actually is the non medical movie. Absolutely non medical. I just, I think it's kind of funny. But that was Friday with of course Ice Cube. Anyway, I just found that kind of cute and very applicable. So now back to the data very quickly. Pcos. I learned this as pcod, polycystic ovarian disease. But disease probably is not appropriate because it's not a disease. It truly is a syndromic issue. It's a syndrome. But back in the day, 1935, it was Stein Leventhal syndrome who first drafted this report titled Amenorrhea associated with polycystic ovaries. End quote y'. All. That was the first paper to actually mention that term. Polycystic ovaries linked with a menstrual abnormality. These women had infertility, had menstrual disturbances and it was the first kind of tracked back to these two authors. It was actually Michael Leo Lieventhal and Irving Stein who published this in 1935. You all know how many patients they studied for this? How many? Hundreds. 00 hundreds. It was seven. Seven women. Good for them. That's why originally this was given their namesake. This was Stein Leventhal syndrome as first reported in 1935. Now that was an end of seven. 1, 2, 3, 4, 5, 6, 7. That's it. Then as we covered back in 2023 because we're always learning and the data is always changing regarding this condition, of course we learned that PCOS is not just one phenotype. It's kind of complicated. Insulin resistance is tied in there. But not everybody has insulin resistance just as not everybody has polycystic ovarian morphology. So there's actually four phenotypes and the most traditional clinical way. Now there's this new lab based option which is also four phenotypes which very loosely is applicable to the four clinical presentation that we're going to cover right now. As a recap, we're talking about the same thing, the take home message. Whether do you use the lab based four criteria or four subtype schema which I'll tell you in just a minute or the traditional A, B, C and D schema that the take home message is the same. PCOS has different presentations. PCOS has different issues. Some have metabolic derangement. Not all of them do. Some have polycystic ovarian morphology. Not all of them do. So that's the take home, guys. That's the clinical pearl. Stop putting PCOS patients into a box. It's not a box. It is actually a spectrum. And sometimes a patient may jump from A to B. She can go from B to A because it changes as the system and the body changes and adapts. They don't. They're not locked into one phenotype. It's not a contract. All right, so this is, this is the body and this is just at this moment in time. A patient may have phenotype A, which is classic pcos, or may have phenotype B, which is non polycystic ovarian morphology pcos. So let's get into this briefly now, just as a point of recap. Remember, most people use. Even though there's other clinical criteria, most people use the Rotterdam criteria. Two of the three necessary for a clinical diagnosis. So very good sensitivity, maybe not so good specificity, but two of the three, remember that is hyperandrogenism, either physical or phenotypic or lab based. Then you have irregular cycles and polycystic ovarian morphology. Two of the three, Boom. Check the box right there. With high sensitivity but specificity, something else. You meet criteria for Rotterdam for pcos. Okay, so that's the diagnostic issue. However, it's a little bit deeper than that because there's actually four phenotypes that build on that Rotterdam criteria. Now, some use NIH criteria, American Andrew or endocrine Society criteria. I get that. They're. They're basically the same with small flavor differences. The seasonings are different, but the meat stays the same. Wow, that was cheesy. All right, anyway, the four different phenotypes, I feel kind of sassy tonight, y'. All. I finished a very long call. My team killed it. Killed it, rocked it out. I think we had six C sections today. Six within like a 12 hour span. Not in, you know, in addition to the triages, the usual labor with two vaginal deliveries. So overall, yeah, like eight deliveries in 12 hours. Pretty good. Pretty good. Anyway, so this is the end of the day. Yeah. You know, somebody did beg me to do this tomorrow. I don't want to do it tomorrow, I want to do it now. So thank you, Michael, for hanging in there. Here we go. So phenotype A is classic pcos. Classic. That is hyperandrogenism, that is ovulatory dysfunction. You know, periods of amenorrhea and polycystic ovarian morphology. They got the triad that is cinquena, perfect pcos. All right, that is phenotype A. Phenotype B is pcos, but without the polycystical varied morphology. So they have hyperandrogenism check. They've got ovulatory dysfunction, check. But their ovaries, little good. You got two of the three. That is phenotype B. Some have phenotype C, which is ovulatory pcos. So they have hyperandrogenism. Again, either lab based or phenotypic, but they have super regular periods. And then you do an ultrasound and lo and behold they've got polycystic ovaries 18 to 20, little cysts around the ovarian cortex, kind of thickened endometrial stroma. Well, so that's ovulatory pcos. Wait, you can have regular periods with pcos. Of course, homie, of course. Phenotype C. Then there's phenotype D, which is non hyperandrogenic pcos. So either biochemically by lab or phenotypically, there's no hirsutism, but their periods are all jacked up. And then you do an ultrasound and sure, lo and behold, chocolate chip cookie appearance, polycystical variant morphology. Those are the four phenotypes. A, B, C, D, A, B, C, D. Classic non PCO PCOs, ovulatory PCOs and then non hyperandrogenic PCOs. That's the most traditional in terms of super easy. I'm just without a bunch of labs. That's the easy way. Just literally in your interview with a patient who comes in with ovulatory dysfunction and are concerned for PCOs, quick to go, okay, I think you meet Rotterdam, but maybe you have phenotype B, or apparently you seem to have phenotype C. And then we do labs, which may increase the specificity of that. All right, of course it is true. Phenotype A, which is classic pcos, is the most common and that typically presents with a typical triad. All right, Phenotypes B and C tend to have milder symptoms and they also tend to have lower risk of metabolic complications. Phenotype D, remember that's the one without hyperandrogenism. But they do have ovulatory dysfunction and they also have polycytic ovarian morphology. That is phenotype D, that tends to be the least common. And it can actually that's where it gets kind of confusing. People are like, well, you don't look hirsute well, man, please don't fall into that gap or that hole that is phenotype D. But based on statistics and several reports and publications that is, that does seem to be the least common. Okay, so phenotype A is the more common or the most common, which is the classic phenotype D, which is non hyper androgenic. PCOS seems to be the least common. All right, none of that's new. None of that's in this new publication. This is all in the old stuff. That's the stuff that we covered back two years ago. Over two years ago, actually in 2023. Now we're going to get in into this new publication.
- [17:25]
Michael (Producer)
I told you, I told you.
- [17:28]
Dr. Chapa
Yep. Because it's pretty much the same thing with a new twist. Now in this new publication, authors do describe these four phenotypes using a little bit more biomarkers. All right, so they talk about anti mullerian hormone, luteinizing hormone, total testosterone, are they obese? So it's more of a lab based slash, you know, metabolic picture than the simple phenotype clinical base, which is the A, B, C and D criteria which we covered again two years ago. All right, so here's first of all, before we go into the specifics on this, we'll do this very quickly. Let me just read you ACOG's news communication for today, November 4, 2025. This is the email blast that comes out. And hey, here's some ideas of things that are in print. Quote, Researchers examined commonly measured variables that could distinguish clinical subtypes of PCOS using unsupervised clustering of nine clinical variables. Nine clinical variables, y'. All. So that's, that's in other words, both history and hyperandrogenism. LH level, anti mullerian hormone, hormone level. That's why I said it's a little bit more clumpy. It's a little bit more complicated than what we told you two years ago anyway, but it was in close to 12,000 affected women, so that's good. And just as an aside, it actually says nine clinical variables in 11,908 affected women. I'm just glad it says women and not people. It's a small victory there. All right, so anyway, so yeah, kind of what we talked about. So we're going to get into this, okay, we're going to go into the specifics and let me read you the main aim of this publication. We'll take a quick break to let that settle, let that simmer, let those neurons fire. And then we're going to come in. I'm going to tell you just the quick nitty gritty of what they found. And we're going to call it a day. Call it a day. Okay, so as the authors state, quote, our current study aimed to identify a set of commonly measured variables. All right, everyone. So that's labs as well as clinical findings. All right, so labs as well as clinical findings. They go on to say commonly measured variables that could distinguish clinical subtypes of PCOS using cluster analysis in a large discovery cohort. Those are all fancy words that validate these subtypes in independent cohorts of different ethnicities. So the different ethnicities are China, the usa, baby, Europe, Singapore and Brazil. Those are the five different ethnicities or cohorts, China, Europe, Singapore, Brazil and US of A. Those are the five different locations that they looked at this. They did throw in the IVF outcomes and the pregnancy outcomes, which, again, it just verified what we already know. These patients have a lot of metabolic derangement. And while IVF does work, there tends to be slightly higher risk of pregnancy loss. And the same thing we already talked about, pregnancy outcomes. What you would expect is exactly what they found. Higher rate of gestational diabetes, y' all think. Higher rate of hypertensive disorders in pregnancy, y' all think, Guys. And I'm not minimizing this at all. I'm just saying, didn't we know this already? I think we did. Let's take a quick break. We come back, we will tackle just the quick specifics of this, what they call the four different phenotypes. Remember, ours are A, B, C and D. And then we'll wrap it up. So we will be right back. This is, excuse me, a damn fine cup of coffee podcast family. Unique to the Chop up podcast community, the Strong Coffee Co. Offers 20% discount to whatever you purchase online through the link in our show notes. That's right. It's unique to our podcast community. The Strong Coffee Company is not your routine cup of coffee. It is coffee 2.0 and it's coffee that works as hard as we do. There are latte options. There's whole bean options as well. And this comes with collagen as well as L theanine and adaptogens to boost overall performance and mental acuity without the caffeine crash. There's actually published peer reviewed evidence from this from July of 2024 in active clinical nutrition. So this combines my two favorite things, my love of coffee and my love of data in my morning cup of coffee. So the strong Coffee Co. Offers 20% discount through the link only in our show notes. So as a thank you to being part of our podcast community, the strong coffee company has partnered with for a 20% discount on anything purchased online.
- [22:11]
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- [22:55]
Dr. Chapa
All right, amigos, let's get back to the quote unquote new information on pcos. Even though we covered that two years ago.
- [23:03]
Michael (Producer)
See, I done told you. I done told you.
- [23:08]
Dr. Chapa
All right, so here's where we're going. This new publication, this new publication, it kind of breaks up. What we did mirrors it. Using more lab based criteria. Very easy. I'm tell you this, we're going to call it a day and be done. Let's get out of here. So first of all, they described first a hyperandrogenic subtype. That sound familiar? So they called that HA for hyperandrogenic pcos. Fine. That was characterized by high testosterone or high DHEAS levels, along with some metabolic disorders. So that is the hyperandrogenic subtype. Great. HA pcos. Then there was a subtype associated with obesity. They called that object not for ob, like in pregnancy, but OB as in obesity PCOS that was characterized by, you guessed it, obesity, higher bmi.
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Michael (Producer)
Sorry.
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Dr. Chapa
Oh my gosh. I almost almost died. I couldn't do it. Sorry, Michael. That was okay. I mean, of course it's got a higher bmi, hence why it's called obesity. Oh my goodness. All right, so OB PCOS that also had some metabolic derangements like fasting hyperglycemia or fasting insulin level that was elevated. Fine. So that is basically obesity with metabolic dysfunction. But they called it OB pcos. No surprise there. The next group they called shbg. Shbg. Guys, what is that? That's sex hormone binding globulin. That is high sex hormone binding globulin type of pcos. Remember I told you guys. So it's just, it's the exact same thing. Four different phenotypes, but now using lab criteria and or biochemical classifications. Whereas what I told you was A, B, C and D as phenotypes. We're talking about the same stuff. Pick a schema, it doesn't matter. It's like some use Carpenter calcin, which is what ACOG prefers for GDM testing, some use National Diabetic Data Group. It's okay, those are different levels and cutoffs. Just use one and be consistent. The take home message here guys, is whether you call this phenotype A, B and C or ha, PCOS or ob, PCOS or shbg, pcos, whatever. Just know that there's four different phenotypes and then the last phenotype was actually one associated with high LH and anti mullerian hormone subtypes. So LH amh, remember anti mullerian hormone is also a reflection of course of follicle development. So there is a LH PCOS which has high levels of LH and follicle stimulating hormone and anti mullerian hormone because all the little follicles are making those. It makes sense. And of course FSH and LH are high because you don't get that negative feedback. All of this makes sense. None of this is new. It is four different classifications of PCOS using more lab based criteria. Sex hormone binding globulin, total testosterone, LH or AMH using fasting insulin levels, fasting glucose. All things that you should be checking anyway for your PCOS patients because they have an overall higher rate period of metabolic dysfunction. So whether you call it again, and we're going to start wrapping this up, phenotype A, B or C on the clinical side or more lab based, my point is threefold and then we're done. Number one, nothing new under the sun, obvious. Number two, PCOS is a constellation, a plethora of different symptoms, if you will. And it is not cookie cutter. Not everybody fits into one box. So four different styles. So if you're asked on the oral board, tell me about pcos. Oh, I'd love to. Would you like to know about the Rotterdam criteria, which is a very quick assessment at the bedside to put them into that box as a whole of pcos. And then we're going to divide them out into four other little sub boxes called subclassifications. And there's a clinical subclassification which is A, B, C or D. And then there's a more lab based subclassification which is based on lab criteria like sex hormone binding globulin, lh, anti mullerian hormone, fasting glucose, fasting insulin, overall metabolic derangement and or their BMI for the ob pcos. OB meaning obesity so what would you like to know? So that's the answer. PCOS is a constellation of issues. Some have polycystic variance, some do not. Some have had a more metabolic derangement than others. Not everybody has that, although some have some flavor of it, but more to some degree higher than others. All right, last thing, just to be fair and complete very quickly, a quick little blurbs on the IVF outcome, because they did cover that. I want to be true to the paper and the pregnancy maternal outcomes we already got. It's what you would expect, so I'm not going to dwell on that one. But in this publication, just in this publication, the good news was, is that the clinical pregnancy rate for the four subtypes of PCOS for in vitro, if they're going to choose that way of fertility management, was all over 60% in each category. That's good news. So in hyperandrogenic PCOS, it was 66%. In the obesity classification, that was 62%. That actually was the lowest. Again because obesity carries more of a high oxidative stress, maybe other metabolic arrangements that go with it. So it kind of dropped, but still over 60%. Still good news. In the sex hormone binding globulin PCOS flavor success for clinical pregnancy was 67% after in vitro, again, very, very good. And then in LH PCOS, that's the one with high LH and high anti mullerian hormone levels, it was 66%. That's all good news. That's actually higher than the control group. So that is good news. The not so good news is what we've also already known for a long time, which is that there tended to be a higher rate of pregnancy loss also associated with each of those four subtypes, which hangs around somewhere around the upper 20s to the low 30s in the percentiles. So while they get pregnant, they do have a higher rate of loss for reasons that we've already discussed many times before on this show. Metabolic derangement, oxidative stress, poor implantation, poor vascular response, yada yada, the whatever you can think about. Okay, and then the last thing regarding IVF is again, what we've known for at least 30 years that PCOS patients who have stimulation done specifically for in vitro, they do have a higher rate of ovarian hyperstimulation syndrome. Ohss, Ovarian hyperstimulation syndrome. We've known that for a long time. And they saw that again here. Okay, so podcast families, we get ready to wrap this up. I just found that super interesting. And again, I'm not bashing any. Any study at all. I'm just saying I love how things come out. Like, oh, hey, something is brand new.
- [29:57]
Michael (Producer)
See, I done told you. I done told you.
- [30:01]
Dr. Chapa
Is it really new? Is it, though? Is it, though? So, once again, I'll put the show notes. I have the show notes, and I'll put the link to our 2023 publication just to make that clear that that's a more clinical, kind of an easier way to think of things, using the exact same stuff that is discussed publication, kind of on a more streamlined version. But get the labs. I mean, I think labs are fine. I check all of my PCOS patients. Of course, for fasting hyperglycemia, we do a hemoglobin A1C. We get a fasting insulin level. We should do that. And there's different ways to do that. There's different ratios or different calculations to try to assess metabolic dysfunction. That's okay. You should do that. We also look for thyroid abnormalities, which is much more common in PCOS patients and in women in general, but especially with any kind of endocrine dysfunction. Thyroid dysfunction is part of that eval. We do that and we look for other causes. We don't just do clinical. We do an ultrasound. We look for polycystical variant morphology so we can better put them into their sub classifications. And we educate our patients about this. We don't want them to be uneducated about this. And we show them the data.
- [31:08]
Michael (Producer)
See, I done told you. I done told you.
- [31:12]
Dr. Chapa
Podcast family, that kind of brings us to our wrap. We have covered a new publication that just came out recently regarding the four phenotypes of pcos, which I done told you already back in March of 2023. Podcast Family, as always, we're thankful for you. We thank you for your great messages of support that you send us. Thank you for your wonderful words of encouragement. I just got something earlier today on our Instagram which said, I'm just gonna paraphrase briefly, thank you for. For what you do. Thank you for your boldness, both with things in medicine and for other things. So I feel, you know, thank you for that. That's very encouraging. As always, we're glad you're part of our podcast community, Michael. Come on now, let's take it home. This has been Dr. Chapa Zobi Gyn, no Spin podcast podcast family. Thank you for your support. Thank you for listening. And as always, we'll see you on another episode of the no Spin Podcast. Sam.