Thinking About Ob/Gyn
A fresh and evidence-based perspective of all things related to obstetrics and gynecology. Follow us on Instagram @thinkingaboutobgyn or visit thinkingaboutobgyn.com for show notes and more.
Thinking About Ob/Gyn
Episode 11.13 PMOS, PCOS, and the Metabolic Truth
Use Left/Right to seek, Home/End to jump to start or end. Hold shift to jump forward or backward.
Howard and guest hose Sivani Aluru unpack why the new PMOS name matters, how PCOS got tied to “cysts,” and what the evidence actually says about diagnosis, metabolic risk, and treatment. We also challenge a few habits we have all inherited, from pre-op antibiotic dosing to the way we talk about hormones, weight, and fertility with patients.
• the evidence gap behind 2 g vs 3 g cefazolin in obese cesarean patients and how practice inertia forms
• why PMOS shifts attention toward insulin resistance, metabolic screening, and multidisciplinary care
• how NIH, Rotterdam, and androgen excess criteria shape who gets diagnosed and who gets missed
• SHBG and free testosterone as a practical way to explain symptoms when total testosterone looks normal
• why ovarian follicles are not the same as painful ovarian cysts and why ultrasound can mislead
• patient frustration with “just take birth control” and how we explain progesterone protection for the endometrium
• lean PMOS, weight-focused bias, and realistic conversations about lifestyle change, GLP-1s, and bariatric surgery
• fertility takeaways from PPCOS II, metformin limitations, and what lifestyle trials suggest preconception
Be sure to check out thinkingaboutobgyn.com for more information, and be sure to follow us on Instagram.
0:00 Welcome And Guest Introduction
2:01 The 3-Gram Ancef Habit
12:02 PCOS Becomes PMOS
12:55 How The Criteria Got Complicated
22:00 Insulin Resistance And Free Testosterone
30:40 Hormone Panels And TikTok Myths
32:30 Ovarian Follicles Are Not “Cysts”
36:03 Treating Symptoms Without Dismissing People
46:12 Fertility Trials And Lifestyle Results
57:27 ACOG At 75 And Why Join
Follow us on Instagram @thinkingaboutobgyn.
Welcome And Guest Introduction
SPEAKER_00Welcome to Thinking About OBGYN. Today's episode features Howard Harrell and Savonny Alaru discussing PMOS.
SPEAKER_01Howard?
SPEAKER_02Savani?
SPEAKER_01What are we thinking about on today's episode?
SPEAKER_02Well, a couple of things, but we're gonna talk mostly about PCOS.
SPEAKER_01Sorry, what?
SPEAKER_02PCOS, polycystic ovary syndrome.
SPEAKER_01Oh, you mean PMOS, polyendocrine metabolic ovarian syndrome?
SPEAKER_02Okay, yes. Yes, I mean that.
SPEAKER_01Thank goodness you have me on here to get you guys up to date. I've never heard you guys talk about PMOS before.
SPEAKER_02Yeah, it's existed about a week, hasn't it? So we've only talked about PCOS in the past. You're always one-upping me, I see. Anyway, for our listeners, let me introduce my friend Savani Olaru. Now, when people say Aluru, I get mad because it's Olaru. Is that right? Aluru.
SPEAKER_01It is Aluru, yes. I tell people it kind of rolls off the tongue.
SPEAKER_02Alaru, it does sound Italian. I don't know. She's an OBGYN in Chicago, and she and I have become buddies through our involvement in ACOG, where she served as a junior fellow college advisory council chair. And we talked a few months ago about maybe having her on to talk about the 75th anniversary of ACOG and opportunities and ways for folks to get more involved in ACOG. And we've both done a lot and continue to do a lot for our professional organization. So we can talk about that some. But then when this name change thing happened for PCOS, I thought that Savani would be perfect to talk a little bit about this new topic as well. So let's do both.
SPEAKER_01Yes, thank you so much for thinking about me. I see so much on the daily of people coming into the office and wondering do they have PCOS? What is PCOS? And this is such a great opportunity to talk and educate a little bit more. So now in the last episode, you and Antonia brought back the things we do without evidence segment.
The 3-Gram Ancef Habit
SPEAKER_01So we have to keep that going today.
SPEAKER_02Yeah, people do like that one. Have you got one for us?
SPEAKER_01Absolutely. So how about giving three grams of cephazolin or ANCF as a preoperative antibiotic instead of two grams for obese patients? A long time ago, the standard preoperative dose of antibiotics was actually just one gram, but bariatric surgery found that to be inadequate, and surgical site infections were reduced with two grams being administered. So eventually two grams became the standard. But a little bit over a decade ago, three grams became recommended for patients who weighed more than 120 kilograms. This was recommended by the American Society of Health Systems Pharmacists and the Infectious Disease Society of America, as well as the Surgical Infection Society and Society for Healthcare Epidemiology of America.
SPEAKER_02Whoa, so many societies. Well, how about ACOG, though?
SPEAKER_01Absolutely. So with ACOG and Practice Bulletin 199, which was reaffirmed in 2018, there's a comment that consensus guidelines have increased the dose to 3 grams in patients that weigh 120 kilos or more who are undergoing non-obstetric surgery. But data from obstetric populations are conflicting so far. They specifically talk about two clinical studies that supported the increased dose, while two clinical studies actually didn't. They also talked about surrogate markers of measuring the minimal inhibitory concentrations of RAM-negative rods in patients that have different doses, but these weren't clinical outcomes. And then actual clinical studies say that the actual tissue penetration wasn't too significantly different between the two groups. They also cite a retrospective study that didn't show a difference in infections. So to answer your question, ACOG actually doesn't recommend a three-gram dose and they defer to other professional societies for non-obstetric surgeries. But I will tell you, if a patient weighs more than 120 grams and is on my operating table for a C-section, I will dose three grams of ANSEF because of all the evidence from the other societies.
SPEAKER_02Yeah, I did it this weekend actually, and was thinking about this coming up. But it's just routine. We've done it for years and years and years.
SPEAKER_01Exactly.
SPEAKER_02So well, I think you've mostly answered the question, haven't you? But I do think it's interesting. And it's another example of something that we talk a lot about on here of how we institute a standard of care without necessarily the final data or great data. It's evolving. But then it's very difficult to unravel that later on. So this in I call it inertia of practice. Well, you're a bit younger than me, and you've never probably operated in a circumstance where you weren't diligently making sure. Your whole training has been to make sure that everybody above 120 kilos got the three grams. So it's hard sometimes for us to get away from that practice pattern, that inertia. And this puts a lot of emphasis on making sure that we don't adopt policies or recommend things that don't have a great evidence basis to begin with. But as you said, the three gram recommendation came from a pharmacokinetic study by Edmondston et al. published in 2004. That was the bariatric paper. And of course, many of these decisions are made locally, and a lot of hospitals didn't adopt that recommendation, and others did. And then the societies eventually came together around 2013 and then adopted the extra gram. So and when we talk about societies making recommendations like ACOG or any of that alphabet soup that you mentioned a minute ago, these are just people like you and me who volunteer to participate in their organization and they come together and they look at the evidence that's available to them at the time and they try to do the best job they can. And well, as a side note, that really emphasizes the need to get involved and to be a voice. And you and I have tried to do that in ACOG.
SPEAKER_01Oh, absolutely. I've been really privileged to serve on CPG, which is the Clinical Practice Gynecology Committee. And you're going to be seeing some of the new evidence that's been undertaken by these incredible clinicians with not only the research-based experience, but also the anecdotal and seeing this in practice level experience too, for things like GSM, genital urinary syndrome of menopause. We've done work with the new adnexal masses guidelines. And as we're about to get back to now, the newest ad the newest project is going to be a little bit more about PMOS.
SPEAKER_02Great. Well, that's relevant for our conversation. But yeah, they're just people. And I guess my point was A, get involved, volunteer for your professional societies committees, try things like that. Try to talk to people who are working on these committees and share your opinions and perspectives. But they are living documents that change. We are undergoing a change right now in how we treat recurrent bacterial vaginosis. And the most recent thing that ACOG has, or at least the Green Journal had an expert review, all it really says don't treat the partner. It's like two years ago. But then new evidence comes. And so this is a constant process. And I guess one thing I'm saying is don't get marred to the way things have been and where they were, but look for new evidence. So well, back to cephazolin. Since those 2013 sort of consensus guidelines, there have been over 30 studies that looked at two grams versus three grams that use real world data and then see if this change mattered. And an example of this is a paper that was just in the Green Journal in 2015. I guess not just in, that's gosh, I'm getting old. Where Mazda and colleagues did a five-year retrospective cohort, and they found that three grams of ANSEF in an obese cesarean population didn't change the rate of infection compared to two grams. Speaking of which, can we still call it the Green Journal? You changed the colors on us.
SPEAKER_01I did, I did. But I will say the Green Journal is an institution, so that one is still saying. I think the Teal Journal and the Teal dark pink and yet and maybe mustard yellow journal, they just don't have the same ring to it.
SPEAKER_02Yeah. Well, anyway, you can go off on as many changes as I do, I think, but you see, people see why we're buddies. I think we're both spazzy. But there's a ton of other studies in ortho cases, trauma cases, colorectal surgeries, bypass cases, and there are studies that look at cesareans. And so one of these is the Pevsner study in 2011, and in that study, it was underpowered to see a difference in infections. But it's interesting because it really looked at the adipose tissue and the concentrations of the antibiotic there and these sort of surrogate markers. And this is sometimes typical of older studies. You just want to get it published and look at it. So you look at a surrogate marker, and that's how we got into this spot in 2012, is because you had these tissue concentration studies that looked at surrogate markers, but not the real life outcomes. So we get ahead of ourselves. We recommend the extra because it makes sense that higher tissue concentration at the time of incision would matter and things like that. We do this a lot with we do it with infectious control processes, where we look at the bacteria count on our hands or on surfaces and things like that. And then we do the trials and we find out that those differences don't actually matter in terms of real-world infections, for example. So that's what happened in this original Edison study in 2004, and they looked at tissue levels in different times, different places in gastric bypass surgeries, and they saw a slightly improved theoretic benefit in terms of tissue concentrations, and then they made all the recommendations based on that. Now, they found no difference in clinical outcomes, but of course, it was underpowered to see that. So the assumption's always that if we did a larger, better powered study, we would see those things. But we changed our recommendations. And anyway, now though, we have dozens of studies that say in real world outcomes-based matters, it doesn't make a difference, both in the general surgery world and in obstetrics. So yes, this is turning out to be a thing we do without evidence.
SPEAKER_01I think the more we discuss things and the more hospitals and clinical systems are used, are using things like surgical sight infections as a marker, it brings up the topic of the safe prevention of NTSV and gives into a whole host of other rates as to how metrics per se as to how we are graded as clinicians. So I'm really glad you brought this topic up because it opens up a whole host of we're talking about doing things in practice without specific evidence just yet. Well, the other thing that we can go off on a tangent about would be do you close the subcutaneous layer to prevent surgical wound site infections if it's greater than two centimeters? So more tangents to come.
SPEAKER_02Yeah, in obstetrics versus gynecologic patients, and is there a difference? And yeah. I think the other thing too, just sort of related to this, is hospitals more than ever are looking at surgical site infections.
SPEAKER_01Absolutely.
SPEAKER_02And in obstetrics, there's a certain number of surgical site wound infections that are probably unavoidable. And so that's always the problem, is where hospitals are driven to be better than they were last year, and you say and you're often making guesses off of limited data sets. It's harder, or I guess it's easy to come in and say, oh, that one could have been prevented, and maybe we should do this and the other. And you turn around and you're doing 50 things, but you still have occasional wound infections. So we really do need to limit the sort of policies in your department to things that do have a really good evidence basis because it's easy to it we just need to accept that some people are going to have infections. We'll see this changing in gynecology, where I think that pretty soon we'll be recommending routine metronidazole for hysterectomies in addition to the ANSF dose. That's evolving. It might be a little bit ahead of the evidence. The evidence is mixed, and we've talked about that before, but don't be surprised if that happens. There's a new study out recently, I think from New Orleans, that showed where they did an implementation and required flagell for hysterectomies, they had a like a dramatic reduction in wound infections. Does that mean it's true? We don't know yet. And it could be that they had a really bad run of things and then they had a really good run of things, and so ultimately randomized controlled trials in a benign gynecology practice are what matters. But okay.
PCOS Becomes PMOS
SPEAKER_02Well, can we talk about PCOS a bit?
SPEAKER_01I'm sorry, I think you mean PMOS.
SPEAKER_02Ah. How many years is that going to take? So speaking of difficulty in changing old habits, how long will it be before I stop saying PCOS, or our patients do, or our literature does? Even since this change, there's several new papers that have been published, of course, that call it PCOS. So they people talk about this 17 years to adopt a new guideline or a new evidence-based practice. And I think one of the things is that by the time you if it takes you that long, it's changed again by the time you get there.
SPEAKER_01Aaron Ross Powell How many of you guys still call it IUGR instead of FGR?
SPEAKER_02I try. I try. I need one of those dog collars and AI-driven, and it just shocks you every time.
SPEAKER_01I trained in the FGR era, so.
SPEAKER_02Yeah. So it sounds weird to you when us old fogies mess it up. Well, let's talk for a little bit about how we got here.
How The Criteria Got Complicated
SPEAKER_02So Antony and I, a long time ago, we talked about that old disease called PCOS and a bit of history around it. In fact, that was way back in season five, episode five. But let me give a brief history segment. We used to do that a lot too, about how we got here and how these criteria have evolved. So back in that episode, we talked a lot about the early Stein-Leventhal syndrome era, which started in 1935 when Irving Stein and Michael Leventhal published their landmark paper that describes seven women with irregular periods, hearstatism, and enlarged polycystic-looking ovaries.
SPEAKER_01Okay, I do need to point out that Stein and Leventhal were both born in Chicago. They both went to Rush Medical College and did their work at Michael Reese Hospital on the South Side. Later they were both faculty members at Northwestern. So just pulling in a tie-in to my district six folks.
SPEAKER_02Oh, so these are your people, huh?
SPEAKER_01Absolutely. 100%.
SPEAKER_02Yeah. Do you like the weird hot dogs that Chicago people eat?
SPEAKER_01Don't call them weird. I don't think ketchup belongs in a hot dog. I think everybody else is weird for putting stuff that doesn't belong on there. But this is the part where I split between being from the Chicagoland area and being from Milwaukee. So I I played the fifth on this one, officially.
SPEAKER_02Okay. Yeah. Okay. Well, before you get too attached to them, because their it was their thinking that led to PCOS being treated as primarily an ovarian disease. And then a lot of the early treatments were either things like bilateral ophorectomies or wedge resections, some treatment of the ovary. But then eventually we were able to study and able to order and look at labs and able to measure things like glutenizing hormone in the 1950s and plasma levels of testosterone, not until 1961, and then we started to learn about the hormonal underpinnings of the condition. So eventually in 1990, we had the NIH consensus criteria, which said that a patient must have both ovulatory dysfunction, usually presenting as irregular menses, and hyperandrogenism, visible either clinically or measured in blood work. And at that time, there was no ultrasound or imaging of the ovaries required in that 1990 criteria.
SPEAKER_01Yeah, I think it's fascinating that the emphasis on ovarian imaging was really added later. And I have women that come into my office all the time and say, can you just do an ultrasound to confirm I have PCOS? And I tell them the same thing. I'm like, I can listen to you for about two minutes, and I would like to let you know based on these symptoms, you have PCOS, girl, I believe you.
SPEAKER_02Yeah.
SPEAKER_01You don't we don't need to get ultrasound for it.
SPEAKER_02Yeah, I always tell people a lot of times we're doing labs to look for comorbidities or to exclude other worse things like other androgen secreting tumors or things like that, not to diagnose PCOS. I guess the other connection there is that transvaginal ultrasound wasn't routinely available in a practice setting back in '90. And as new technologies come about, we sometimes for good or bad change things. So we started ultrasounding everybody and maybe returned the emphasis back to the ovary a bit. And now you might see that a little bit with antimalarian hormone. But anyway. Well, in 2003 we got the Rotterdam consensus. Now, by 2003, transvaginal ultrasound was a routine part of office-based gynecology. And the Rotterdam consensus, there'd been well, it was one of these two sort of competing systems. And for a long time in debates, academic debates, depending on where you trained and who you worked with, people would argue over these two sets of criteria. But the Rotterdam consensus said that a patient needed two out of three features. So those features would be irregular menses, obviously meant to imply an ovulation or irregular ovulation, and then clinical or laboratory evidence of high androgens, and then polycystic appearing ovaries on ultrasound. It was also around that time that folks started talking more about the lean PCOS and the different phenotypes associated with it. And of course, this was rife for overdiagnosis as polycystic appearing ovaries, now that we added the ultrasound component, were much more common than polycystic ovary syndrome. Something like 20-ish percent or a little bit more of women on ultrasound will have polycystic appearing ovaries, not women not on birth control. But we've never thought that the incidence of PCOS or PMOS was as high as 20-something percent. I'll also add that the other argument with the Rotterdam consensus has been that one of those three diagnostic criteria had to be the anovulatory cycles or the irregular menses. So this still centers the disease around ovulation. And I'll admit that's how I've always viewed it, when that's a hangover of the NIH criteria where you had to have irregular menses. And then, could in other words, with Rotterdam, could you have polycystic appearing ovaries and hyperandrogenism, but have clockwork periods and have PCOS? That's been a debate my whole career. And it's certainly possible that someone would come in who ovulates 13 times a year, but they have elevated testosterone and they have polycystic appearing ovaries. And so a lot of us, including me, have thought that wasn't the spirit of the criteria.
SPEAKER_01And I'll be the first to admit I used to I heavily rely on the Rotterdam criteria even today when I talk to patients about this in the office. But because of what you just mentioned about having clockwork ovulation and no oligomenorrhea, a lot of people have been missed in this diagnosis. And one of the confounding factors for that is talking about the age of diagnosis too. So I've always told people we really cannot, and the Rotterdam criteria does hint at this, we really cannot diagnose the official PCOS until a woman is seven years out from her first menstrual cycle because of accounting for the immaturity of the HPO access.
SPEAKER_02Yeah. But they may, but then common sense too. You may have a 15-year-old or a 16-year-old who's not seven years out, but is clearly struggling with what we would now call PMOS. So lots of debates and lots of variables in there. And maybe sometimes those variables don't matter that much. Whatever it is, whether you meet some strict criteria or not, it's it's like you said, when you're talking to the patient, it's obvious what's going on.
SPEAKER_01It very much is a clinical diagnosis. And I also get a lot of referrals for people who are 15, 16 years old who their PCPs would order an ultrasound or they're seeking an ultrasound, and it comes back with enlarged ovaries with multiple follicles, as pretty consistent with somebody who's in that puberty phase.
SPEAKER_02And now folks will be coming in with elevated antimalarian hormones. What does that mean? So okay, well, then just three years after the Rotterdam criteria in 2006, the Androgen Excess and PCOS Society pushed back against the Rotterdam criteria a bit. And this group really wanted to center the diagnosis around hyperandrogenism rather than the ovary. And they argued that hyperandrogenism was the key feature, and then you just needed one of the other two. So again, I've definitely seen this battle in my career where a patient's with a completely normal cycle were diagnosed with PCOS because they met that androgen excess criteria. The problem, again, for me with this is that there's always lots of reasons why a person might have an elevated androgen level. And I guess when we've called it PCOS, we were looking for some ovarian connection to that. Plenty of patients have excess hair in a male pattern, or they have acne, or they have other clinical evidence, or they have on testing, they have an elevated testosterone or something like that. And they may not have the other metabolic or reproductive issues that we've classically associated with PCOS. So that's been the debate. And I guess this also is where different perspectives come in. For a gynecologist, we care about menstrual cycles and we care about fertility. But for other specialists who are not gynecologists, well, they may start at a different place, the dermatologist, the endocrinologist, the primary care doctor.
SPEAKER_01And I think the best part about as we're going to be talking about what the new name change really signifies is it does account for everybody seeking, everybody starting off in a different specialty as well. I specifically like the changes that talk a little bit more about the endocrine component and sex hormone binding globulin.
SPEAKER_02Yeah. Okay. Well, then the next big change, and something we've discussed previously on the podcast, was the this addition of antimalarian hormone testing as a potential diagnostic criteria. That happened in 2023. And that likely didn't change much in terms of who would be diagnosed and the absolute values of how high the anti-malarian hormone needed to be. They were not part of that original sort of recommendation. And there's been a few studies. I reviewed an abstract of another study more recently of what number is that, what how high should the AMH be. But anyhow, that quickly gets us to this year and PMOS or polyendocrine.
Insulin Resistance And Free Testosterone
SPEAKER_02Metabolic ovary syndrome.
SPEAKER_01So this name change really moves the emphasis towards a metabolic disease, where many of these problems are driven by insulin resistance. So maybe 70 to 80% of the cases are in fact driven by insulin resistance. So we're still using the Rotterdam criteria, but emphasizing a more universal metabolic workout workup to focus on insulin resistance, glucose tolerance, and lipids for all of our patients seeking this diagnosis or somebody that we have the clinical suspicion for. High levels of insulin stimulate the theka cells of the ovaries to produce excess testosterone. And insulin levels are inversely correlated with sex hormone binding globulin, SHBG, which it leaves more free circulating testosterone in the body. So we can see the effects of the elevated testosterone, whether that presents as ovulatory dysregulation, ovulatory dysfunction, increased herstetism, worsening acne, or even the lighter part of that with more oiliness too.
SPEAKER_02Yeah. The total testosterone might be normal, but because the sex hormone binding globulin is low or dysfunctional, there's been mutations described in a sex hormonal binding globulin starter, the starter region of the gene that essentially makes it not bind well, then the unbound or the free testosterone will be elevated and have all those effects.
SPEAKER_01And I'll tell you, as a gynecologist myself, as somebody who was wondering for years why I had persistent acne despite all these interventions, it wasn't until I ordered a testosterone panel and saw these exact, well, my partner ordered it for me. I'm not ordering my own laps.
SPEAKER_02She's ethical people.
SPEAKER_01100%. It wasn't until I saw this exact finding in myself that after years of struggling, everything clicked. So you're unlocking these diagnoses and seeing that the evidence is changing to prove to people you're not crazy. You know your body best, and it's time for us to figure out the root of what's going on.
SPEAKER_02Yeah. Well, the original idea way back really with Stein Leventhal was that the ovary itself was the problem. But there and then there was a shift, and the idea was that high androgen levels were the main problem. And of course, androgens could come from the adrenal glands, and you could have other issues for having high androgen levels. So that that distinction is still important to make a difference, to make a distinction between ovarian sourced androgens and adrenal source androgens. So I think we're still talking about ovarian sourced androgens here. And now we've shifted away even from both of those a little bit and centered this more around being a primarily metabolic issue. So I also think it's nice to not emphasize the ovaries. Again, not just for the reason of overdiagnosing it due to polycystic appearing ovaries, but because many women with PCOS don't have polycystic appearing ovaries. And actually, there's a new study that we can discuss in a minute that goes more into that.
SPEAKER_01Absolutely. I'm going to correct you again for PMOS, also, so I remember this for myself. But also, it's so interesting that you bring up the source and the root of where these high androgens are coming from, because a lot of people are trained to order things like DHEAS along with their elevated testosterone workup and not really realize women that have this condition can also have an elevated DHEAS. Does it not necessarily mean that we're looking for adrenal secreting tumors here or tumors from the adrenal gland that are secreting androgens.
SPEAKER_02Yeah. Yeah. Well, right. And sex hormonal binding globulin would still apply there too. The total levels could still be normal, but the unbound portion could be elevated.
SPEAKER_01We just need new brain.
SPEAKER_02You guys don't know it, but her job normally when we're together is to correct me. So this is she's gonna keep hitting me with this. I'm horrible. PMOS. Okay. Though the study that we're gonna talk about, which was just published, still uses PCOS in the title.
SPEAKER_01So everybody can follow along.
SPEAKER_02Yeah. Yeah, yeah. Well, I've always emphasized the last word of the name, whichever one it is, which is syndrome. And the syndrome, of course, is just a constellation of symptoms, but it doesn't imply a specific pathophysiology. So we've just described the you are described the sort of insulin resistance theory, which is a dominant theory now, or at least the pathophysiology that explains a large portion of cases of PMOS that we see. But there are certainly others. The hypothalamic pituitary ovarian axis defect deals with abnormal pulsatility of ginetotrophin releasing hormone, where the hormone is released too rapidly. And the absolute levels may not even be different. It's the pulsatility and the rapidity of the pulsations. But that will give you this high LH to FSH ratio that we used to talk about a lot if you if you have a patient with that particular constellation. And then this in turn prevents dominant follicles from fully maturing and ovulating. So this has been another one of the overarching theories for decades. You still see people all the time try to diagnose it just off of LH to FS ratios, and half the time they're not checked on the right cycle day. And you see a lot of stuff like that because people have memorized that LH to FSS ratio thing in review books when they were in med school. But that's been an overarching theory, and it's probably true for a lot of our patients. There's some ideas about how ganadotroph and releasing hormone pulsatility is determined by mimicry of the maternal pulsatility, so that this can be a heritable change, either a genetic one or an epigenetic one, or just by exposure in utero. There's some thoughts that the fetal pulsatility is set in synchrony to the maternal pulsatility. And then that's another dominant causation theory is that prenatal androgen exposure. So think the mom has PCOS and has higher androgen levels while pregnant. And then the epigenetics related to that due to either high maternal androgen levels or even things just like high stress and insulin levels in utero that can alter gene expression. In other words, what we would probably call an epigenetic cause. And then this programs the fetus to develop PMOS later in life. So lots of evidence that this may happen with mothers with PMOS or gestational diabetes, I think insulin resistance, or even just premature birth, where there's high levels of insulin-like growth factors and this stimulated catch up growth that epigenetically alters these expressions in the infant, in the newborn, and other stressors in utero, stressful environments that cause epigenetic changes. And there are some specific genetic causes like mutations. I mentioned a mutation in the starter region of sex hormonal binding globulin gene, which in turn just alters the function of sex hormone binding globulin gene. There are a few other single gene type mutations that people have looked at, and lots of other reasons why. But anyway, this constellation of symptoms, then look something that looks like PMOS or PCOS will develop. And so that's why there's all this debate over the criteria, is because we're not talking about one disease process. We're talking about literally probably a dozen or 20 or 30 disease processes, but it comes in, we see it as a constellation of symptoms, and that's what a syndrome is. So we have to keep that in mind that we're not discussing a particular pathophysiology. But in 2026, where we have higher rates of obesity and higher rates of insulin resistance in our baseline population, it is likely that insulin resistance is the more dominant cause.
SPEAKER_01I agree. And I do see, especially in 2026, with this issue being discussed a lot more and more people coming forth now qualifying for this diagnosis, raising more awareness of it. I get asked all the time, can you check my hormones? Can you order a hormone panel? Or there are companies that are ordering hormone panels. So I talk specifically about the pulsatility of GNRH and how, unless I'm testing you hourly every single day, I won't be able to determine your FSH to LH ratio. We don't know where you are in your cycle. And also it's not necessary for that diagnosis. Also, with testing insulin resistance, too. I know we're going to talk a little bit more about this, but that A1C is not the best marker to let me know if you have insulin resistance or not. It's going to let me know are you prediabetic or not? Or do you actually have diabetes? But the Rotterdam criteria does not account for insulin resistance or any type of diabetic disorder into the diagnosis, too, as part of the syndrome or constellation.
Hormone Panels And TikTok Myths
SPEAKER_02Well, especially now we have so much sort of functional medicine and social media-driven health influencer ideas about hormone levels and stuff like that. So I get obviously people come in and checking it too. And what one of the things that's happened is in that space that our patients are watching on TikTok, they've treated these sex hormones and even insulin to a certain degree, but the sex hormones kind of like thyroid, where you expect thyroid to be steady state, and I can check it at every stage of life and every phase of life and all that, and it be relatively standard and constant throughout. But sex hormones, of course, not only do they vary widely, but as you just said, with the pulsatility of ginetotrophin, the level that you check, which sometimes is an average over time, doesn't even reflect the functional pulsatility of it. So these levels just don't mean what a lot of health influencers are telling us that they mean. Yeah, right. And certainly the interventions they're recommending just don't seem to apply to that. We need studies that say the interventions do something. Insulin, fasting insulin levels are also interesting because we have the sort of this, again, functional medicine approach to what a fasting insulin should be. In a common TikTok reel is that up to 25 is normal. Well, we know it's not normal, but the question is what does it mean and at what level do we start to worry about it? But but it's probably not less than five either, probably up to nine to eleven or something like that. There's a lot of research to be done there, and we don't have guidelines around what we do with that. But that's where you would start to see insulin resistance is somewhere in in that area. And then what do you do about it? Do you put everybody on metformin because you see that? Or do you work on lifestyle changes and the underlying causes? So whole other discussion there. But okay, well, I did mention this new article.
Ovarian Follicles Are Not “Cysts”
SPEAKER_02It's actually from JAMA Internal Medicine in May of 2020. Um I'm sure they submitted it for publication before the name change, but it still talks about PCOS. And so don't correct me when I talk about it for the next couple of minutes and say PCOS. I'm just quoting the article.
SPEAKER_01That's okay. We have a safe space, and I'll be the first to admit I don't always say PMOS, so I need some correcting as well, too.
SPEAKER_02Okay, well, that's probably true. So one of the things that they point out in this article is in a survey of 7,000 respondents, 85% of patients and 62% of clinicians associated PCOS with ovarian cysts. But that, of course, the these cysts are not necessarily problematic for people. They're small antral follicles, not large cysts that we think of as sometimes causing pain or other issues like that.
SPEAKER_01Yes, doesn't really take specifically into account that if somebody has a large population of anal follicles and an enlarged ovary from that, that you can feel that ovarian heaviness, but not specifically addressing the type of cysts that grow in size or have complex components or become hemorrhagic or lead to rupture and residual pain.
SPEAKER_02Yeah. We when we talked about the episode of the pit that dealt with ovarian torsion, we They said that she had PCOS, yes.
SPEAKER_01Yeah.
SPEAKER_02They said she had PCOS. And it is possible that the ovary gets so bulky that you could have torsion from it, but very unlikely. And I think they conflated what we're talking about here. They conflated these larger cysts with that, and and so that that sometimes leads to problems. But okay, well, this study looked at Finnish women who didn't did not meet the clinical criteria of having PCOS, and then 313 who did meet their Rotterdam criteria.
SPEAKER_01Wait, isn't Antonia Finnish? Is she gonna be mad that she's not here to discuss this article with us? Oh no.
SPEAKER_02That might be an issue.
SPEAKER_01Sorry.
SPEAKER_02Well, maybe she won't listen. Well, she'll probably be mad, but I won't say any of the author names because I always rely on her for that. So and then she tells me where they're from and where they went to high school. Anyway, they excluded women who were on hormonal contraceptives, of course. And then they found that 12% of the women with PCOS still had greater than 20 follicles on ultrasound. And at the same time, only 62% of the women with PCOS had greater than 20 follicles on ultrasound. They also looked at total volume, and only 40% of the women with PCOS had ovaries that were greater than 10 milliliters compared to 5% of women without PCOS. That size greater than 10 milliliters has often been a surrogate or something associated with PCOS. So I guess the point is that you don't need polycystic appearing ovaries to have PCOS or PMOS, and you don't have PCOS just because you have polycystic appearing ovaries, and that the cysts that you have are not likely to be the cysts that are associated with pain or hemorrhage or other dysfunctions, and probably not ovarian torsion or things like that if you have PMOS.
SPEAKER_01Yes, if I could just if in a way record you saying that, barring the fact that we are on a podcast and this is recorded and get that out to everybody. How do we my whole career is going to be focused on how do we make sure that people are feeling heard for their symptoms without trying to be paternalistic and tell them actually it's not this type of cyst? Your symptoms are real, but this is not the type of cyst that is going to grow and rupture. These are actually these cysts are the oocytes that we had since we were fetuses. They just didn't leave us.
SPEAKER_02They just didn't leave us.
Treating Symptoms Without Dismissing People
SPEAKER_01They didn't.
SPEAKER_02Well, let's talk some about some of the controversial areas and how the name change may play into that. So the first one that comes to mind from me is that many patients, particularly those influenced again by social media, are frustrated by the sort of standard medical response to PMOS, which is take birth control pills if you're not wanting to be pregnant. And if you're wanting to be pregnant, then we'll give you letrozole. I think patients are frustrated by that, particularly in an era where there's so much, well, anti-birth control sentiment on social media and so much talk about finding the quote root cause and treating that instead of just masking it with pills. That's what you see on social media. So the name change will focus us more on insulin resistance, but I'm not sure that it changes our management right now that much. It may fine-tune some research, but we've still have to treat the symptoms and the problems with it and maybe we'll learn more about root causes, but I'm not sure that the name change is going to make people less upset about the fact that we tend to throw birth control pills and lifestyle interventions at folks.
SPEAKER_01No, I definitely see that. I actually had somebody in the office that's like, I don't just want to band-aid specifically saying those words. Let's focus on the root cause. And I use this as an opportunity to try to educate in the sense that absolutely, let's talk about the root cause and looking specifically at what the issue is. Is it hersitism? Because then as we're talking about how you have decreased sex hormone binding globule and increased free testosterone causing these effects, perhaps a combined oral contraceptive pill, if you're a good candidate, can help reduce the amount of circulating testosterone. So can it prevent you from getting pregnant? Absolutely. But is that the main reason why I'm using this medication? Not at all. And that's something that you're open to trying. If you want a non-hormonal medication to do that, let's talk about medications that could possibly serve as testosterone receptor blockers, things like testosterone or things like spironolactone, which is now permeated into the social media space as well. Specifically, when we talk about the oligomenorrhea aspect, a lot of what we as clinicians need to do is educate on the risks of unopposed estrogen on the uterine lining and how that can actually translate to pre-car to precancerous changes too. So I do a lot of progesterone is protective. I say that three times. I had a high school bioteacher that said if you say things in threes, people will remember it. So thank you, Mr. Donahue. I use that every single day in the office. Progesterone is protective, progesterone is protective, progesterone is protective. So am I helping to treat the oligomonorrhea and the irregular periods? Yes. Can certain forms of the progesterone we're using prevent you from getting pregnant? Absolutely, if that's the goal. But my job is to focus on your overall health and let's talk about protecting your uterine lining while we continue to manage the syndrome. And then, yes, we talk a little bit about the weight. I'm sure you hear this as well, too. A lot of people say because of my PCOS, it is very difficult for me to lose weight. They're not technically wrong, but I use this as an opportunity to tell them, yes, it is more difficult to lose weight. Let's talk more about what types of exercises and how a 10% reduction in body weight can actually trigger your ovulation naturally, too.
SPEAKER_02Yeah. And the thin type patients, the they can't lose more weight. I mean, patients get frustrated by that. And I think we feel frustrated by talking about it. And they the patients know they're overweight. And maybe maybe the answer there is, like you said, really working on even minimal gains are important and then enabling them with tools.
SPEAKER_01Yes, they don't fit that traditional stereotype. And I know from experience with working with these patients and also having been a patient myself, it is very difficult when you're looking for answers or you're looking for that solution to have somebody that you're paying for medical advice tell you something you already know, right? And I'm not doing it to weight shame, absolutely not. That's just what I tell every single person. But if you have the true endocrine dysfunction where you have the elevated testosterone, your body's going to be more akin to building muscle. So let's use it. Let's use this testosterone to our advantage. I say this as somebody who's a physician who talks about this every day, clearly passionate about this. But I also say this as somebody with PMOS myself who worked on a 40-pound weight loss journey. So I tell people, listen, I'm not playing games here. I can tell you exactly how we do this. There's different ways of managing your symptoms. I believe you. But if you already have a normal BMI, the issue is not going to be, the solution is not going to be weight loss for you.
SPEAKER_02Right. Well, people are frustrated by that, the idea that losing weight will cure it. And you see in social media, patients are frustrated when their providers seem to only focus on weight loss. And although they're also asking for root cause, so it's the other extreme of what we just talked about, how we have greatly underdix uh underdiagnosed PMOS maybe in thin patients. And the truth is PMOS may be nearly as common in thin patients as in obese patients, but we have so focused on the weight issue that we don't see those patients and we've underdiagnosed it.
SPEAKER_01Absolutely. One of the things I did want to point out too is sharing a little bit of my own journey. I did not realize that I myself had PMOS until I lost the weight. I thought a lot of my comorbidities, I was never officially pre-diabetic, but I always felt that fatigue. A lot of it was diet-related, of course. I'm not even going to talk about the stress of medical training, which I don't have to tell you twice, or any of our listeners because they're going through it right now. I empathize, I feel with you. But it wasn't until I lost the weight that I started having symptoms of worsening acne and my skin started showing this. And I realized it took the gynecologist in me, working with my dermatologist, to realize, oh, I lost all the adiposity. I'm not having the peripheral conversion of the testosterone to the androgen in my cells. And because of that, the testosterone has nowhere to go but on my face and my oil glands. So oftentimes you see these things unlocking themselves in a progression, and it has nothing to do with the weight loss. The weight loss helped improve my metabolic function, my mental clarity, and overall just my life, but helped me realize, oh, there's other things at play here. So I tell people, I agree, weight loss alone isn't the solution.
SPEAKER_02Yeah. Okay. Well, another area, patients with PMS often receive very fragmented care. They come again to us with the menstrual abnormalities or the fertility issues. They go to the dermatologist with acne or hair loss or male pattern hair. And they may go to their PCP or their endocrinologist with diabetes or prediabetes issues. They may go to the weight loss clinic or their PCP with obesity or challenges losing weight. They may go to cardiologists because of dyslipidemia. So one of the things that's always been missing for patients with PMOS is a comprehensive care program that addresses all of these issues. And I think one of the hopes, at least, is that this name change will emphasize the need for a multidisciplinary metabolic approach. In fact, I put a link to an open access article, anybody can read it, just published in Gynecologic Endocrinology, not a not the most important journal in the world, but it's a good article in an editorial that gives some opinions about this particular issue, I think.
SPEAKER_01Yes, I think the editorial really emphasizes that polyendocrine, the use of that word specifically, acknowledges that multiple endocrine axes are now dysfunctional because of this syndrome. Metabolic elevates the metabolic health aspect of this too to a core component of the disease name. It encourages earlier screenings and preventative long term management too. The ovarian syndrome still retains the word ovary in order to respect the critical reproductive and fertility impact that we see, not just with the infertility world, but also in the future with the GYN oncology world and endometrial hyperplasia from unopposed estrogen. But it does not define the entire condition by what's going on specifically with the ovaries and the cystic morphology alone. And I think retaining the use of the word syndrome really acknowledges the super diverse phenotypes. I mean, in this conversation alone, we've discussed every we've just we haven't even we probably have not been able to name all the single ways that this disease really presents and the clinical presentations, the different causes, how everybody's uh treatment is highly individualized. It is a lifelong, very complex disorder. It has a lot of intricate interactions between endocrine, metabolic, reproductive, and uh also coming to the psychosocial pathways and the effect that this has on people's day-to-day lives. So I'm really happy about the way that this has been elevated and acknowledged. But like we're about to talk about specifically, it's just changing the name doesn't solve all the issues at play.
SPEAKER_02Yeah. Yeah. It maybe gives us a moment to think. We do this where we change names of things periodically. A lot of times because there's a new insight, and sometimes they stick and sometimes they don't. I always think about amniotic fluid embolism was changed to anaphylactoid syndrome or pregnancy, but it never took off. And I think everybody's gone back to saying amniotic fluid embolism.
SPEAKER_01Or cholestasis is like cholestasis of pregnancy, not intrahepatic cholestasis.
SPEAKER_02Yeah. Yeah. Or intrauterine growth restriction to feel. Yeah. Yeah. We do these name changes because we have new insights or a better understanding or a refined understanding. And so the name change alone is not that important. It's what people take away from it and what work comes from it. So obviously, if we're shifting our emphasis to the underlying metabolic causes or at least associated conditions, then the treatment and management should necessarily shift and change a bit as well. And the research should change and shift a bit as well. And we've already mentioned that it is starting to do that. We've gone a hundred years ago from oophorectomy as a treatment to try to manage these metabolic issues. And now obviously we laugh at that a little bit today. So cringe.
SPEAKER_01Mega cringe, honestly.
Fertility Trials And Lifestyle Results
SPEAKER_02Let's talk for a few minutes today about some of the more important trials in the last 15 years or so and how they affect the management of PMOS. Yes, let's do it. So one landmark trial was the pregnancy and polycystic ovary syndrome two trial or PPCOS II trial, published in the New England Journal of Medicine back in 2014, which was just like yesterday to me. And when they started this trial in 2012, the standard of care for infertility at the time was clomaphine. But they did a double-blind multi-center trial that randomized 750 women to receive letrazole or clomaphene, and then of course followed all the important outcomes. And they found that letrazole was associated with a higher live birth rate and higher ovulation rates among infertile patients with PCOS. So this was a game-changing study that changed in my career.
SPEAKER_01Absolutely. I would say in the era that I trained and the era that I practice in, when people are looking, when people are found to be candidates for ovulation induction medications, if they meet send if they meet symptoms of PMOS, I'm already thinking in my head, well, let's see what letrosol could do, and let's have them test their ovulation first to see if there is going to be a benefit there.
SPEAKER_02And prior to that trial, not only was clomophene used for that, but we also would use metformin for a period of months before trying clomaphine. But a previous landmark trial had shown that metformin by itself did not improve fertility rates. And there's still more to learn here about what metformin might do. Subsequent studies looked at adding metformin to letrazol or clomaphine with mixed results. And now some newer studies are looking at adding clomaphine to letrazol-resistant patients. And so that's interesting too.
SPEAKER_01Yeah, I feel like a broken record whenever I see somebody for a fertility evaluation and they say something like, Well, I'm on metformin and oh, I've been told I have PCOS and that metformin is going to help me. My soapboxes, metformin monotherapy is not proven to increase live birth rates. But I think the metformin does get to the point of addressing the insulin resistance slash endocrine dysfunction aspect of it too. So there was a meta-analysis in July of 2025 and with BMC Women's Health that included 10 studies that had 931 PCOS patients. They looked at letrozole plus clomaphine and actually improving pregnancy rates by 50% and increased the rate of ovulation by 29% without any change in adverse outcomes or other surrogate markers. So that's really interesting to me too as a practicing clinician, because I could never imagine really using both of these in the generalist OBGYN world.
SPEAKER_02And whether that's plus or minus metformin, particularly in an insulin resistant patient. We've been using steroids for letrazol-resistant patients, and there's good data there too. So I think we're going to see more of that. But yes, that's I've not actually done that yet, but there's several new trials out to the point that we have a meta-analysis. There's several trials that indicate this could be a therapeutic option for letrazol-resistant patients. And rather than gonetotrophin injections, which of course get into the world of higher order multiples and lots more problems. Okay. Another important fertility aspect is what to do preconceptually. So there's a trial uh called the OWL PCOS trial or ovulation with lifestyle in PCOS trial.
SPEAKER_01Okay, high key. I love a good acronym. I love the abbreviations there, but I think we should possibly do a little bit of a better job. OWL PCOS doesn't really roll off the tongue. Maybe we should get the job of naming new medications as well, too.
SPEAKER_02Yeah, we could do this. We could just name these trials. I people sp people must put they must pat themselves on the back when they come up with some.
SPEAKER_01You need more of an alliteration. You basically need like a pre-pregnancy PCOS portfolio. So I would be like the quad P trial. Give me that job.
SPEAKER_02Some of them are just too clever for their own good. But anyway, in this trial, OWL PCOS, they randomly assigned, I can just imagine the author loves owls or something. They randomly assigned 150 women to three arms. So one arm was a series of lifestyle modifications, and another arm, the patients took oral contraceptive pills, and then the third arm they did both. They took, they did the lifestyle modifications and they took birth control pills. In the lifestyle modifications group, they had caloric restriction with meal replacements. They had weight loss medications, and they increased their physical activity with a goal of promoting 7% weight loss. And this was done over 16 weeks. And this was done before GLP1s were a thing.
SPEAKER_01I can't even begin to tell you how difficult the actual journey is without GLP ones and really focusing on macros, caloric restriction, and increasing physical activity in a safe way that does not make you feel lightheaded or dizzy all the time.
SPEAKER_02Yeah. And maybe we could talk about this too in another episode, because I also had a 40-pound weight loss journey.
SPEAKER_01Yes, we talked about it.
SPEAKER_02And I wrote about it years ago. Yeah, I wrote about it years ago and talked about it. I need to do it again. But in any event, it is difficult.
SPEAKER_01Well, that's what they don't. This is like we are the two perfect people to talk about it because it is a lifestyle thing. You don't just lose weight and then everybody pats you on the back and it's over. You lose weight and then you are presented with the next set and next era of your life. So completely agreed. That's a great weight loss regimen that they put for ARM one of the OL study.
SPEAKER_02Yeah. Well, so it was intense to do all this over 16 weeks. But what they found was a 26% live birth rate with the lifestyle group compared to 12% with the ones who took oral contraceptive pills alone, and 24% with the combined group. So really no difference. It was the lifestyle modifications that made a difference. Now, we don't have a placebo, so we don't know if the birth control group was better than the placebo group, but clearly lifestyle mattered.
SPEAKER_01Yeah, and I think it's interesting that they really just compared the two head to head. It would have been nice to see a placebo effect with the oral contraceptive group as well, too. Treating the underlying metabolic issue is clearly important. And we see that with the rise of GLP1s, and I'm sure you've also seen this, the Ozempic babies, where these poor patients were told for years and years there's no way you can get pregnant, but not really understanding how and what was causing that ovulatory dysfunction. Or you hear people say, I lost weight with the GLP1s, or naturally, and my menstrual cycle returned. So I've even been seeing people who are like, Well, I was told I was in menopause when this happened at 44 and now I'm 51 and my menstrual cycle has come back. So without talking specifically about that impact on the post-menopausal world and perimenopausal population, which I will also talk your ear about because I love. But when we talk about ways of lifestyle modifications, how do we present it in a way to patients that shows maybe you actually do not need medications? Maybe there is a lifestyle strategy here. Well, not maybe. There has been proven to be a lifestyle strategy here before we implement things like letrozole or other ovulation induction medications or even combining letrozole with uh glucosensitizing medication.
SPEAKER_02Right. And we know they're going to have better pregnancies too. If there's weight to lose, that's a healthier way. So we don't do a good job of this. And it's we don't, as medicine, we don't do a good job with lifestyle modifications. I mean, we know the things to say to people, but then translating that into action and having results from it is just very challenging. And and again, as two people who lost 40 pounds the old-fashioned way, it is hard and it's a very difficult thing to ask patients to do. And so we get frustrated with it. Nobody likes to fail. Our patients don't like to fail. We don't like to fail. We don't like to make them feel like we're shaming them or anything else. And so we don't do this good.
SPEAKER_01Right. And I also say that there is no right way to lose weight. The only right way is making sure that you are not actually putting yourself in a state of starvation. So the time is really the emphasis here. I had this weight loss journey after I completed my residency, took my written boards, and before I started my attending position. That is literally when I scheduled it into my calendar because I was not working a full-time position. Yeah. Howard is laughing because he knows how type A I am and he knows that my calendar is my life. So that is full, yeah. That is when I actually put it down to the schedule to dedicate time to doing this. And I can say this because I do not have children. I did not have a job at the time. I did not have the other responsibilities that our everyday, our patients are going through every single day. So it absolutely is difficult to lose 7 to 10% of your body weight if GLP1s or a medically assisted weight loss track, or even I bring up the topic of bariatric surgery to patients. There's no, there's nothing wrong about this. The time is the factor. And perhaps maybe if you are a 41-year-old and you're a little bit worried more about advanced maternal age pregnancy versus if you're somebody who is 25 and has several reproductive cycles ahead of you still, we can talk about how quickly do you want to accomplish this? So I try to bring that up in a very non-confrontational way.
SPEAKER_02And lots of good studies now about having bariatric surgery and improved pregnancy outcomes. So all of that's on the table. And we don't talk enough about bariatric surgery. Okay. Well, there were some secondary studies that came out of this owl trial. And one of the things they concluded was that while birth control pills do the hyperandrogenism, it was the lifestyle induced reduction in weight and visceral body fat that was the strongest independent predictor of overall health and psychological well-being and sexual function.
SPEAKER_01Absolutely. So it just goes to show that not only are we seeing this now presented on the evidence side, our patients are seeing this as well, too. And they're educating themselves on this and coming to us with likely a treatment plan already in mind.
SPEAKER_02We might call some of our patients, I guess we talk about letrozole resistant. We might call some of our patients lifestyle resistant. They're a cohort of lifestyle resistant patients. And so that enters the conversation about GLP1s, and there's new studies, obviously, about fertility and GLP1s coming out. And they essentially show what we already know. If you can lose weight, many of these metabolic issues improve and pregnancy rates increase. I do think it's interesting how every new GLP1 study is, oh, there's less cancer, oh, there's less heart disease, oh, there's less whatever. Yes, those are all things associated with weight loss. And I worry that people are giving GLP1 some independent magical power in them of themselves. We don't, to my knowledge, have any data that weight loss by any form is better than weight loss by another form. But if you lose weight, you'll have higher fertility, you'll have lower cancer rates, you'll have all of these things are true, whether you do that with GLP 1s or bariatric surgery or caloric restriction or whatever.
SPEAKER_01Yes, I guess the only thing that comes to mind would be from the bariatric surgery world about dumping syndrome and nutrient deficiencies. But before I lose track of some of the most incredible years of my life, I haven't really been able to talk to you about ACOG on our 75th anniversary.
ACOG At 75 And Why Join
SPEAKER_01So you do know it was founded in Chicago, right? In District 6, and it was founded in 1951.
SPEAKER_02You're really into this Midwest vibe, aren't you?
SPEAKER_01I mean, I'm a Midwesterner. That's the major thing that I claim to be. You can tell that by how it's really hard to say bye to me. I'll talk your ear off, and then we'll I'll talk you, I'll say like bye to you as we're going through the door out together, walking down the street. It's called the Midwest goodbye.
SPEAKER_02Oh, as opposed to the Irish goodbye where you just disappear?
SPEAKER_01I'm very loud though, so everybody would notice if I had left a party. They're probably like, thank goodness it's over.
SPEAKER_02Well, yes, ACOG was founded in 1951 in Chicago as the American Academy of Obstrics and Gynecology. And this grew out of several different regional organizations that already existed. In 1956, though, they changed the name to the American College of Obstetricians and Gynecologists from the American Academy of Obstetrics and Gynecology. And this was done to sound more like other organizations, specifically the American College of Surgeons, which was founded, by the way, by an OBGYN named Franklin Martin.
SPEAKER_01Yes, also in Chicago. I did a brief stint at Northwestern before I started medical school, and we shared offices with the ACS building. It's just an awesome plaque to see.
SPEAKER_02Yeah. Well he, yes, in fact, he worked in Chicago and was working in Chicago at the time that the ACS was founded. And but you're gonna like this one even better about Franklin Martin. I have his biography. He was born and grew up in Wisconsin. Woo-hoo.
SPEAKER_01That's where I went to medical school and grew up as a little girl.
SPEAKER_02Yeah. Well, and then the Green Journal was started in 1953, and then they moved the headquarters to Washington, D.C. in 1971 to get away from Chicago.
SPEAKER_01I can't imagine why. But when you become a fiduciary of the college, as in you are an officer, a newly elected officer, you join as a volunteer leader. In your orientation, you learn about the state of Illinois tax code because that's where things are rooted in. Yes. So we always have some. We have some Illinois love here. I'll take it. DC's fine, but it's not Chicagoland.
SPEAKER_02Well, they established the Creog in 1976. And in any event, that gets us why we just had the 75th anniversary and the logo change and the new color scheme in the next 75 years, I guess. So you and I just got back from DC and we had a gala for the foundation celebrating the 75th anniversary. And actually the ACOG Foundation technically is the original ACOG. But because of some of that tax stuff you're talking about, different tax statuses and what different nonprofits can do, there was a switch around. And so the ACOG Foundation that exists today is actually the true older organization.
SPEAKER_01It's just, it was such a beautiful time. For me, it was a true honor to be able to finish that board of directors role and have the 75th anniversary be that culmination because everybody at headquarters, the staff, everyone worked super hard. I can now say this because we're not violating any privacy laws, but I think it's very well known that Mrs. Michelle Obama was our keynote speaker. And the amount of hard work that went into that, I can't even fathom just getting to see that live. What I really want to emphasize to people who are thinking about joining ACOG, because we get a lot of what does ACOG do for me? What is the benefit? I would not be here today without ACOG. I would not have discovered my joy for both clinical practice but also organized medicine. I would not be able to say things to my patients like when I tell you I'm an OBGYN advocating tireless tirelessly for the benefit of my patients. I can say that like wholeheartedly. There's no stone left unturned. And I tell people, I don't truly see myself as being an OBGYN without having that involvement too. I think our field is so perpetrated by stereotypes. And there's so many people who don't have the expertise that OBGYNs do that are trying to control the narrative. So it's thanks to, and I got to meet people like you, incredible hardworking physicians who not only advocate for their patients locally, but do it nationally, do it on a visible stage and really care without soapboxing too much, because I know I've talked to you quite extensively about ACOG, but I joined as a resident. I technically joined as a medical student for the clinical information because it's unparalleled the information that ACOG releases. But I joined as a resident. I started residency in 2020 in COVID. And I just needed a connection to everybody else in my field. Why are we doing this? Why are we putting on the mask every single day? Why are we forcing these families to separate, to give birth in a hospital, right? And have the baby being like held up by a staff member so other family members can see it outside the window. Or how come we're not allowed to do a stat COVID C section if there's a true emergency? So, and why does the N95 grate into my face? So I found my network. It was horrible that and then I think a lot of people thought that they might have had acne, PCOS acne. It turns out it was just skin irritation. Right. It was skin irritation.
SPEAKER_02Through my work But nobody saw.
SPEAKER_01Actually, yeah, that's the story I tell people all the time. It wasn't until the end of the second year of my residency that when the masks officially came off that our nurses on labor and delivery are like, oh, that's what you look like? I had no idea. Patients know what we look like too. Yeah. So ACOG has gift gifted us so much. Me personally, I just I love this organization. And now I've gotten a lot more involved on the clinical side too. So getting able to talk about research developments, making sure that the organization is at the forefront of information, things like PMOS and updating everybody on the incredible work that we do and people like you do. So thank you for this opportunity.
SPEAKER_02Well, thank you for being on, and we're definitely gonna have you back on. We'll pick something else interesting for us both.
SPEAKER_01Love to talk more about the weight loss.
SPEAKER_02The weight loss, the weight loss. I knew I'm gonna try to lose weight before we record that episode.
SPEAKER_01I'm going through it right now. So there's no struggle is real. Well, there's no right or wrong way to do it as long as you are not starving yourself. Please don't starve yourself. We need you.
SPEAKER_02I'll survive. All right. Well, thank you. And I think we both have to go to work. The babies are calling.
SPEAKER_01Babies are calling.
SPEAKER_02All right, we'll see everybody in a couple of weeks.
SPEAKER_00Thanks for listening. Be sure to check out thinking about obgyn.com for more information, and be sure to follow us on Instagram. We'll be back in two weeks.