Fertility and Sterility On Air - TOC: September 2025

Take a sneak peek at this month's Fertility & Sterility! Articles discussed this month are:  

04:20 Poor intracytoplasmic sperm injection outcome in infertile males with azoospermia factor c microdeletions

10:17 Patients with a body mass index of ≥45 kg/m2 can safely undergo oocyte retrievals and anticipate similar assisted reproductive technology outcomes

21:26 Increased endometrial thickness up to 12 mm is associated with increased odds of live birth among fresh and frozen-thawed autologous transfers with or without preimplantation genetic testing

34:21 The chorionic bump is a predictor of miscarriage: a retrospective analysis of 13,656 in vitro fertilization pregnancies

47:01 Prospective validation of anti-Müllerian hormone cutoff to determine polycystic ovarian morphology: HARMONIA study

58:21 Effect of glucagon-like peptide 1 agonist medications on weight loss in patients with and without polycystic ovary syndrome

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Welcome to Fertility and Sterility On Air, the podcast where you can stay current on the latest global research in the field of reproductive medicine. This podcast brings you an overview of this month's journal, in-depth discussions with authors and other special features. F&S On Air is brought to you by the Fertility and Sterility family of journals, in conjunction with the American Society for Reproductive Medicine, and is hosted by Dr. Kurt Barnhart, Editor-in-Chief, Dr. Eve Feinberg, Editorial Editor, Dr. Micah Hill, Media Editor, Dr. Pietro Bortoletto, Interactive Associate-in-Chief, and Associate Editor, Dr. Kate Devine.

Welcome back to Fertility and Sterility On Air. We're in September 2025, Volume 124, Number 3. I'm Micah Hill, the Media Editor, and I'm joined this morning by Eve Feinberg and Kurt Barnhart and Pietro Bortoletto. Good to see you all today.

Good morning, everyone. Great to be here, Micah. I look forward to another great discussion.

It is so good to be back. I missed you guys last month. I listened to the episode.

It was fantastic. I was suffering in Sydney at the Australia New Zealand SREI meeting. I just want to give a shout-out to them.

This is the fourth year in a row they've invited Fertility and Sterility to be there and do a journal club live. We had an amazing discussion. Their fellows are awesome.

We've met them before, some of them at ESHRE, at the Embryo Transfer Course, and a huge shout-out to Allison Gee for inviting F&S there. Just a fantastic meeting. We were delighted to be there.

Kurt, I want to talk to you first about the journal this month. It's the 75th anniversary this year of Fertility and Sterility. We're kicking part of that celebration off by talking to past editors-in-chiefs.

Just tell us, what does it feel like to be at the helm of the journal, 75 years? What are you getting out of these talks with the prior editors-in-chiefs? It's a cliche, I know, but it really is an honor and a privilege to be able to usher this journal. It's meant a lot to our field. I mean, 75 years, it is almost born at the same time as ASRM, and much of what we know and how we practice today has been litigated in this journal, and the quality has increased immensely.

And today, I mean, we've never had more papers submitted to the journal than in the history. We can pick the best of the best, and it really allows me to pick the papers that are really going to drive many things, not only how we practice, but our scientific curiosity, good science, and most importantly, peer review, where scientists get to critique each other and bring their ideas forward. Fertility and Sterility is just a wonderful journal because it's so close to us, and it really does help us on an everyday basis, which is why it's wonderful to hear that we're invited to Australia, and we have literally a global reach, so I'm flattered.

It's amazing, and so for those who haven't heard it yet, there is a podcast that is out there that has the last four editors-in-chiefs of the journal talking about their experience. It's a fascinating listen. I highly encourage you to listen to that.

So we have a Views and Reviews led by Peter Schlegel, one of our editorial editors this month, and this one is truly fantastic. I think one of the best things about F&S is the quality of our editorial content that our editorial editors puts out, and this one is really spectacular. Peter's looking at the future innovations or current innovations that are being studied for severe male factor.

He has an article on stem cell-based therapies, looking at in vitro gametogenesis, the use of testicular organoids to study in advance male infertility, intratesticular PRP injections, and male pre-puberty fertility fertilization. Wow, I'm really stumbling over that one. You tried that instead of me.

Right, but this is a fantastic article, a set of articles. It's stuff I'm more familiar in the world of oocytes and on the female side, and it's really cool to see where the science is at on the male side in this, so highly encourage you to look at that. We're going to continue the topic here looking at male fertility, and so I have the next article, which is looking at poor ICSI outcomes in infertile males with azoospermic factor C micro-deletions.

So this is a study out of Beijing from a group of authors, first author Zhang, senior author Liu, and so they're looking at the outcomes of men who actually have sperm that is found with an AZFC micro-deletion compared to men that do not have that same deletion who have sperm. So this is not including men who have a dissection and do not have sperm. These are not included in this study.

This is a retrospective cohort, as I said, out of Beijing. They had 293 men who were azoospermic or severely oligo, so they define that as less than a million sperm, versus 363 who also were azoospermic or severely oligospermic, but their Y micro-deletion panel was normal. So I think that's part of the challenge of this study is what's your good control group or good comparison group, and I think that was a very reasonable one that they selected.

Their methods seem to be very appropriate for a retrospective cohort study. They use linear and logistic regression and control for the things that in prior literature would be reasonable confounders in a study like this. So what did they find? Well, as you might suspect, the groups at baseline are a little bit different, and I actually thought when I read that in the abstract that these patients do a little bit worse—I just gave away the ending—that we might see that the AZF group had worse predictions, but actually the differences were all in favor of the AZF group.

They had a lower FSH, LH, a little bit higher testicular volume. They actually had a high rate of these guys having sperm in their ejaculate, so most of them did not need ICSI. 60% almost had sperm in their ejaculate, so this is a little bit of a maybe different AZFC population than what I see, where they're usually azoospermic and we don't get sperm in their ejaculate.

We're using testicular sperm. So if anything, the predictors were a little bit in favor of the AZFC group, which is important because they did control for all of those confounders. So ultimately, what did they find? There were some differences in the sort of embryologic development in these AZFC men.

Those that had sperm, they did worse. They had lower fertilization, lower cleavage, and lower high-quality embryos. I should say that this is a Chinese study.

Most of these are day three transfers, I think. They don't really break it down in day three versus day five transfers, so with high quality, I'm not exactly sure what they mean, but those were worse than these men with the AZFC microdeletion. Ultimately, in their clinical outcomes, they did worse with clinical pregnancy, 45% versus 67%, and worse with live birth, 35% versus 53%.

So almost 20% worse for both clinical pregnancy and live birth, and these again are men who actually get sperm. And then if you move on to the final table, they have 15 embryologic outcomes or other outcomes. The main one is that not having any embryo to transfer was more common in the men with AZFC, 15% versus only 8% in those that didn't have AZFC.

Just a quick comment on table four. They have 15 outcomes. All 15 are acronyms.

I'll just see if you can tell me what these mean. FR, 2PNCR, HQER, BFR, NESTCR, CCPR. So there's a glossary, and you basically have to use the glossary to sort of figure out this table.

So I just want to make a sort of editorial comment. We're trying to reduce the number of acronyms in our articles, and this is a good example of why. The whole idea of writing a paper is to communicate science, and to do that, we should do it simplistically and in a way that communicates what we're trying to say, not in a way that makes it obscure.

I have a pretty high pain tolerance with papers, and this one actually took me quite a while to keep coming back to it because I had to have this running glossary of what these acronyms meant. But overall, I think this is an interesting study. It actually shows differences than what prior studies have showed.

Prior studies have shown if you get sperm, these men tend to do as well as other men who, if you can get sperm, who are azoospermic but don't have a C microdeletion. So this is novel in that it's a little bit of a different finding. They don't really delve too much into the biologic plausibility of why this might be, other than saying that they did notice these men had less morphology, or poor morphology, and less motility in their sperm, and they think maybe that's what the issue is.

But they're using ICSI in all of these. I did, again, find it surprising that the majority of these men had sperm in their ejaculate, and that's what they're using. That's just not been my clinical experience.

But this is a very interesting study. I think it challenges somewhat of a dogma, at least which I have thought. If you get sperm from these men, they're probably going to perform similarly to other azoospermic men.

So I think there's some value in that addition to the literature. Kurt, Eve, curious about your thoughts. I agree, and I think it really does a nice job of challenging that dogma.

I think we've always said it just takes one sperm. We need one sperm for one egg. But maybe that's not entirely true.

And so I think as we learn more about genomic changes and epigenetic changes in sperm, I think we'll start to uncover why that might be the case. Yeah, I also think it's uncovering incrementally, but importantly, you know, that the genetics of the sperm matter. It's not just a single sperm will do the job, that there really is subtlety to it that we're just starting to uncover.

You know, it might contradict other studies because all the other studies were, for lack of a better word, unscreened. We didn't know what the genetics were. So as we get more precise, I think we can learn more.

And they also had larger numbers than most of the other studies, which I think is a big advantage of these very high volume centers doing this amount of fertility care. They can sort of answer questions that maybe we didn't have power to sort of look at before. So very interesting study.

Eve, we're moving on to assisted reproduction now, and you're going to be talking to us about BMI, difficult egg retrieval, something I know you're interested in and even have a views and reviews in fertility and sterility about. This is a fascinating topic, and I think one that's evolving, especially as GLPs are coming into the scene and being used more and more frequently. I can't help but wonder if in three years we're even going to be having this discussion, to be honest.

The objective of this study was to evaluate whether patients with a BMI of greater than 45 experience more anesthesia complications or worse ART outcomes compared to those with a BMI of 40 to 44.9. Given that high BMI is often a barrier to accessing fertility care, and many centers have a cutoff. In our center, we take care of patients who have a BMI up to 45 in our procedure room, and then if somebody has a BMI over 45, we take them to the operating room for their retrieval, which I will say it's a couple floors down from us, but it's a huge utilization of resources, and to be honest, it's painful. I really enjoyed this study, and I want to give a shout out to Marissa Luck from OHSU, who just graduated her fellowship.

She was a former Northwestern resident. Marissa, I'm so proud of this work that you've done, and I can't wait to see what's next for you. This study took place both at Oregon Health Science University, OHSU, and Seattle Reproductive Medicine, and all patients with a BMI greater than 40 were included.

What I found interesting, and this is probably regional differences, but in five years where the study took place from January 2018 to January 2023, there were only 98 patients who met criteria, which again, I find this astounding. While I haven't counted the number of patients that we care for with BMIs over 40, I would say it's in the hundreds, if not over 1,000 in our center annually. So there were 56 patients with a BMI of 40 to 44.9, and 42 patients with a BMI greater than 45.

So I think right off the bat, we have to take this with a grain of salt, just given the low numbers. All patients underwent thorough preoperative anesthesia evaluation, transvaginal ultrasound for ovarian accessibility, a full H&P, and airway evaluation preoperatively. The ART protocols were really not so different between groups, and then the egg retrieval was done under conscious sedation, so not MAC.

They used midazolam and alfentanil. They did not use any propofol, and retrievals were performed either under transvaginal or transabdominal ultrasound guidance. The primary outcome was anesthesia complications during egg retrieval, and what they classified as complications were laryngeal mask for oxygen desaturation, desaturation to less than 90%, use of continuous positive airway pressure, placement of an oral or nasal airway, use of vasopressors, and the need for intraoperative or direct post-op admission.

Secondary outcomes that they looked at were operative time, ART complications such as OHSS, or the inability to access an ovary. They looked at embryologic outcomes, looking at the number of mature eggs, blasts, and euploid embryos for those that did PGT, and then they also looked at pregnancy outcomes, clinical pregnancy, miscarriage, and live birth rates. They looked at demographics and clinical characteristics between the patients.

They compared these with CHI-square and Fisher-Exact tests due to low numbers. They did a multivariable logistic regression, and they used that to examine the association of adverse outcomes with a BMI greater than 45 adjusting for age. And then for secondary outcomes, they used multiple linear regression models for clinical pregnancy rates and live birth rates.

So what did they find? And I think that these findings are interesting and important, especially as we think about these BMI cutoffs and is a BMI cutoff, you know, speaking from my center's experience, is a BMI cutoff of 45 a meaningful cutoff, and are there differences between groups? And so what they saw was that 93% of patients had no anesthesia complications. 7% experienced oxygen desaturation to less than 90%, but there was no need for advanced airway management, so they did not need to use an LMA or intubate any of these patients. And there were no significant differences in these complications between the patients with a BMI of less than 45 and a BMI of greater than 45.

Not surprisingly, they saw that the operative time was a little bit longer in the over 45 BMI group. The agrotrivial took 26.8 minutes versus 22.3 minutes, and that was a statistically significant difference, but there were no differences in sedative doses between the groups. Looking at their ART outcomes, they also did not show significant differences in the number of mature eggs retrieved, the number of blasts, the number of euploid embryos.

Their pregnancy rates were excellent. They were 58% overall with no significant difference between groups. Their live birth rates were lower.

Live birth rates were 31% overall, and while there were no significant differences between groups, I would guess that if they were to compare that to patients with a normal BMI, they would have seen a higher rate of miscarriage, which has been reported in many groups, including data from our own group and SART data. Christina Boots from our group has really spearheaded those data. Looking at miscarriage rates, there were really no differences that reached statistical significance, although, interestingly, 19.2% versus 6.4%, so I think a big difference, but the numbers are small.

Overall, their conclusions were that egg retrievals can be performed very safely in an outpatient setting up to a BMI of 50. I know that challenges, again, traditional dogma of over 40, where many centers have a cutoff would love to use these data at our center, although I think it's pretty rigid because it's across an entire hospital system that anything greater than a BMI of 45 goes to an operating room, but I think that this provides some really nice data to show that egg retrievals can be performed safely. Again, I think with the advent of GLPs, are we even going to be having this discussion in three to four years? Micah, Kurt, what do you guys think? Very good summary.

I agree with you, the GLPs are going to change things, but just before we give the impression that they're going to save everything, there's a lot of work that has to be done in that group, too, to make sure that it's safe in early pregnancy and things like that, but I'm getting off topic, and I'm going to go down a rabbit hole. I find this paper very, very valuable, and let's talk a little bit about the situation we're in. Why did we make that hard cutoff? There's a couple reasons I can think of.

One, it's the focus on the numerator rather than the denominator. People are very risk-averse. One bad adverse event is going to drive policy rather than all the people that can be helped, so clearly they're focused on avoiding one bad case rather than helping lots of people.

The second is there still is a stigma for high BMI, and I think that plays into it a little bit. Then finally, it's efficiency of practice now. This goes into the infertility is more of a business than it is a health procedure, and therefore, practices would rather not deal with the high BMI because it takes longer, requires more staff, it makes your whole practice less efficient, so we're fighting against two important issues here, which is do we get more people access to healthcare with infertility, or do we limit it to make sure that the healthcare we can do really, really well, really efficiently, and not bother our practices? It really, really is an interesting article to bring up all those topics.

Well, and I think even here, I mean, this is a collaboration between Seattle Reproductive Medicine and OHSU, and so the patients from Seattle who have a high BMI have to go to Oregon to have their egg retrieval, and we're seeing similar trends in Chicago where the private practices have a BMI cutoff of 40 or 45, and so patients who have a higher BMI are flocking to our center where we can care for them, but it is a burden on our center as well, and it is a cost burden to the patient as well. It costs more money for them to have an egg retrieval in an operating room where they charge per minute as opposed to in our procedure room where it's more fixed pricing, package pricing for an IVF cycle, and so I think the overall challenges that we face are multifactorial with patients who have an elevated BMI, and while I do think that reducing BMI pre-pregnancy is probably the right answer, I agree that we need more data on that. I think it is somewhat of a discrimination issue, and we don't discriminate against patients who have other complex medical issues, and we don't say that we're not going to care for them.

We take care of lots of patients who have cancers, lots of patients who have significant cardiomyopathy, endocrine issues, and we don't flinch taking care of those patients, and so I think it really is a challenge on many levels, and it's one that we battle internally within our practice as well. Yeah, and that's why this paper is great, to give evidence on the pro side that it can be done safely, and many of these rationales for not doing them can be challenged, and this is just the beginning to challenge that, but the cynic in me says it's going to be an uphill battle to change the outpatient requirements or goalposts or whatever we're calling them, restrictions. I was told point blank that our anesthesia group would not change, no matter what data we showed them.

Yeah, I think that's the challenge. So this was our discussion at the ASRM Journal Club last year live in Denver, and I think overwhelmingly the panel agreed that we should get rid of these limits, and we took that conversation back to our own practice and had it, and the doctors were generally very much in favor of raising the BMI limit, but we couldn't get our anesthesia team to agree, and they're the ones saying it's their license at risk if they have a bad outcome, and they weren't willing to budge either. So I think I don't know.

I agree with you, Kurt. I think that is an uphill battle. I don't know how we overcome that, but more data is certainly always good and helpful.

Yeah, again, decisions on which papers get in the journal, this is an easy one. This is the kind of data that needs to see the light of day, whether it changes practice today is yet to be seen, but it's a step in the right direction. We're staying in ART, and we have yet another paper on endometrial thickness and outcomes.

We're diving back into this topic, which I think should be a very familiar one for all of us. Tell us about this paper. So thank you, Eve.

I have a paper that I think is well done and will add to our learning, and it's a topic that we argue about all the time. So this paper is titled Increasing Endometrial Thickness Up to 12 Millimeters is Associated with an Increased Odds of Live Birth Among Fresh and Frozen-Thawed Autologous Transfers With and Without Preimplantation Genetic Testing done by a lovely group. Julian Gingold is the first author out of Albert Einstein, and the senior author is Sangita Jindal, also out of Einstein and also Montefiore.

This is using a SART database. First of all, I have to digress a little bit. I'm very happy that the use of the SART database isn't in the title.

The importance of the paper is what you study and find, not that you use what database. That's a method. But anyway, I digressed.

So this paper looks to evaluate the impact of endometrial thickness on live births, and it looks at, as I mentioned, the SART database that the years are for 2016 to 2018. It's got a lot of patients in it. It's got, you know, more than 182,000 patients undergoing more than 260,000 transfers.

And essentially, it's relatively easy to ID their methods. They basically break the endometrial thickness into categories, and those categories are based on thickness, and they go down as low as less than 6, and then they have a category 6 to 7 millimeters, 7 to 8, 8 to 12, 12 to 15, and greater than 15. Obviously, they don't overlap like that.

I'm just rounding them for you to get the categories. And what they do is they're using the 8 to 12 as the reference group. So whenever I'm now comparing things, they're comparing it to what we thought was the sweet spot between 8 and 12.

They also have a little bit of novelty in this paper in that they look at all transfers together, but then they break it down into what happens if we're just talking about a fresh transfer. And then in the category frozen transfer, they look at it with only embryos that have been tested, PGT-A tested, and only embryos that have not been PGT-A tested. So there's some, for lack of a better word, sensitivity analyses here.

So let me go through one line of data to give you an understanding of what we're talking about. It basically says that when all fresh and frozen transfers were combined, the birth rate increased basically as your endometrial thickness increased. And let me just throw some numbers at you, although it's much better to look at the table.

There's a lovely figure that shows a continuous inflection curve, which shows you that it kind of plateaus, and you'll hear the take-home message in a second. So starting at the lowest category, we're starting at a pregnancy rate of 31.2 percent, increases to 40.8 percent, then increases to 45 percent, then to 46.4 percent. That's the reference category.

I'm sorry, the 45 is the reference category. Then you go up a little higher to 46.4 percent, and eventually 46.2 percent. So if you could read those numbers in your mind, you're basically seeing an increase up until around the reference category of 8 to 12, and then a very modest increase after 8 to 12, but it does seem to increase a little bit after 8 to 12.

And the take-home message, but please read this paper and look at the numbers, is that you find that in all groups, not just the fresh category, but also in the frozen categories with and without PGA testing. Now there's a little bit of noise, but the trend seems to be there. And they also did another sensitive analysis in only women with uterine factor fertility.

And in that group, it's because you have the SART database, that it still gets a relatively large group of women only with uterine factor infertility. The increase in endometrial stripe also increases pregnancy rates in the same way. So that's the take-home message, which is, I don't know if that's becoming consensus or not, because there are lots of papers that are saying the opposite, but there are also lots of papers that say the same.

So it adds to our momentarium. But the biggest issues that I want to bring out are, this paper is telling you what happened. It's not telling you what to do with a thin endometrial stripe.

And you can be smart with your own journal clubs. It also is limited because this is people that received a transfer. We don't know about all the peoples that canceled their transfers or got a better stripe on their second attempt or that was the best stripe they could get.

So there is some residual bias here about the individual women themselves. And I found a couple things in here that I want to bring to your attention that really taught me something. The stats were good, and I'll go into them a little bit.

So I'm not worried that there's lack of control in here. But they did point out some things that I probably knew, but it wasn't just so crystal clear for me. So women with less than six millimeters were statistically older, lower BMI.

As a history, were less likely to have a live birth and more likely to have a miscarriage and smoked. So there is some inherent differences between these people. Now, again, you can control for that to some degree, but that tells you that women with thin stripes are different.

Interesting. You guys remember that endometrial smoking is one of the few risk factors that decreases endometrial cancer because it decreases proliferation. I just never saw smoking outside of that context that it's hurting.

It's an interesting observation. I That's great. Yeah.

The other thing is that when you look at people that had, they looked at people that had below and above an eight millimeter stripe, and those are different patients. The women that had less than an eight millimeter stripe for a transfer were more likely to be ovulatory dysfunction, DOR, uterine factor, and women that had a greater than eight millimeter stripe were statistically more likely to have tubal ligations than the male factor. So again, there's population differences in what you're walking into here.

Interestingly, the live birth differed by your stripe, but the miscarriage, ectopic biochemical rate didn't differ, which struck me as being a little bit weird. Both because I thought it would differ, but two, like how can you have an increase in live birth and not have a decrease in miscarriage? It seems to be that the increase in thickness is promoting a pregnancy. It's not the opposite, that the thin stripe is promoting loss, if you follow my logic.

So let me get into the weeds a little bit, because it's interesting, and it gives my chance to be a statistical geek here. They appropriately stratified their analysis by the presence of PGT-A, not controlled for PGT-A. The goal of controlling something in statistics is to make the two groups similar.

But when you have like a dichotomous, you got tests and you didn't, or the analysis I learned on was whether you had a C-section or didn't, there's no like, you got half a C-section or you got half a PGT-A. They're different groups. So you really can't control for it.

You have to do it stratified. What's the answer in this population? And what's the answer in that population? And then look at it. In this case, it looked like that there were similar trends and overlapping percentages and confidence intervals.

So they were able to say that the effect was the same in all groups. And therefore, the decrease in pregnancy rates with STRIPE isn't due to the embryo, so to speak. That actually is due to the uterus.

So as I mentioned before, this paper says, look, we're the first SART paper to do this with PGT-A. We're the largest SART paper. There's another paper, the National US Data, that found similar results.

There's a Canadian paper that found similar results. There's a paper in China. There's a paper in the UK, all saying we find the same things in registered results.

But there's also a paper, most notably from Baris Ada, also for Trillium Serulidae a couple years ago, that says we don't find a difference. And in fact, there is no linear relationship between a threshold of EMT and a live birth rate. In that paper, the Ada paper, they found a receiver operator curve of 0.54, which is basically flipping a coin.

And it didn't matter whether you adjust it again for age and BMI. Endometrial thickness was not an independent sample. So this is a convincing paper that, as a population, it matters.

But it's not a convincing paper in saying what you do about it. And is there a therapy that you can do? And should we be canceling people with a thin stripe or waiting for them to get a thicker stripe? That's the reflex that we all get from data like this. But it basically says that people that have thin stripes are different.

They probably have lower pregnancy rates. But waiting to get their stripe thicker or trying to intervene to get it thicker may or may not overcome that. So what do you guys think of that? That was interesting.

And again, I think challenges the dogma of we usually say seven or eight is sufficient. And I think this showed less of a plateau than other papers that have looked at it similarly. And I think that the strength is really in the numbers and the stratification by groups.

So I really liked it. I think the authors did a fantastic job. And I think it's an interesting, I think it's going to make me think about things a little bit differently moving forward.

I want to end by, there's a very good inklings on this by Kate Schoyer. And I think she purposely challenges both ways. The first comment, which may not be correct, it may be a challenge is, well, maybe by this data, we should be having a higher threshold.

It shouldn't be seven because this data shows that it increases even when you get above 12. Maybe our threshold for endometrial thickness should be 12 or nine rather than seven. So that's one challenge.

And the other one, she is the complete other direction. She also mentions the one statement that I found really intriguing in this paper and really is the whole premise of this paper, which is quote, our models assume that the endometrial thickness is an independent and modifiable factor. And we don't know if that's true.

So this whole premise is based on all these women can have differences in their endometrial stripe or endometrial thickness, and we can look at pregnancies better here or not, because it must be an independent factor and modifiable, but it might not be. People in the lower group are different people than in the higher group. So it's an interesting question, both epidemiologically, but also in clinical practice.

Yeah, I have to say, I agree with that sentiment. And I think that it's modifiable to a point. I think that women have different ranges of thickness that they can experience, but my patients who have an endometrial thickness of five to eight are never going to fall into that 10 to 12 range.

And so I think that there are some key differences between these women that we're not, I think that we're not appreciating. And so when I say that this is going to make me think about things differently, I think it's probably not going to change how I practice, but I think that patients do have these inherent differences that maybe we're not realizing so much. Yeah.

And then the final piece, I'm surprised Micah hasn't jumped in on this, is that this is a statistical term. I'm not saying wrong. This is a gross measurement, meaning it's a very nonspecific measurement.

All we're doing is literally measuring something on ultrasound when there's probably much more specific, better markers of endometrial preparation. I'm not talking about going back and doing an ERA test. I'm just saying, but it might be that morphology is more important, or it might be gene expression in different ways or many other things.

It's not just what I measure on my ultrasound. When we think about the complexity of implantation in the endometrium to reduce that to a single millimeter measurement, I think we can all understand is incredibly crude, but it's what we have in the SART dataset. It's the only thing we have that assesses the endometrium in the SART dataset.

So I think that's why there's so many studies on this. It's what we got. To me, the thicker endometriums, yes, they did better statistically, and this study had very large sample size in those thicker women, so that's helpful, but the difference is 1%.

So they're saying it's higher. It's 45 versus 46% for thicker. So are you going to cancel someone? Well, you'd have to cancel 100 cycles and know that you could get them thicker and know that getting them thicker would improve their outcome to make that worth it in those 100 women.

So to me, it's just, I would say it confirms what I already thought. Over a certain thickness, we sort of plateau. Yes, if we get a big enough study, we'll find statistical variation is 1% clinically meaningful.

I don't think so. No, not going to change my practice. So we're moving on to early pregnancy now.

Just a reminder that Fertility and Serility is not just an IVF journal or infertility journal. We love gynecology. We love early pregnancy.

This is a really cool study called the chorionic bump as a predictor of miscarriage, a retrospective analysis of almost 14,000 IVF pregnancies. This is out of RMA New Jersey, first author Zhang, senior author Bergh with colleagues in EVRMA in Valencia, Spain. So what is a chorionic bump? I actually got asked about this last week for the first time ever in my career, which to me was strange.

A nurse practitioner said, how do you counsel patients with a chorionic bump? And I was like, what's a chorionic bump? I hadn't read this article yet. She told me, I Googled it and I was like, I don't counsel them anything. We don't know that it's associated with any outcomes.

And then I read this study. So it's something that I guess I need to think through a little bit more. So what is the chorionic bump? They have a nice picture of it.

It's this protrusion of the chorionic wall into the gestational sac. So it just looks like this white protrusion into the gestational sac next to the embryo with its fetal heartbeat. It's got a central hypoechoic region with a peripheral hypoechoic rim without vascularity.

Most of the thoughts on the etiology of this have to do with a bleed. So a bleed in the intravenous space of the chorionic villa that extends into the gestational sac. But other people have hypothesized it's a placental cyst.

Other people that it's a loss of a twin that did not make it to an embryonic stage. But some MRI and histologic stuff suggests that it might be a bleed in that space. So their exposure was having a chorionic bump and their controls were those that didn't.

They used only patients that had PGT. So they're removing, at least to the best of our ability, to aneuploidy as a cause of this being detected. Now I think it's important to note that they did their database search and if it had the term chorionic bump in it, that went into the study group.

And they did evaluate every ultrasound image to make sure that those patients have it. So they're essentially trying to remove false positives. So you don't have patients that are falsely diagnosed with it.

If they looked at the image and did not think it was a chorionic bump, they moved them into the control group. But they didn't do that for the controls. In other words, they couldn't look at the controls.

They had almost 14,000 of them. They couldn't go through those many images. So there could be false negatives.

There could be people with chorionic bumps that are in the control group. The second weakness is that there is no definition of what a chorionic bump is. And they don't really say how many of their practitioners note this.

Is it something they emphasize in practice? I don't think it is in our practice. So I think if we're documenting this, those might be exceptions rather than the rule. But interestingly enough, they ended up with 159 patients that had a chorionic bump out of these roughly 14,000.

That ended up being a prevalence of 1.1%. This is a little bit higher than what's reported in the literature, which is as low as 0.1%. So 10 times higher, up to 0.7%. So roughly 50% higher. Maybe this is a detection bias because these are IVF pregnancies. We're obviously watching these much more closely.

Or maybe it's a prevalence in our IVF population. We don't really know. So what did they find? What's the important thing? Out of these, there was a higher pregnancy loss rate, clinical pregnancy loss rate.

So 24% of these pregnancies ended up miscarrying if they were in the chorionic bump group versus 13%, 14%. So that's 10 percentage points absolute difference. Live birth was the same.

It was 10 percentage higher if they did not have a chorionic bump, 86% versus 76%. Again, these numbers are high because we're talking about people that have pregnancy. So those that have a pregnancy that make it to an ultrasound.

They did look at all the OB outcomes that they had available in their data set, and they didn't find any difference in any of those. So that was reassuring. I was curious how well these are documented.

So like how well are these in the range of what's normally reported? Because we don't catch all of these outcomes, at least in my database. But these were actually in the normal range reported. For example, gestational diabetes was about 8%.

That's what CDC reports around 8% being in the overall OB population. So I don't think that there's maybe detection bias there. So overall, what was the conclusion of this paper? If you had these chorionic bumps, you were more likely to have pregnancy loss and therefore less likely to have a live birth.

It was 10 percentage point difference in both of those outcomes. So contrary to the previous study Kurt talked about where we couldn't explain the difference in live birth, here we can. It's the exact same percentage that are lost in association with the chorionic bump that makes that difference in that live birth.

So we have that explanation. So that's reassuring that if you make it through that first trimester, those pregnancies do exactly the same. There's no difference in OB outcomes.

There's no difference in their chance of making a live birth. I think it's very interesting that there's this higher detection in this patient population. I think some of that's certainly IVF.

I didn't see it hypothesized, but the snarky critic in me wondered if the trophectoderm biopsy itself, these are all PGT, could that lead to a chorionic bump? We're messing with the trophectoderm at an early point. That is placentation. That's where we're seeing this bump or what's hypothesized as a bleed.

I don't think so, but we've had it hypothesized that PGT, trophectoderm biopsy, is associated with hypertensive disorder. Val Baker has a paper in F&S that postulates that from retrospective data. So maybe that's part of the prevalence.

I certainly think there's a detection bias. But what's great about this paper is the other studies we have did not show an increase in out-bad outcomes. And this, again, is challenging a dogma of what we thought we knew on this new phenomenon that I wasn't aware of, the chorionic bump.

This suggests that maybe there is. I think this is like when Kurt says let the science wash over you, there's a lot of ways I can critique this paper, but I think it's really nice in that it sets us up for this whole new area of research that I think can be done. Often it takes hundreds of papers to get to a final answer scientifically of what this phenomenon even is.

I think we need a definition so that we even know what we're talking about. Here we're limited to whatever the ultrasonographer said their definition of chorionic bump is, and we don't know what that is. So we need a definition.

Then we can get larger confirmatory studies. It'd be great if we had AI tools, and we can probably do this now, where we could take those 13,000 images from the normal pregnancies and have AI scan those and see if it picks up similar things. So we can actually then go look through those images and actually have a defined patient population, see if we see the same effects in those studies, same associations.

Then the final thing is just the authors did a post-talk analysis on the type of progesterone supplementation. I think that probably came from the reviewers because the commentary talks about that as well, hypothesizing that maybe adequate progesterone supplementation and IVF might help avoid this. I have no idea if that's true or not.

It's hypothesizing several lines down the lines of inquiry that I'm suggesting. I think we first need to have a standard definition. We need replicative studies to see if we see the same association with that standard definition.

Then we can look at what's associated with those bad outcomes. And then way down the road, we can see if we can change those outcomes. But overall, they did find a study that challenges what we thought about this phenomenon.

I think it's very interesting. Kurt, Eve, what did you think? I really liked it. And I will say chorionic bump is something that I've been paying attention to for a long time.

When I was newly in practice, we had an ultrasound tech who was really astute, who picked up on these and pointed them out. And I dove into the MFM literature many years ago. And actually, this was much more reassuring than the MFM literature, which shows greater than a 50% chance of miscarriage in the setting of a chorionic bump.

And so I can't help but wonder if a chorionic bump from an IVF pregnancy is maybe less significant than a chorionic bump that arises without embryo manipulation. And I don't know if those are the same phenomena or if what we're seeing is slightly different. But I really liked the study.

I thought it was reassuring. I always worry when I see a chorionic bump. And I'm still going to worry, but perhaps I'm going to worry a little bit less than I would otherwise.

So I think it's great. Back to your comment on AI, I do think that's a new frontier for AI is looking at early pregnancy and having the ability to predict whether or not a pregnancy is going to make it to term. I think in the AI of my brain, I usually can adequately worry when the yolk sac looks too big or the gestational sac looks too small relative to the fetal size.

But I think that's just clinical gestalt from looking at thousands of OB early ultrasounds. But I think that's a really novel area for AI in the future. Yeah, I agree.

I'd like this paper. I enjoyed ushering this through the process because I enjoy studying early pregnancy. And I think this is like science developing in front of our eyes because it really is an observation somebody made where I'm difficulty quantitating it and defining it.

Yet it seems to be, despite that variance in a research study, they're still finding significant findings. So it's kind of like I noticed something, the crude way we study it now is showing that I think I should pay attention to it. I think I can do a much better job in the future.

And I can then decipher whether IVF is different than regular pregnancies and MFM and things like that. So it just really is like opening up this line of research in this crude, but well done study. I'm not saying the study is bad.

I'm just saying our definitions are bad and our outcomes are different. But I also, having studied early pregnancy for a long time, it's a little bit frustrating because what are you going to do about it? Make the patient, you have a chorionic bump, I'm really worried. You're not going to change anything.

So sometimes these predictions are frustrating because all you can do is just wait and say, oh yeah, I was worried about it. Or I guess my worry wasn't bounded. But the missing piece is the therapy.

But maybe we'll get there eventually too. Maybe AI can help us with that. I like that final comment, Kurt.

You guys know I always like to talk in numbers needed to treat or harm. It's a 10 percentage point difference in loss. So for every 10 women with a chorionic bump that you counsel that you're at an increased risk of miscarriage, one of those will have an additional miscarriage compared to women who are the same that don't have a chorionic bump.

So is it worth telling them that when nine of them will have a good outcome and having them worry about it and we can't intervene? I don't know. I think we all have different approaches to how we counsel. And then do what? Give them more progesterone? Tell them to go on bed rest? Tell them that they can't go on vacation? What's the therapy? Be anxious? So I'm not saying withhold patient information.

I'm just saying predicting a miscarriage is a difficult thing because all you're doing is adding anxiety. I think the hardest part is with the 21st Century Cures Act. When we document that we see a chorionic bump and we don't talk about it with the patient, then the patient has full access to their ultrasound report, sees that a chorionic bump has been identified, looks into chat GPT, Google, which quotes a much higher loss rate, freaks out, leads to multiple messages, and why didn't you tell me this was there? So my approach is really transparency in what we're seeing in counseling, but now I think that I can counsel with more certainty that it's probably not as significant in an IVF pregnancy as has been reported in a pregnancy without medical assistance.

I agree with that, Eve. I think if you're going to document it, you should counsel the patient on it. I like that approach of transparency.

And it's good, I didn't know about the MFM literature, so I'm glad to know that you were reassured by this, that at least the absolute risk was a little bit lower than what's reported. Yeah, at first when I saw the paper I was like, this isn't novel, like this is well known that it's associated with miscarriage, but I really liked this paper. Yeah, I think the difference is, I don't want to say that IVF pregnancies are different than unassisted pregnancies, I think the difference in MFM literature is it's much farther along and much larger, so therefore it's a more severe finding, whereas you hit it on the head earlier saying we monitor so early and look for very small differences that ultimately might not have the same effect.

So I'm not sure it's the IVF that makes a difference, I think it's the monitoring that makes a difference. Yeah, I agree, they often don't see the patients before 10 weeks. Eve, we're moving on into reproductive endocrinology and you're going to tell us, can AMH help us predict PCOS or determine, not predict, determine PCOS, diagnose it? This was another really good paper, it's very technical and scientific, but I liked it and I think it may ultimately change how we diagnose PCOS, probably not right off the bat, but over time.

I think, Kurt, what did you say, how many papers do we need to change how we practice? So I think everyone on this podcast knows that PCOS is the most common endocrine disorder in women and it affects globally one in eight women. Right now, we're mostly using the Rotterdam criteria, which require two out of three features, so oligo and ovulation, hyperandrogenism, or polycystic ovarian morphology. But I think as we all are aware, transvaginal ultrasound has limitations.

It's costly, it's less accessible in a primary care setting or in a rural setting, and it may be culturally or anatomically unacceptable for some women. So the 2023 international PCOS guidelines introduced AMH as a potential alternative to transvaginal ultrasound for identifying those patients who have PCO morphology. There was a previous retrospective study called Aphrodite that proposed an AMH cutoff of 3.2 nanograms per ml for this purpose.

This present study called Harmonia aimed to prospectively validate this cutoff, and this study was done by Terhi Peltonen from Finland with senior author Riikka K. Arffman from Roche Diagnostics. So what they did was they did a prospective population-based non-intervention study. They enrolled participants over a two-year period in two sites in Finland, and they had 948 women aged 33.9 to 37.2 years.

They broke PCOS down into four phenotypes, which they called A, B, C, and D, and I think the important thing to know is that three of the phenotypes had PCO morphology, and one phenotype, which was B, which was just a LIGO or anovulation plus hyperandrogenism that didn't have PCO morphology is the one that didn't have PCO morphology, and the other three did. So they had 128 cases that were PCO morphology positive PCOS cases and 820 women who were PCO negative controls, and so they looked at serum AMH measurement, and I think it's important to know that it's really only validated on this Roche Elecsys AMH plus immunoassay, and that the 3.2 may not be translatable to other like Beckman culture or other forms of AMH testing. So they determined PCO status using transvaginal ultrasound, and then the primary objective was to verify in this independent prospective cohort study the AMH cutoff using this specific AMH immunoassay, and then what they wanted to see, the primary endpoint was the concordance between AMH-based levels and transvaginal ultrasound-based PCOM morphology.

So what they found in their cases was an AMH of 6.2, and then in the controls, the PCO morphology negative, they had an AMH of 2.16, and in phenotype A, which was a LIGO anovulation, hyperandrogenism, and PCO morphology, so what I call the real deal, the AMH in those patients on average was 9.05. And so when they looked at the diagnostic performance of using the AMH cutoff of 3.2, they reported overall a very high sensitivity of 92.2 and a specificity of 77.9, and the overall agreement between these two was 79.9, so 80% agreement between using an AMH of 3.2 and looking at PCO morphology on ultrasound. The area under the curve was 94%, so really looking at quite a good cutoff, looking at that ROC curve, and something that I think we can confidently say has a pretty good sensitivity and specificity for identifying PCO morphology without doing an ultrasound. They looked at this in certain subgroups, so they looked at the influence of BMI, and they found that that AMH cutoff remained effective across various BMI categories, which I think is really important.

They also looked at the influence of age, so are patients who are less than 35 more likely to fit into this cutoff versus patients who are older than 35, and they found that the cutoff was pretty consistent along age groups. Overall, the conclusions of this paper was that an AMH cutoff of 3.2 is a valid and accurate tool for identifying PCO morphology in patients who have a PCOS diagnosis, and that AMH testing can offer a non-invasive, accessible, and cost-effective alternative to ultrasound. These data support the integration of AMH into routine PCOS diagnostic workflows, especially for patients who are in a primary care and a non-gynecologic setting and really argue that AMH can be part of the diagnostic workup.

So, a couple things that I want to highlight. There's a narrow age range when we talk about less than 35 and greater than 35. I think it's really important to highlight that this study only included patients who were 39.2 to 37, 30, sorry, let me re-say that.

I think it's important to highlight that the narrow age range that was included in this study is a limitation. The youngest patient was 33.9, so this really cannot be applied to young patients where we often struggle to make the diagnosis of PCOS, so in teenagers or those who are in their 20s. And similarly, the oldest patient was 37, so I think it really limits the generalizability, and I think if you're talking about incorporation of a blood test for widespread use, then you can't be so specific in that age range.

I also think there's limited racial and ethnic diversity. This is a Finnish study, so 97.5% of these patients were white and European, and do we know whether or not that applies to South Asian? Does that apply across the board? I think that in order to introduce a new blood test to be universally used, you have to have a wider population base in which you're testing it. They also excluded oral contraceptive users, which I think is fair, but I also think that if you're looking to do a blood test on somebody in lieu of an ultrasound, then I think you may want to consider including OCP users into that study population.

I think the interesting thing is the study really only focused on the four different phenotypes of PCOS. It would have been really nice to have a control population that did not have PCOS, and so they're looking at the PCO morphology with and without inclusion of that PCOM morphology, but I think the more adequate comparison group would have been a population of patients that are normal ovulatory without PCOS. They're really just looking at it in this very specific subgroup.

I think the findings are limited. I think it's interesting, but I think more work needs to be done before we abandon the use of ultrasound in the diagnosis of PCOS. I agree with all that, Eve.

Very interesting. I think it makes sense that AMH should be able to be used for this. I think other studies have shown it makes sense it's going to correlate with AFC.

If we're using AFC as one of the criteria for PCOS, then it makes sense to use AMH. We don't usually get ROCs of 94%. Kurt, what did you think about that? Very impressive, but with the caveats of a lot of what Eve said, what's the population and what are you trying to predict here? I find this area fascinating.

What was the question? Can AMH be a diagnosis? The question was very narrow. The question is really, can AMH be used in a PCOS population to identify PCO morphology? That's different. It's not saying, is AMH a diagnostic criteria? It's basically saying, does AMH correlate with PCO morphology on ultrasound? I think we will all say it does.

The bigger question, which they were dancing around, which is, should AMH be part of the diagnostic criteria? I've had lots of discussions with people about that. Why? Are we having trouble diagnosing PCOS? Is that the goal? That does make for interesting science and a good use of data and a good paper to discuss. I think that the inter-assay variability, though, really limits the generalization of this paper, that they validated this one specific immunoassay in their one specific population.

I can't just take that cutoff of 3.2 on our Beckman-Coulter and say that it's the same. I think it's really interesting. It's very scientific.

It was beautifully done, but it's a very narrow question in a very narrow subgroup. I don't even know that most people think about phenotypes, ABCD, that dogmatically. I think that's a good point.

I think if we think about the origins of the ROC curve and what we're talking about here, can we diagnose PCOS morphology in people with a PCO diagnosis, getting it right or getting it wrong? We think about the origin of the ROC. It's in London during World War where they're being bombed. It's like, do you sound the alarm and send everyone to the underground because it's a flock of geese and you cry wolf too many times, nobody goes underground anymore? Versus if you miss the bombers from Germany that are coming over, people are going to die because it gets bombed.

So maximizing that sensitivity and specificity and finding out where you make that cutoff so you're not sounding the alarm too much but people aren't getting bombed is a much different scenario than sort of this, where they already have a diagnosis of PCOS, can we predict their ovarian morphology? Which I think we all say we agree we probably should be able to do with AMH, which I think explains that really high AUC that we almost never get in our area. So it was fun to see that high of a value. Yeah, the curve was beautiful.

Kurt, we have one more and we're staying sort of in reproductive endocrinology and we're going to talk about GLP-1 agonist. So hot topic, we've touched on it today, let's dive a little bit deeper in our last paper. Sure, so the effect of a glucagon-like peptide 1 receptor against, I'm sorry, agonist medications on weight loss in patients with and without polycystic ovary syndrome.

This is an article that was known to me as it was getting published because it comes from a few of my colleagues at some unknown place called the Perlman School of Medicine and senior author Anuja Dokras who's been working in PCO and is quite an expert for a long time. And congratulations to Emily Gleason and Lindsay Levine who are working in our research group and are in training and get a nice publication. Anyway, I'm not just saying it's a nice publication because of the people with that.

And I think this is an interesting and well-done use of a research letter. This is a research letter and the hypothesis basically saying can GLP-1 work as effectively in women with PCOS as they work in other women with obesity. You might say that's an interesting question or maybe not as an interesting question, but why would it work any different? But women with PCOS are different because of the metabolic disturbances of PCOS than your prototypical obese patient.

So it was a legitimate question to say, you know, do these weight loss medications work similarly? And I guess that's the question because this is a relatively small study in a research letter, not a full study. So they did a nice job of finding people that had PCOS with a very strict definition, finding women that were a control group to that or a good match to that. And they ended up assessing the use of the GLP-1 and the outcomes in around 92 patients or 92 patients in one group and 110 patients in the other.

And I guess in retrospect, there's no surprise that there was really no difference in those that lost greater than 5% of their weight. The actual weight loss was similar and there was no difference in people that maximize the weight loss after 18 months. Now there's a lot of subtle differences in who took them and for who long and side effects and things like that.

But the outcome of this paper is basically saying that there really isn't a difference in who uses these medications in their weight loss. And so why is it a research letter? Because I think it takes an important point without needing a huge study to say, yeah, we have questions that the metabolism might be different. Maybe it's better because these drugs were developed for type 1 diabetes.

I'm sorry, for type 2 diabetes. But it's possible it doesn't work in women with PCOS for a lot of reasons. So the idea that you can relatively convincingly say it doesn't really matter and it can be used in this population removes a stigma or allows the medication to be used in populations that haven't necessarily been studied in the phase 3 trials for these medications and things like that.

So, you know, you might ask me, you know, why is a negative study and a small population accepted as a research letter? And I think that that's what I'm trying to say is that's the difference here. I think this is a really good idea. It's not hypothesizing and trying to prove that it's better or worse.

It's basically trying to get enough data to convince you that it's similar enough that these patients can use the medication. It's not trying to say it's more effective or less effective. And it is novel and it is a timely question and it is rigorously done.

The statistics are terrific and the explanation is in good shape. So that's why I think an important negative study as a research letter can impact care without being the definitive study on the subject. We can go farther into the realm of research like now why would somebody want to do a huge phase 3 trial on the difference between PCOS women? You know, there maybe is an interest to spend the time and the energy in doing that study when you've got data that shows at least the very difference it's similar.

They're not saying equivalent. They're not saying better. They're not saying worse.

They're just saying this population can be treated with these medications just like anybody else. And I think that's the importance of it. There's a nice reflection on the paper too as well.

It does point out some limitations. Again, if you want to impress people at your journal club, it does mention that there's a lot of differences in the different medications that were used. It's not just one medication.

There's different brand names. Yes, it is still a relatively small sample size. Yes, there are other potential confounders that can't be controlled for.

But it doesn't take away from the fact that at the end of the day, women with PCOS had the same effect with these wonderful medications than people without PCOS that were trying to reduce their BMI and get out of the obesity range into a normal BMI range. Any other comments on it? No, I liked it. And I think it answers a nice nugget of a question of whether or not use of GLPs would have any different impact on those who have PCOS versus not.

So I thought it was a really nice little piece of information. And I was glad to see this in our journal. And I think it loops back nicely to where we started.

We are ending sort of where we started talking about the increased use of GLPs in the fertility realm. And so I truly think we're not going to be having these BMI 50 debates for much longer. Yeah, I also think that this is a population that is probably the most obvious to use it.

I mean, if PCOS and obesity is part of the cause of their infertility, fixing that can be a benefit. And maybe people don't need to go through IVF. But I also agree with you, obesity with and without PCOS needs to be treated and can be treated, even if we are going to treat them with invasive things like in IVF.

So good summary. Wonderful discussions today. If you watch Pardon the Interruption on ESPN, you know that they always correct their mistakes at the end of the show.

I made two today. So I'll correct those really quick. I said Pietro would be on with us.

As we all know, in the world of medicine, sometimes our plans don't work out. Because of that, we missed two really good articles, including the seminal article from my own fellow Amalia Namath. So I encourage you to log in, read F&S in September.

It's a really interesting article on non-obstructive azoospermia. The other mistake I made is I presented a paper that was not in this month's journal, the very first one. So the one on the AZFC was from July.

Eve caught it and was immediately typing it in the chat. So I apologize to first author Maultasch on a similar article that's also in this month. And I just printed up the wrong one.

But we got bonus coverage from back in July. So I apologize for those. Final shout out is to a fellow in REI in Barcelona.

He's a Swiss gentleman, Yannick Hurni. He wrote a beautiful thing on LinkedIn saying how podcasts became my unexpected classroom. It started with F&S on air two years ago, doing long ski tours.

I would listen to episode after episode with absolute fascination. There's something romantic about the human voice like the golden age of radio. You get attached to the hosts eagerly awaiting for the next release.

I love to that. So thanks, Yannick. And please come find us at ESHRE next year.

I used to be kind of upset that people are learning from podcasts rather than reading the journal like they used to in my generation, you know, all that commotion. But the idea that we're reaching people on the ski slope or on ski trips now just warms my heart. So this this is great.

So keep listening wherever you're listening. Glad you're listening. And I hope that it's contributing to your knowledge.

As always, there's lots of great content we did not cover in the journal. I encourage you to print all those articles and read them. Kurt is off to the SREI Fellows Symposium this week.

We'll have a live journal club there from our editor in chief. I encourage you to listen to that. And by the time we listen to you next, it'll be close to ASRM.

So we hope to see all of you in San Antonio and have a great month of September. This concludes our episode of Fertility and Sterility on Air brought to you by Fertility and Sterility in conjunction with the American Society for Reproductive Medicine. This podcast is produced by Dr. Molly Kornfield, Dr. Adriana Wong, Dr. Elena HogenEsch, Dr. Selena Park, Dr. Carissa Pekny, and Dr. Nicholas Raja.

This podcast was developed by Fertility and Sterility and the American Society for Reproductive Medicine as an educational resource in service to its members and other practicing clinicians. While the podcast reflects the views of the authors and the host, it is not intended to be the only approved standard of practice or to direct an exclusive course of treatment. The opinions expressed are those of the discussants and do not reflect Fertility and Sterility or the American Society for Reproductive Medicine.