Fertility and Sterility On Air - TOC: November 2025

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

(03:03) A Randomized Controlled Trial of Counseling and Educational methods on Preimplantation Genetic Testing for Aneuploidy (PGT-A) for in vitro fertilization (IVF) patients

(14:02) Healthy euploid dizygotic twin birth after transfer of non-mosaic aneuploid embryos

(25:05) Validity of completely omitting endocrine and ultrasound monitoring in hormone replacement therapy protocols for frozen embryo transfer in good-prognosis patients undergoing single blastocyst transfer

(38:52) Cost-effectiveness of single euploid frozen embryo transfer in a true natural versus a hormonal replacement cycle

(44:29) Modified Versions of Natural Frozen Embryo Transfers Do Not Impact Live Births

(55:28) Soy consumption and the risk of laparoscopically confirmed endometriosis in a prospective cohort study

(01:02:42) Optimizing In Vitro Maturation Outcomes of Oocytes Following Gonadotropin Priming in Premenarcheal Girls Undergoing Ovarian Tissue Cryopreservation

View the November 2025, Volume 124 Issue 5 of Fertility and Sterility at https://www.fertstert.org/issue/S0015-0282(25)X0012-1

View Fertility and Sterility at https://www.fertstert.org/

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 everyone back to Fertility and Sterility On Air. We are in November 2025, volume 124, number five. We're recording this the week that we're all traveling to ASRM, and I am so excited to have Eve, Pietro, and Kate on.

Good morning, everyone. Morning. Good morning.

It's so good to be back. I missed last month because I was admittedly a little bit jet-lagged coming back from the Fertility Society of Australia and New Zealand, and I just want to give a shout out to all of our friends down under. They are the most loyal listeners, the most loyal welcoming hosts, and it was a fantastic meeting.

So, hi, everyone. We are glad to have you back, Eve, and excited to see all our down under friends from Australia and New Zealand that are coming to ASRM here this week. So, we're going to jump right in.

This is a really interesting issue. When I saw these articles, there were some clear themes that were coming out. There's PGT.

There's frozen embryo transfers. We have the luteal phase expert of the world, Kate Devine, on to give us some insights into this, so I'm really excited for this conversation. As always, there's some interesting front matter.

Anuja Dorcas, one of our editorial editors, has a great series on PCOS, all the fellows out there. This is a deep dive. I recommend you read this.

There's probably also a change in the title of PCOS that's coming out. You've probably, if you're an ASRM member, received that survey. Anuja talked to us about this this month on our editorial meeting, so we're looking forward to that.

Also, not surprisingly, Eric Widra has a great inkling, private equity in IVF. It's not a golden ticket, but it's one way to get to our destination. I always appreciate hearing the perspectives from Eric.

I think this is something that we all think about, and again, people like Kate and Pietro and even you, Eve, have walked the balance between our traditional academics, our traditional private practice. I think those lines are blurred. I don't even like dichotomizing those things anymore, because I think we're all trying to advance the field, so it's great that Eric has an excellent inkling on this topic.

Pietro, we're diving straight in. We don't often get good sort of educational and counseling articles. This one scored incredibly high from the reviewers.

It's a randomized trial on how we counsel about PGT. I'm really interested in the conversation that we're going to have about this. Thanks, Michael.

Yeah, it's not often we see an educational RCT. RCTs in baseline in our field are rare, but well-done, useful, clinically actionable RCTs even more rare. So really delighted to see this published in Fertility and Sterility.

The article's entitled Educating IVF Patients on PGTA. Does the method matter? By Dr. Singh et al. So this is a really cool prospective randomized control trial with three arms.

They enrolled about 105 IVF patients plus 97 partners, and these were all patients undergoing their very first ever IVF cycle. And they randomized them to three potential interventions. As we were considering the use of PGTA in their ART cycle, one group was randomized to REI counseling only, or what we would consider standard care, me telling the patient the pros and cons of PGTA.

The second arm was the standard care plus a literacy-optimized handout, so a small handout that patients would get after their visit that they could then digest and have some more, hopefully, permanence to some of the counseling. And then the final intervention was the three-pronged approach where you had the standard care REI counseling, the handout, but then this group also got a 15-minute genetic counselor session. And so you can see kind of escalating levels of education and multimodal patient education on the utility of PGTA.

The primary endpoint of this study was to see what was immediate post-visit knowledge scores. What percentage correct did these patients get when asked a series of PGTA-specific questions after their visit? And then the secondary endpoints, which I think are super interesting, were knowledge retention at two weeks. It's great if you remember stuff immediately afterwards, but what about two weeks later when the fog has lifted? Decisional conflict and decisional regret, which I think are super pertinent to our field where we're trying to really incorporate patient-centered decision making.

So what did we find? There were massive jumps in knowledge. With even a simple handout, we went from 47% correct with REI-based counseling to 79% once we added a simple handout. And I think probably most interesting here is when we added the genetic counselor session, that number only increased to 81%, so a very small delta from the handout to a 15-minute genetic counseling session.

Interestingly, these effects all persisted at two weeks for patients in both intervention arms, but only partners in the genetic counseling group retained knowledge. Man, does that make sense to me. Think about this.

A handout gets handed out, who takes it home? It's probably going to be the patient who actually reads it. It's probably going to be the patient. The partner probably didn't have a chance to spend time with the handout, and if you scheduled an extra 15-minute visit with the genetic counselor, it's just an opportunity to capture that partner's attention.

That totally jives with what I would have thought. One important point, and this kind of speaks to the secondary analysis, is despite the higher knowledge, there was no reduction in decisional conflict or regret that was detected. So the authors mentioned that they were likely underpowered for these outcomes, which makes sense, small cohort powering to the most important outcome, but I think an important point to highlight of this study.

And if you're a skeptic of PGT and wondering, is this just a ploy to get people to utilize more PGTA, planned and actual PGTA uptake did not increase across the intervention arms. The education improved understanding, but did not drive utilization, which I really love that the authors highlighted and pointed out, because I think we all have our bugaboos about PGTA and the general infertility population. This was great to see that it wasn't driving utilization.

So what do we make of this? A simple optimized written handout, written at a fourth grade literacy level, was just as effective as a live genetic counseling visit for patient knowledge. Partners needed a little bit more reinforcement. A handout alone wasn't enough for retention.

That genetic counseling visit, at least for the partner, proved to be worthwhile. And while knowledge improved, regret, conflict with that decision making remains the same. And unfortunately, we really were just able to move the needle on comprehension.

I'm going to stop there for a second. I love, love, love this study because I do standard care. But I love the idea of adding a handout to kind of drive home the point of my counseling.

And I'm wondering if the in-between point is maybe provide two handouts, one for the patient, one for the partner, because we all know the genetic counseling time is hard to come by and it's tough to add an extra burden to the patient's already busy clinical schedule. What did you guys think of this study? And how does your practice for PGTA counseling potentially change after reading this? I thought that was a great review, Pietro, and I couldn't agree more that, you know, there's a commentary in this issue that found these results to be somewhat sobering to some extent because of the fact that the genetic counseling moved the needle so little for the patients themselves. But I kind of see the glass as half full here, that there is such a low-cost intervention that really showed such significant improvement.

And that's also so intuitive, as you said, right? So, it really reflects what we know about good pedagogy, that repetition is key, that different folks learn differently. You know, there's auditory learners, there are, you know, kinesthetic learners, all of these things. Some people, you know, are visual learners.

And so, to kind of provide multiple passes at the information and in multiple formats to me makes perfect sense. And when it's cheap and easy, that's even better. So, yeah, I'm all about instituting handouts, and I would imagine that it applies to multiple other types of knowledge that we're trying to impart.

Yeah, I couldn't agree more. And I tell all my patients that it's an iterative process getting them to IVF, that we have several opportunities for education. And my counseling session is the first of several.

We also utilize written handouts. We utilize engaged MD. We do utilize for those patients who want a genetic counseling session, we use a genetic counseling session.

But I think that, to your point, Kate, people learn in different ways. And I think that having all methodologies available is fantastic. I'm going to hold my second point on this paper that's more linguistic and not scientific per se until we're done with the discussion.

But I'm just throwing that out there because I really want to cover a different point. Before we get to that point, Eve, I just have one comment on there was a financial part of the counseling and knowledge assessment that I thought was really interesting in the handout. So, at baseline, more than 80% of patients did not know whether PGTA was an insurance covered benefit.

And interestingly, when they surveyed patients between two to four weeks, the confusion actually grew post-visit. I think this highlights a potential learning or further exploration opportunity. There's a lot of financial opacity, not just genetic illiteracy that drives some of this decisional tension and patients trying to make tough decisions about where to allocate their resources.

So, I think it highlights the need for transparency around out-of-pocket costs associated with PGTA in addition to educational gaps that they're trying to close. Eve, tell us your point about language. Wait, before I go to that.

So, the other thing that I was surprised on was that the average patient age was 32.2 and 33.9. And would this study have been a little bit different in an older population that might have really needed to use PGT, therefore may have had different literacy for PGT coming into the visit? Okay, my linguistic point. We are not REI providers. The word provider has a really sordid medical history.

And I'm smiling because I say this all the time. But I want to use this platform just to get it out there that the word provider emanates from Nazi Germany in the 1930s. Pediatricians were the first to be strict of their titles as doctors and called providers.

The rest followed suit. And as physicians were dehumanized and strict of their titles and strict of their medical licenses, they were demoted to providers. And so, it's just, it's really painful for me and I think very painful for many people to hear us being called, quote, an REI provider.

And when I searched this paper, the word provider was used 22 times. We are REI physicians. Healthcare providers are ancillary staff, nurses, APPs, non-physician entities.

And I think when we spend four years in medical school, four years in residency, three years in fellowship, we are physicians. And I think that that's really important for all of our colleagues to be mindful of the really horrendous historical perspective on the word provider. And in the same way that we have switched our verbiage from master bedroom to primary bedroom because of the origins in slavery, I think we need to really keep top of mind that physicians are physicians, not providers.

Well said, Eve. I think that's a great point on how language matters and how we can all be a little bit more tactful in our academic writing. I know, Eve, that's a point that you're very passionate about as we're discussing who should best provide care for infertility patients.

I think it's especially important that patients are just very clear on who it is that's talking to them, what their role is. That includes fellows, their primary REI physician, the nurse practitioners. We just need to be clear on patients.

We don't want to obscure things for patients. I think that's the really important point. Yeah.

And I think that Medicare particularly lumps providers together. So like in the U.S., the origin of the term provider came from Medicaid and Medicare like in the 1960s. And it's a transactional word to describe somebody who provides care, who renders payment.

And nurse practitioners through Medicare sometimes are paid the exact same as physicians, and it actually lowers physician reimbursement to be lumped into the category of provider. Really interesting article. Thank you, Pietro, for breaking that down for us.

Eve, we're sticking on the concept of PGT. We don't usually publish case reports, but occasionally we do if they're exceptional. Tell us about this case report we're talking about.

Yeah, this is an exceptional and kind of a scary case report. First author, Dr. Teiss, senior author Ruth Lottie, and this paper comes from Stanford. It's titled Healthy Euploid Dizygotic Twin Birth After Transfer of Non-Mosaic Aneuploid Embryos.

And I think everyone who listens to this podcast and probably more than that knows that PGT for aneuploidy is a selection tool. And we talk about this a lot that it's not an embryo diagnostic tool. And I wish Kurt was here today to drive that point home.

And PGT is widely used in IVF to select embryos that are believed to be chromosomally normal or euploid for transfer. Embryos that are aneuploid with abnormal chromosome numbers are typically discarded due to presumed poor outcomes. And I would argue at this point in 2025, it's well recognized that embryos that are called mosaic can result in healthy live births, although at a lower implantation rate and lower live birth rate.

I would also argue that there's strong data showing that embryos called aneuploid have been convincingly shown not to result in live birth. And I think one of the best studies on this we reviewed a while back is Teigs and others by what they did, what they called a non-selection study and transferred embryos without knowing the PGT results. When they unblinded the data, they demonstrated that no aneuploid embryos resulted in live birth.

So this case report describes something totally new. And it's a 42-year-old woman, G7P5, who shared three sons and two daughters with her 49-year-old partner, actually two sons and one daughter, as one of their daughters unfortunately died in a drowning accident. They presented to the infertility clinic at Stanford for PGTA to have a girl.

And this was in 2017. Stanford at the time used a commercial PGT reference lab with NGS-based PGTA, and they did not tell us what company, with the same amplification and sequencing technology that is currently used, Ion Single-Seq and Ion Repro-Seq. This couple's first cycle yielded one euploid male 46XY embryo, and their second cycle yielded three aneuploid female embryos.

One had monosomy 5 and monosomy 18. One embryo had monosomy 11P, and one embryo had monosomy 7, monosomy 9, and monosomy 18. And those last two embryos were graded at 4CC.

The couple who strongly desired a female, hence the reason that they undertook PGT in the first place, really wanted to transfer their female embryos, even though they were aneuploid. So at Stanford, they set them up for genetic counseling. They brought this before the ethics board and made the decision to transfer all four embryos, the euploid male and the three aneuploid female embryos.

On first trimester ultrasound, they noted that there were dichorionic-diamnionic twins. There were first trimester screening that were slightly abnormal and concerning for trisomy 21, but the couple declined amnio because they decided they would not terminate. They delivered at 36 weeks via vaginal delivery, and they had two female infants in postnatal genetic counseling via peripheral blood karyotype and chromosomal microarray showed that both females were normal euploid females.

At the time of this writing, these twins are seven years old. They are healthy. They have no developmental concerns, and genetic analysis was done and suggested that the twins are dizygotic and likely originated from two of the aneuploid embryos.

So this case report was written really as a preface to a study that Stanford is conducting called the TAIM study. TAIM is Transfer of Mosaic and Aneuploid Embryos, and it's a prospective research study that was initiated at Stanford, and the study aims to evaluate the outcomes of mosaic and aneuploid embryo transfers and currently has over 100 participants. And all patients who are undergoing this study have to go through genetic counseling.

They do single embryo transfer after this case, and patients are exhaustively counseled that this is a research study and research protocol. But looking at these data and looking at this case report, I think what's so remarkable and the reason why this is published is it is the first documented case report of healthy dizygotic twins born from transfer of two aneuploid embryos. And the authors really make a strong case for why we should consider transferring aneuploid embryos in the setting of patient-centered care, reproductive autonomy, and just realizing that PGT may have some flaws with it.

So I'm so curious to open this up for discussion, but I think it has the potential to open up a huge can of worms. It does concern me about the accuracy of PGT, but I think I'm more curious really about is it an error of one specific PGT reference lab and their algorithm that they're using, or is this really, truly generalizable to all PGT? And were these embryos mosaic, and were they called aneuploid because of the threshold of where that copy number cutoff was set? Or are we really discarding embryos that have true reproductive potential? And if we think back five years ago, we weren't transferring mosaic embryos, and now we are. And I can't help but wonder, will the same hold true for aneuploid embryos? What do you guys think? I agree that it's a can of worms.

And I also agree that it really behooves the REI physician to counsel patients that we cannot say with absolute certainty that any embryo has no reproductive potential. And so it's terrifying, as you kind of started, in terms of what patients hear when they're given the option to discard embryos. And so I think, actually, we have just revised version 4,000.2 of our consents to make even more clear that we are not encouraging patients to discard anything, nor are we saying that there is any embryo that has no true reproductive potential.

Patients really need to understand and hear that loud and clear that that is their choice. And unfortunately, this case report is case in point that there's just so much that we don't know and don't understand. I find it interesting that two of the female embryos that were transferred in this case were complex aneuploid embryos.

And one of them was aneuploid of four chromosomes. You know, there's been emerging data that increasing numbers of aneuploid chromosomes in an aneuploid result may actually have a higher rate of euploidy than single chromosome aneuploidies, and whether that is because of bioinformatic noise, and again, to your point about the platform, and perhaps some of these embryos really ought to be called no call, as opposed to, you know, four, five, six chromosomes abnormal, chaotic, as one lab has called them. So lots to learn.

This is something we're actually looking into at our site in a rebiopsy study of some of these higher numbers of aneuploid, but really kudos for the team study and doing it in such a rigorous way with appropriate counseling. I really think we're all going to learn a lot. I mean, this ties in so well with the study Pietro just told us about when we're talking to IVF patients.

I mean, 10 minutes at least to explain the pros and cons of PGT, its limitations, and I still feel like half the time the patients don't understand it. Most of these platforms are just validated against cell lines. They're not actually clinically validated.

You mentioned the Teagues paper. I think there's maybe two of these that have been clinically validated. Most of these have not.

This is hard. I think even as physicians, we don't always understand it well. We spend a lot of time teaching our fellows how to understand this.

How in a few minutes do you help patients understand it and make an informed decision is very challenging. I wish they could do DNA fingerprinting and figure out exactly which of these embryos these babies came from. That would really have made this next level, but obviously these happened a long time ago, so that's not an option.

That would have been very, very cool. Yeah, I think we have to remember that all of these tests are screening tests. They're not diagnostic, and we have to approach their utility with a certain amount of humility.

They have limitations, and patients should be aware of them, and we should do our best, be it with a handout or a genetic counselor, to try to expand on those as thoroughly as possible, because there is decisional regret, and there are really cool case reports like this that come up that I think further expand our understanding of the technology. Yeah, and I think to the point of policy, that every clinic needs to have a policy that is written, that is clearly communicated to the patients a priori, that this is what the test is, this is what the test will show, this is the uncertainty, and this is our clinic policy with regard to aneuploid embryos, and maybe that policy changes over time, but right here, right now in our clinic, we will not transfer aneuploid embryos, period, and so I think it is good to know for our listeners out there that your patients can take their aneuploid embryos to Stanford to be evaluated to see whether or not they qualify for the study, and maybe there are other centers that are transferring aneuploid embryos, but I love that they're doing it under IRB with close surveillance and proper counseling mechanisms in place. A huge shout out to Dr. Lotti and the Stanford team.

She's an incoming president of SREI here in another year, and we love these studies that Ruth is doing. These are fantastic. So Kate, obviously anytime we do PGT, we have to do frozen embryo transfers.

I know this is a thing that you're very interested in with your synchrony studies, your sustained trials with all of the luteal phase research you do, so tell us, can we make it simpler for our patients? I like that lead-in, Micah, much foreshadowing, I would say, because I think this study answers that question to some extent, but not as much perhaps as I would have liked. So Zoglu et al. and the co-authors out of Turkey conducted here a retrospective cohort study of 218 programmed single untested, so no PGT here, despite them all being prior freeze-only cycles, single untested blastocyst transfers with conventional hormone and ultrasound monitoring, and 76, so somewhat of an asymmetric cohort size, so 76 programmed single untested blastocyst transfers with no monitoring at all.

So the study period was recent from June 2023 through October 2024, and the endometrial preparation in both arms was with oral estrogen, two milligrams, three times daily, starting on the second or third day of the period, and then when progesterone was started, typically 10 to 12 days later, that was given 25 milligrams twice daily as a subcutaneous injection. It's unclear what type of downregulation was used for these patients, and I think that's relevant, whether it was, for example, contraceptive pills or an agonist or nothing, they were all good prognosis patients. Everybody was younger than 37 years old.

In fact, the overwhelming majority were younger than 36 because apparently most patients at the center in Turkey who are older than 35 undergo double embryo transfer and were excluded. So all the patients had achieved a tri-laminar lining of greater than or equal to seven millimeters in an antagonist IVF freeze-only stimulation previously, and none of them had had more than one failure. It's not clear exactly what they meant by IVF failure, but clearly this is a good prognosis population.

All the patients had to have had a normal uterine cavity and bilaterally patent fallopian tubes on HSG, and severe male factor, and patients with known endometriosis were excluded. So essentially, that left only unexplained infertility, PCOS, and they explicitly stated by Rotterdam criteria, mild male factor, infertility, or a combination. So the primary outcome evaluated was ongoing pregnancy per transfer, and this is, again, between the group of patients that had standard hormonal and ultrasound monitoring versus those that had no monitoring at all.

Ongoing pregnancy was defined as viable beyond 12 weeks, and the authors found that 46% of the patients in the group with no monitoring achieved an ongoing pregnancy versus 49% in the group that was monitored. The odds ratio was 0.88, and the 95% confidence interval was 0.52 to 1.49. Typical secondary clinical outcomes were assessed and were similar between the groups as well. Notably, neither live birth nor cumulative live birth were assessed or presented in these data.

In terms of the baseline characteristics, authors didn't find any differences between the groups in terms of the age at time of transfer, BMI, duration of infertility, infertility diagnosis, or any of the cycle characteristics that were assessed. And they do purport to have conducted a multiple logistic regression analysis accounting for potential confounders and calculated an adjusted odds ratio, but to me, anyway, it was not clear which variables were actually included in that model or whether the odds ratios that are presented in the tables or the text were the adjusted or unadjusted odds ratios. So, you know, I'll stop there and hear a little bit about what you guys thought about the study.

I think it's fascinating, and I think it's super, I would say, helpful to those patients who are good candidates for this potentially. As Barbara Lawrence mentions in a really helpful reflection as well, patient selection here is going to be key, right? So these patients all, you know, were good prognosis patients. Beyond that, 64% of their population had PCOS.

And so these patients are pretty unlikely to ovulate, or less likely, I would say, than ovulatory patients to ovulate, right? And so what we're trying to pick up in cycle monitoring for frozen embryo transfers is whether they have ovulated through the estrogen before we start the progesterone. The authors also did exclude the three out of 218 patients, so 1.3% that were found to have ovulated, to have had an elevated progesterone at the time of their lining check. So, you know, one could argue that that was probably not a good methodologic choice.

Ultimately, that is exactly what we are trying to pick up. So if you add them back, you know, there still is not a statistically significant difference in their primary outcome. That said, you know, we would need a very large population to pick those patients up, especially in a largely anovulatory group.

So I really want to be able to make IVF and frozen embryo transfer more accessible. I think if we can do this for more of our patients, it'd be great. That said, I think we need a more generalized cohort to evaluate.

And I think kind of really the Holy Grail is when we're going to be able to have patients do home progesterone monitoring. And then we get to have our cake and eat it too. I love this article.

This is something that I have been thinking about a lot in the last six to seven weeks as we've been opening up our new clinic and trying to think about what are the kind of creative novel things we could do that are evidence-based. The thing that I always struggle with when you really push the envelope like this study did is what is the patient acceptability of this kind of change? A lot of these patients that come through our doors are patients who have done IVF before at other centers and there's a certain amount of being married to the monitoring. They monitored me very closely or they did extra monitoring for me and the perceived value of that extra monitoring is really hard to disentangle.

We all know that there's a sweet spot. There's a Goldilocks amount of monitoring, but more does not mean better outcomes. But the psychology of the patient and totally eliminating monitoring, that's tough.

And it's really tough for patients who have experienced it before and if they don't get pregnant or don't have a good outcome. But even more so like what is the rest of the community doing in the city? There are a certain amount of like we all kind of practice in a similar way and you don't want to stand out too hard in your local practice environment. Would love to hear from the larger network clinics like Mike and Cade and Eve in the academic setting.

Is this something that you think would even be feasible in your programs with the hefty amount of patient counseling? Well, I just want to methodologically, I have a little bit of an issue with this paper in that it's not a prospective trial. So to be clear, they sort of did this without any IRB, without any patient consent. They just went ahead and they didn't monitor patients and they did frozen embryo transfers.

And then they looked retrospectively at their data comparing the two groups, which I really take issue with. I find that very difficult and I can't speak to that, but that really jumped off the page of me. And I'm curious about what you guys think.

But to your point, Pietro, I feel like statistics don't apply to the individual. And while on a population level, I think, yes, it's probably fine for the majority of patients. What about those few patients who have one embryo and you are not detecting that they have ovulated prior to transfer? I think that's a huge disservice for something that I think is relatively easy to pop into a clinic.

And even if you just do a blood draw and maybe you make that easy and they do a blood draw at a local lab and not come all the way to the fertility clinic, but somewhere where you can get results prior to the time of transfer. It doesn't even have to be same day results. You can start progesterone, await the progesterone level.

And then if it's elevated, you can cancel the transfer because you're not warming the embryo until the morning of. But I think for a relatively simple intervention like a blood test and a relatively high stake procedure of a precious embryo that is very difficult to get for many patients, I think it's careless. And I don't really care what the climate is in Chicago.

I would not be proud to offer that level of no monitoring and no intervention when we all know patients will ovulate through. It's just a matter of who will and who won't. And while the majority won't, on an individual level, I take issue with it.

If you had a better way, Eva, finding out who those patients are a priori that are at higher risk for premature ovulation or in an incomplete lining development, would that change your rationale or your approach to implementing something like this? I have been doing this for 20 years, and it still surprises me. Patients who ovulate through in one cycle often don't ovulate through in a different cycle with the same protocol. So I am not sure that there is rhyme or reason to identify a prototype of patients who will ovulate through a program cycle.

But yes, if we could, absolutely. But I don't think that that exists. I will push back on that a little bit.

I mean, I think we know what the risk factors are for ovulating through a frozen embryo transfer preparation, and they're not in this population for the most part. So that's one thing that sort of makes the results a little bit less useful. But I agree with you that in most settings to check a progesterone, and that's really what we're getting at, we need that progesterone prior to starting the exogenous, is so easy to do.

And it's going to get easier. The home-based assays are, you know, they're getting to be extremely good. But to Pietra's point of our patients saying more is more and please monitor me more, it takes some frame shifting in terms of people's idea about what's entailed in good care during ART before this becomes something that is widely adopted.

And I'm really glad you got to that point about this being a retrospective study. I mean, that's always relevant, but here the authors give very little information about how they selected patients for monitoring versus not monitoring. And oftentimes we can try to adjust for that in terms of a really rigorous evaluation of the baseline and cycle characteristics that said they did not provide any data about the gravidity or parity of these patients.

Again, they're 64 percent PCOS. They said they'd only had up to one IVF failure, but they didn't say what the rate of failure was in each group. They also didn't say how many other low-tech treatment cycles they had done and whether that varied between groups.

And so when this is a patient and provider choice, essentially there could be huge differences between these two groups that are not represented in these data. So I would call this a hypothesis-generating study. I think especially in resource-poor settings, something that we should consider, but I wouldn't be diving right in based on this paper.

Great summary. Thank you, Kate. I personally didn't find it unethical to do it retrospectively.

I think practices are often changing how they monitor. I know practices that monitor everybody on day four of fresh IVF, day six, and I've talked to people like Paul in Seattle who are pushing that to can we start monitoring people on day seven, day eight, and maybe just monitor them twice during an IVF cycle. I don't necessarily think that needs patient consent prospectively, personally, because there's no practice documents that say you have to monitor this way and do it on this time.

So I think as long as patients are educated and you're doing it smartly, as Kate's saying, with the patient population, I would have liked to see this be a non-inferiority design. That was my main thing. You can't do a superiority trial with small numbers and say there's no difference, therefore it's the same.

I think if Kate was doing this and saying we're going to implement this, it would be a non-inferiority design. What's that margin? These odds ratios are huge, so I think it probably would have crossed that margin, and you would have said we can't say it's non-inferior based on this study. So to me, that's the big take-home point.

As Kate said, it's hypothesis-generating, but we can't say let's implement this in our patients today. We're going to stick on this same theme. We're staying in FET cycles, and we're talking about the cost-effectiveness of single-euploid FETs in a true natural cycle versus a hormone replacement cycle.

So I just want to unmute the mics real quick and go around. Pietro, what's a true natural cycle? Oh man, you're singing my song, Micah. A true natural cycle should not be called natural.

It should be called unmedicated, and it should include no ovulation induction agents. It should include no ovulatory trigger and should include no luteal phase support. Right.

That's Pietro's definition. Eve, what's your definition? True natural cycle. Same thing.

You ovulate, you monitor timing, and you transfer in an ovulatory cycle with no trigger, no luteal support. No luteal support. All right.

Kate, your definition of a true natural cycle? It's unanimous. Okay. So in this case, we're talking about a hormone replacement cycle, which was given estradiol and then giving micronized vaginal progesterone.

A true natural cycle was monitoring for a LH surge, but giving supplemental progesterone. I think this conversation just highlights that we don't have standard definitions. I actually think this is a good place maybe where the practice committee could step in and just give us a definition.

I think when we talk about natural cycle, generally we're talking about, is there a corpus luteum or is there not? How do we get to that is really the crux of us talking in different words. And Eve already talked about language matters. And so I just think it's important that we're clear on what we're talking about here.

So in this cost-effectiveness study, they're giving the same progesterone in the natural cycle versus the medicated cycle. Really the only difference in the medicated cycle is you're giving estrogen to get them there. In the natural cycle, you're monitoring them.

So I'm just going to keep this simple for the sake of time. They found that the natural cycle was more cost-effective. Why did they find that? Well, they had reduced miscarriage rate.

And this gets to a study that maybe Kate has done because they're talking about FETs with vaginal progesterone in the program cycle and the natural cycle. Kate has a study that PIO has lower miscarriage rates. And here they've also found that their natural cycles had a 10% miscarriage rate.

It was 19%, so almost double in the program cycle, but they weren't using PIO. They did do a sub-analysis looking at Kate's study, but they didn't use Kate's data. They used the cost from Kate's study.

So maybe that changes it as well. Overall, what they found is that the natural cycle is more cost-effective, but it's because it has lower miscarriage. It did have more monitoring and therefore was more expensive because they were using progesterone.

So I was really excited when I read the study and the title. They did a lot of sensitivity analysis really quickly for the fellows out there from a method standpoint. They did the ICER, the incremental cost-effectiveness.

That's cost minus the cost of the other arm over effectiveness minus effectiveness in the other arm. So if something is cheaper and more effective, obviously it's going to be more cost-effective. Something might be cheaper and less effective, but could be more cost-effective depending on what that ratio ends up being.

They did tornado plots. Tornado plots are beautiful. It's essentially a sensitivity analysis looking at each assumption you make in your cost model because those assumptions are really important.

And not surprisingly, the assumption of how big the miscarriage rate is and how much you spend on monitoring for these different arms were the things that drove the difference. So you could have different assumptions and maybe come up with different conclusions. And then finally, they did Monte Carlo simulations.

That's 10,000 simulations changing the model to see how much it changes this. They decided to limit those simulations to within 10 percent of each assumption. So that makes these relatively narrow simulations as far as how much those will change the model.

So I think this is an interesting study. I think the NAPRO data coming out is going to really drive a lot of this discussion. How much does it change preeclampsia? How much does it change disorders of pregnancy? I know Pietro has thoughts on that based on the population that was selected.

But as always, I think this comes down to any cost effectiveness model is really driven by the assumptions you make. This assumption was driven by the differences in miscarriages. The difference in miscarriages was driven by the progesterone supplementation that they did in their program cycles, in my opinion.

I know we have experts on this call, so I'd love to hear what you think. I can't say it better than that, Micah. To me, it's an endorsement of systemic progesterone if you're doing a program cycle.

Yeah, their data certainly supported that. Yeah. Yeah, I think your summary said it all.

Can you please get the practice committee on a working definition for us all to speak the same language, will you? Pietro, I use your chart from the views and reviews that I put together, and I use that frequently. That spells out what is natural, what is modified, what is modified natural, and what is programmed. And I think to date, I love that.

With the pluses and minuses, when it shows estrogen, progesterone, trigger, corpus luteum, to me, that is the gold standard. So, strong work there. Thank you.

I think Curt is really rubbing off on all of us. We're really becoming sticklers for language and terminology, and nothing is spontaneous, except maybe one, historically. And if something is natural, that implies something else is unnatural.

And in my older years, I'm becoming more and more like Curt, which I guess isn't a bad thing. We're coming into that holiday season. So, great reference, Pietro.

Kate, we're sticking with this theme. So, I love it when these articles have a theme. We're still talking about modified versus natural.

Does it impact live birth? What did we learn from this article? Yeah. So, in this article, Hargreaves and co-authors, one of whom is Pietro's brilliant partner, seek to evaluate different modifications to natural FETs. And unsurprisingly, they adhered to Pietro's terminology, probably not a coincidence.

It's a retrospective cohort study where they looked at 4,806 natural and modified natural cycle FETs to 3,517 patients over a very long study duration. So, from 2014 to 2021 at a single center. So, the four protocols evaluated were a true natural defined as we just discussed, a protocol that used only vaginal progesterone supplementation, so no ovulation induction, no trigger, a group that had aromatase inhibitor ovulation induction, trigger, and vaginal supplementation.

And then lastly, HCG trigger and vaginal progesterone supplementation. So, in an appropriately adjusted analysis, in my opinion, authors found no differences in any outcome. And that included the primary outcome of live birth.

Also reassuring, given all that we discussed about whether frozen embryo transfer results in more substetric outcomes, especially, you know, in the setting of program cycles, which, of course, was not the subject of this particular analysis. That said, they found that the mean birth age was 39 weeks. And that birth weights for each group were normal, ranging, you know, in the 3,300 to 3,500 gram for means.

And these were similar among the groups, which you have to look in the supplementary material to find. And so, since there were no differences in the live birth between the four protocols, they concluded that it's reasonable to modify a natural cycle protocol in any of these ways without fear of negatively impacting the outcomes. So, to me, kind of in keeping with one of the themes of today, you know, this is kind of about convenience.

So, natural cycles are inconvenient, especially those without, even if they are more cost effective relative to program cycles without systemic progesterone, they're inconvenient because they require just a ton of monitoring. And so, you know, at the end of the day, I think this and many other protocol modifications to natural cycles are going to need to be made if we're going to generalize utilization of modified natural cycles or try to give patients whatever benefits may exist from having a corpus luteum present for their frozen embryo transfer cycle. So, we're going to be seeing, I think, a lot more creative protocols coming out to evaluate this.

One thing, though, that I wanted to kind of push on a little bit, it's not necessarily the topic of this paper, is not to throw the baby out with the bathwater in terms of program cycles. And shout out to Alexi Poku who has a reflection in this FNS as well, kind of talking a little bit about really what is the quality of the evidence that we have so far to show that natural or modified natural cycles really result in better outcomes for our patients. There's an accumulating body of evidence.

Unfortunately, almost all of it is non-randomized data. There is one RCT that's been published, but it was stopped prematurely. And so, you know, I, I think, like many others, anxiously await the outcomes of the NAPRO study.

I think that if it shows that there's a benefit in terms of patient safety, then we all need to pivot and pivot quickly and do what we need to do to extend natural cycle protocols in all their variants to our patients. But for now, we don't know. So, you know, there's a lot of convenience to be had in program cycles.

And I think that it's still a very reasonable option for most of our patients. Kate, I'm going to try to get you to blink. Any NAPRO results you can share with us? Good try, good try.

All right, listener, I tried. How much of your cycles for each person on this call are modified natural? Like what percent of your FETs are using a corpus luteum? Eve? About half. About half.

Pietro? The dismay of our lab. Yeah, we're at half right now. I've been as high as 75, 80 percent in previous centers that I've worked in.

Kate? Yeah, I think we're at about 25 percent, just given the size of our lab. We really try hard to not have that be the first-line protocol for our patients yet until we know there's a benefit. Were any of you not using a trigger for your natural cycles? Anyone truly monitoring for natural cycles and any significant percentage? We were.

About six months ago, it was a free-for-all. Everyone was doing what they wanted. We stopped.

We paused. We looked at our data. We talked to our lab, who was really struggling with timing.

We went to a universal trigger and then transfer, with the idea that if they are surging, we still trigger. We transfer six days later. If they are not surging, we trigger and we transfer seven days later.

Pietro and Kate, I see nods. The podcast people can't hear it. You guys also triggering most of those natural cycles or corpus luteum cycles? 100 percent.

Okay. Who is using progesterone even if they trigger them and they have a functional corpus luteum? Guilty. I think we're all using it.

I don't, and I'm getting just the same pregnancies. I haven't been, but I see that on everyone at our practice, so I think we do. We looked at that, too, and our universally lower pregnancy rates when progesterone wasn't used in a natural cycle.

You did? We did. Why? I wonder why. Physiologically, is it the trigger that messes with the LH pulsatility? What do you think is the reason for that? I think it's the trigger.

I think if you are going to trigger, then you have to use progesterone because of the half-life of HCG. We know that gonadotropins interfere with LH pulsatility. In the same way that when we use a gonadotropin stem cycle for IUI, you have to use luteal support.

I think the same holds true for a natural cycle. Kate, you're the luteal queen. What do you think? Yeah, I agree with that.

I think the data are mixed and it's not proven, and again, I think it may vary from patient to patient, but to me, it's, you know, in this case, we're using vaginal progesterone for the most part. It's like such minimal harm that I just really see no downside. I also worry about it, as you know, Micah, because we've discussed this, you know, quite a bit about older patients and corpus luteum function.

So especially in patients who are older, you know, I think we just don't know for sure whether ovarian aging affects the quality of the corpus luteum function as well. Drew, you said you're guilty as well. Tell me why you're guilty.

I think patient expectation is probably my number one, number two, and number three reason. I think there's probably very little difference between the addition of progesterone in the general population, but I agree with Kate. As you get older, there's some biologic plausibility, but I think that's also true for younger patients with diminished ovarian reserve.

I think their luteal function may not be as robust as a 32-year-old with a normal AMH. Agree, and we are looking at that as well. So I would love to be able to do natural cycles and modify natural cycles with more confidence and a larger swatch to the population.

So I think we have a lot of work to do on the research side. I'd love to see that data published. I'll just say the RCTs on IUI cycles, when you use letrozole, when you use Clomid and you do triggers, luteal support does not matter, does not affect it.

If you use gonadotropins and you're really pushing estradiol levels higher than it does, and that makes sense, you're getting feedback, you're going to have decreased OH pulsatility. That's what the clinical trial data shows on IUIs. Clomid has a longer half-life and Clomid probably is still working at the level of the pituitary to secrete gonadotropins, whereas if you don't give Clomid and you're just giving gonadotropins with a shorter half-life, the mechanism of Clomid and gonadotropins is entirely different.

I think it's probably confounding by selection. I think the patient who needs IVF to conceive is not the same as the patient who needs IUI to conceive, and I think along there are probably ovarian reserve, poor prognosis, and other factors that kind of make the distinction more obvious in IVF cycles versus IUI cycles. We're all arguing that progesterone is low intervention and probably low cost.

I know some patients hate the discharge. I'm just saying I don't see the data to support it and I'm doing it without it and seeing good pregnancies. So I'd love to see actual data, actual trial data, on the natural cycle.

Do we need to give them? If we do, why aren't we giving progesterone in every cycle to every woman trying to get pregnant every month if it truly matters? We probably should be. There's a certain sect of people that are doing that. Yeah, there are.

I guess my main point is low harm, low cost. It's still an added intervention, and I know people that take that to the extreme and they're adding 30 interventions to every natural cycle that they do with all these supplements, and at some point, extra stuff is harmful and is costly. Really interesting discussion.

I love hearing that internal data. If we're committed to luteal support in the spirit of trying to simplify medications and cost for patients, what about a little luteal HCG every so often for a couple weeks? Are we accomplishing the same thing and better supporting their naturally or spontaneously occurring corpus luteum better than giving them some progesterone vaginally? That would certainly work. They already have the medication at home.

They've already learned how to give it to themselves. One less medication. Keep it simple stupid.

Well, shout out to Paul Lynn and Eric Widrow who said we need more controversy and arguments when we have these. We agree too much, so I'm trying to throw a little bit of that in there. Good talks.

All right, we're going to switch up. Yeah, keep it spicy. Exactly.

Pietro, I had to throw you the soy and endometriosis surgery. You're a surgical guru. Why did I give you this article? What's this about? Nothing spicy about soy intake and endometriosis risk, but let's talk about it.

So you're probably wondering, we've heard soy is used for different kind of stages in life. Why are we using it? Well, soy contains a rich amount of isoflavones. These affect the estrogen receptors, particularly the beta receptors.

And when you activate the beta receptors, depending on the tissue specific properties, you may be down regulating proliferation and modulating a big inflammatory cascade. And this has been shown in ectopic endometrial tissue over and over and over again. So the thought here was it's going to be really hard to randomize a population of people and look to see if there's any risk reduction by increasing soy intake.

So you have to do these things using large pre-existing prospectively collected data like the Nurses Health Study 2. This included 82,000 pre-menopausal nurses that were followed over 30 years with over 1 million person years of data. My computer is crashing just hearing that statement being said out loud. In total of these 82,000 women, there were 3,800 cases of laparoscopically confirmed endometriosis.

And they had yearly data every four years, excuse me, not yearly data, every four year data reporting on soy and isoflavone intake for these patients. So top line finding here was that each additional serving of soy per week seemed to offer an 8% reduction in the risk of laparoscopically confirmed endometriosis. This was a statistical finding.

The effect plateaued when they reached about four milligrams per day of isoflavones, which was roughly equivalent to one serving of tofu or soy milk per week. It's not a lot of soy, not a lot of tofu. Interestingly, the signal was actually the strongest in the patients who did not have concurrent infertility, suggesting that there's a potential link through this pain inflammatory phenotype, but not so much this subfertility associated subgroup of people with endo.

Now, I think what the researchers are really trying to take away from here is that small culturally achievable soy exposure may offer some non-pharmacologic risk modulation for patients, particularly those who present with pain as the predominant symptom of their endometriosis, not so much infertility. These are impossible studies to do, excuse me, really hard to have a stratified prevention trial with supplements or nutritional modifications, particularly with something as sticky and tricky to study as pain and infertility. I think this is probably the best we'll ever have with regard to the relationship between soy and endo, but really cool to see that maybe we are a little bit more of what we eat than we thought.

And I think it's surprising to no one, you know the things that are good for you, you know the things that are bad for you, and more of the good things might be better. I don't know that I'm ready to recommend soy for all of my patients with endometriosis and pain, but I do talk to them about an anti-inflammatory diet. I do talk to them about the FODMAP diet, where we're purposely trying to remove known inflammatory dietary foods, and I've had a lot of patients who've noticed a small but meaningful difference in their quality of life either before surgery, after surgery, or even in the midst of ART treatment.

Pietro, help me understand this mechanistically. So endometriosis epigenetically up-regulates estrogen production, down-regulates progesterone, so it's an estrogen-dependent disease. This is a dietary estrogen-like thing.

So you're saying the mechanism is that it's anti-inflammatory, but we're giving something that promotes endometriosis growth? How does that work? Not as simple as that, Mike. We generally think that endometriosis is an estrogen-predominant disease, but there's actually a bunch of different subtypes, and when they've done studies where they've biopsied different implants within the pelvis and across different kinds of patients, they've noticed that certain patient groups have more progesterone receptors in their ectopic endometrial tissue. Others have more estrogen receptors, and sometimes you have this mixed alpha and beta response.

So part of what I think will be really cool in endometriosis care in the next couple of years will be this personalization of the minute you have surgery for endometriosis, could you better phenotype their receptor status, kind of like what we do for breast cancer, to better target the appropriate therapy post-surgery for these patients to give them the best benefit. But ultimately what soy is doing in this study is it's down-regulating proliferation and it's modulating inflammatory cascades locally within ectopic tissue, which is why we think it's beneficial for pain, less beneficial for infertility improvement. I'm going to pivot hard on something that Eve and Kate and I have been talking a lot about, which is restorative reproductive medicine.

Pietro is our representative surgeon. One of the big things ERM people are putting out is endometriosis surgery to treat infertility. As someone who does a lot of surgery, what's your take on that data? Great question, Micah.

And we have two really good studies that were done decades ago now, published across the globe, published in meaningful journals like the New England Journal of Medicine. The number needed to treat for patients with symptomatic endometriosis is actually surprisingly high. And for the lay listener, that means that you're going to have to do lots of surgery to be able to maybe improve the chances of unassisted pregnancy for this patient group.

When the reality is we know that ART, defined broadly, be it IUI, be it ovulation induction, or even IVF, can sometimes make that number needed to treat significantly smaller and speed up the time to successful pregnancy for these patients, not only for their first child, but also for their second child. So I think what gets lost in restorative reproductive medicine is that infertility doctors also believe that there is a role for surgery to restore normal architecture, normal functioning, but there are limits to what surgery can do. There's a reason we moved away from tubal surgery.

There's a reason we don't do metroplasties anymore, where we hack out a large portion of the uterus and try to put it back together. We know that ART does better, does faster, and does safer for these patients. So I think we're talking the same language, but just looking at it from different sides of the same coin.

All right. You did not know that curveball was coming, and that was a smashed out of the park summary. Eve, any other thoughts on that? And then we'll pivot to you for the last article.

Oh, I have lots of thoughts, but too many for this podcast, and I'm going to give a teaser for views and reviews that I'm putting together, looking at all of the data on less aggressive therapies, or I don't even want to say less aggressive, because I actually think that a nine-hour endometriosis surgery is far more aggressive than a 20-minute egg retrieval. But more to follow on this. I've got lots and lots of thoughts, and there's too much to say.

All right. Well said. We look forward to that views and reviews.

So, Eve, you have our last article, and we're totally pivoting off the theme here, gonadotropin priming for ovarian tissue cryopreservation. We're on the cutting edge of research here. What did we learn? This is interesting.

This is a paper by Dr. Zhao and others from China. The objective was to evaluate whether short-term gonadotropin priming improves IVM outcomes of eggs retrieved during ovarian tissue cryopreservation in premenarchal girls. So, quite a niche population.

This was a retrospective cohort study in a university-affiliated tertiary care center in China. They had 167 premenarchal girls, and interestingly, the ages were 3 to 18. They had several girls that were in the 15 to 18-year-old age group who had not yet had initial menses.

All of these girls were scheduled for stem cell transplants between July 2021 and September of 2024. Two cases were for Fanconi's anemia, and the rest of the girls had thalassemia. They split the cohort.

There were 124 patients in the gonadotropin group. These girls received three days of HMG, 150 to 225 IUs per day, just for three days prior to ovarian tissue cryopreservation. And then the control group was 43 patients with no gonadotropin priming.

So, what they did was they gave these girls HMG injections. They did a surgical approach. So, they did a unilateral laparoscopic oophorectomy.

They processed the cortical slices. They extracted the COCs from antral follicles, and then they used a biphasic IVM medium, which we reviewed a few months ago on the podcast. And then they assessed maturation of the oocytes at 24, 48, and 72 hours, and they vitrified the mature N2 oocytes, and then they froze the cortical strips.

They also examined the tissue to evaluate gonadotropin receptor expression. And what they saw was that FSH and LH receptors were indeed expressed in granulosa cells and oocytes across all follicular stages. And again, keep in mind that these are premenarchal girls.

So, what they saw was that in the gonadotropin group, the maturation rate was statistically significantly better. So, 49% of the oocytes were mature compared to 36% in the control group. When they looked at this by age, they stratified it ages 3 to 5, 6 to 11, and 12 to 18.

And in the 12 to 18-year-old girls, the gonadotropin priming did not improve the outcomes. And I suspect that's probably because these girls' hypothalamic pituitary axes were already somewhat intact, and they may already have endogenous gonadotropins. They saw the greatest increase in girls who were age 3 to 5 with an odds ratio of 3. And in ages 6 to 11, the odds ratio was 1.67, and neither of those confidence intervals crossed 1. And so, what they concluded was that gonadotropin priming significantly improves IBM outcomes, especially in that younger population.

And it likely involves enhanced follicular development in a favorable environment for transcriptomic changes in the granulosa cells surrounding the oocyte, which I think is biologically plausible. They did not have any adverse events that were observed, and they saw that the hormone levels normalized quickly. And so, I think clinically, if you are going to do this methodology where you are doing IBM from a removed ovary and freezing cortical strips, I think it does sound like it's reasonable to give three days of HMG injections prior to laparoscopic oophorectomy.

I think it's an interesting approach, and I would say in our center we do OTC, but I don't think we're quite doing biphasic IBM at the same time. And that may become the standard of care, but it's an interesting approach to get both oocytes as well as cortical tissue from these girls. Not surprising to me at all that they found gonadotropins might be helpful here.

If you look at some of the IBM trials that are ongoing in the United States, and full disclosure, I do have a conflict of interest with one of them, Gameto. This is a trial, phase three clinical trial, that's giving patients a very short course of clomid and injectable gonadotropins ahead of a retrieval for IBM done in the laboratory setting. And I wonder, in this age group of patients who are young and injection naive, if even something just as simple as clomid might be beneficial to create a similar effect as the gonadotropins, even more cost and patient-friendly way, but it makes intuitive sense that a little bit of a nudge might not be too much of a bad thing here.

Yeah, excited about the innovation here, both in terms of the media, the biphasic approach to both tissue and trying to in vitro mature oocytes. And it's not surprising to me either that it would be most beneficial in the youngest group that are most gonadotropin naive. So I love this paper and great summary, Eve.

Well, this was an awesome discussion. When I saw the papers this week, I was so excited, especially given who we have. We miss you, Kurt, but we have some of the world's experts on these topics that were discussing this.

I learned a lot. We're on our way to ASRM in San Antonio, so I'm going to give a quick global shout out. ASRM and FNS is the society and the journal worldwide for reproductive medicine.

So shout out to the Bedoshi family. We'll see you soon from Brazil. Scott Nelson in Kuwait, we'll see you soon.

Diana Tain, Malaysia, listener of the program, we'll see you soon. Barbara Lorenz, UAE, we'll see you soon. Martha Luna, Mexico, we'll see you soon.

And Yannick Ernie, I can't even keep up with how many countries you're in and where you're doing all these different masters all over the place. Keep up the good works to all our global listeners and my friends. I will see you this upcoming weekend.

Great discussion. And if you see us around the expo hall, tap us on the shoulder, say hi. We love talking with you guys.

And if you play your cards right, Micah will even record a voicemail for you. Micah is going to be wearing his cowboy boots in San Antonio, so bring yours too. Get your boots on and come to the gala as well.

That's the board member of me wearing the development hat. All right, everyone, we will see you next month. Have a great month.

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. Selina Park, Dr. Carissa Pekny, and Dr. Nicholas Raja.