Fertility and Sterility On Air - TOC: March 2025

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

01:46 It is time to rethink coordination of fresh oocyte retrievals with microscopic testicular sperm extraction

02:55 Rescue intracytoplasmic sperm injection improved cumulative live birth rate for cycles with second polar body extrusion rate <50% in young women: generalized additive model

16:05 Success rates with preimplantation genetic testing for aneuploidy in good prognosis patients are dependent on age

26:03 Embryo retention and live birth in frozen embryo transfer cycles: a cohort study

33:45 Long-term safety of controlled ovarian stimulation for fertility preservation before chemotherapy treatment in patients with breast cancer

40:43 Similar accuracy and patient experience with different one-step ovulation predictor kits

51:16 Use of at-home sperm concentration testing in a male hormonal contraceptive efficacy clinical trial

53:34 Association between sleep quality and ovarian reserve in women of reproductive age: a cross-sectional study

61:44 Prediction of menstrual cycle phase using cross-sectional measurements of reproductive hormones

View Fertility and Sterility February 2025, Volume 123, Issue 3: https://www.fertstert.org/issue/S0015-0282(25)X0002-9

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 discussion with authors, and other special features. FNS On Air is brought to you by 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, and Dr. Pietro Bortoletto, Interactive Associate-in-Chief.

Hello and welcome to another episode of FNS On Air. I'm your co-host, Pietro Bortoletto, and I'm joined by my co-hosts, Eve Feinberg, Kate Devine, and Kurt Barnhart. Good morning, everybody.

Good morning. Good morning, Pietro. It should be noted that we are recording this on the morning after the Philadelphia Eagles have won the Super Bowl.

Kurt, we're surprised that you're here. We're surprised that you have a voice and that you're not up a light pole in downtown Philadelphia. Tell us more about how it was.

Yeah, the climbing of the light pole is easy. It's the sudden fall at the end. That's the problem.

That will get you every time. But go birds. Go birds.

Fly eagles fly, right? Yeah. Yeah. We suspect Micah is still celebrating into the wee hours of the morning because he is off this month from a podcast reporting.

But we have a slate of really wonderful articles for you. Our first inkling this month is actually by our very own Eve Feinberg. Eve, you wrote a little bit about, should we rethink coordination of fresh egg retrieval and micro tessie? Is the juice worth the squeeze? What do you think? Yeah, so this came about after we had a failed Lupron trigger with a fresh micro tessie and it was a bit of a scheduling disaster where we had to re-trigger the patient, reschedule the egg retrieval and reschedule the micro tessie, which caused a lot of havoc for our team.

And it really got us thinking, could we dissociate the fresh micro tessie from the egg retrieval? And could we be going through planned egg freezing cycles in advance of a micro tessie and then using micro tessie sperm with those eggs? And our urologists were incredibly enthusiastic about that idea, as was our IVF laboratory. So we started collecting data in our center to look at this very question. And the inkling is a little bit of a teaser in terms of the thought process behind it, what's been published and our question moving forward that we hope to answer.

Well, I suggest everyone take a look at the inkling and keep an eye out for that data. I know of a couple of programs that still are very gung-ho on fresh micro tessie with fresh retrieval. And you're right, it is a coordination nightmare for everyone involved.

We're going to move away from the inkling and we're going to jump straight into our first article under the assisted reproduction section. Kurt, you have something that lives in the same vein. Tell us a little bit more about Rescue ICSI.

And again, is the juice worth the squeeze? I'm not sure I like this analogy. What juices are we squeezing? I don't get this. But anyway, I'm going to talk about what I thought was a really interesting paper in it.

And I hope I can explain it well, because it's a bit complicated, because it's just not what we do every day. So the title of the paper is Rescue ICSI, improve cumulative live birth rate for cycles without a second polar body excrusion of less than 50% in young women. And it adds in the title, although there's an unfortunate typo in the title I didn't catch, generalize additive, not addictive models.

Addictive models would be really something that I think statisticians have to figure out how to figure out, make that work. But anyway, this is a paper that I know we're going to get into this, because you're going to ask me lots of questions. This is a macro paper.

This is not a paper that looks at the outcome of every egg and what happens to every egg. This is a practice-based question. What if we rescue ICSI and a whole bunch of people, what does it do compared to people that we didn't? So I'm not going to be able to give you the details about what happened to every egg and such.

But the idea was that there are some people that have lower fertilization than normal, that don't have no fertilization. And this idea of Rescue ICSI on the next day has been floating around in literature for a long time with a lot of really high profile papers. This particular paper has decided to use Rescue ICSI three to four hours after a look at fertilization.

And instead of using 2PNs as their marker for fertilization, they're using the second polar body exclusion. Now we could talk about that for a long time. It's basically a way to get to the ICSI sooner rather than waiting for the normal 20 or 18, 20 hours that we look for, at least in my lab.

So I know this isn't going to change your practice today because there's some relatively novel embryologic practices, but it's still an interesting concept. So of course it's out of China, which is a lovely institution where they have a ton of patients and they're able to take, you know, a good five years data and drum up, you know, thousands of patients. And what they did was they looked at cycles where apparently they've been doing this Rescue ICSI and they looked at two important things.

They said, how many eggs need to not fertilize for us to say that this is a good model? And then say, and is it, does it work in all people? So the first thing they did use this generalized additive model was to draw a curve, which basically says, let me look at the relationship of Rescue ICSI with how many eggs I needed to rescue versus pregnancy rates and see what the curve looks like. Then they also looked at the cumulative pregnancy rates based on how many eggs fertilized and we didn't rescue ICSI and you know, what the pregnancy runs. And they basically said where those two curves intersected, that gave them a threshold.

That's where these curves came in. Interesting not use of the curves to get a little specific here. The curves, when you get an answer, the curve, if the answer looks like it's close to one, that means the curve is basically linear and the more away from one, it's sometimes unexplainable curve, which is sometimes happens when we plot things where we really can't see it.

So using this kind of intersection is not a bad idea. And they found that the intersection was around 50%, meaning the first finding of this paper was you had to have fewer than eggs not fertilized for Rescue ICSI to really show some benefit. Okay.

The next question is what does benefit mean? So what they did was the group, and by the way, we're talking about, I didn't go through all their exclusion and exclusion criteria, but they whittled down something like 20,000 cycles to about 5,000 cycles with Rescue ICSI versus around 10,000 without. And they basically showed that the difference between those two groups, the groups that got Rescue ICSI because they had fewer eggs and the groups that had normal fertilization, they didn't have a difference in the first pregnancy rate, but they did have a difference in cumulative pregnancy rate. So the whole theory here is not that I'm fixing that egg.

In fact, the egg that got ICSI might not have been picked to transfer, but what they're basically saying is by rescuing the cohort, I've got more eggs, I got more good embryos, and ultimately, I got more pregnancies. So that's the general finding of the paper. They also did a second analysis, which basically said, well, does it work for everybody? And they gave a similar logic with these generalized equations and said that really the cutoff is around less than 37 years old, or I'm sorry, less than 38 years old.

This one's kind of a backwards logic, pardon me. It's basically saying we saw benefit in the young women, but we didn't see benefit in the older women. And they speculated a little bit, is it because there weren't enough eggs in the women greater than 38 to show an effect, or were the eggs more fragile? Those are questions I'm leaving to you because they didn't answer them in the paper, but they're basically saying it worked in the young women, but it didn't work in the old women.

So the gist of the paper was, if you don't get 50% fertilization, they're suggesting you should rescue that cohort with the unfertilized egg, with RICSI early, thus creating more embryos, and then ultimately you have more to work with, it's cost effective, and you'll have a higher cumulative pregnancy rate. And they didn't see any differences in, which was the theoretical reason not to do this, they didn't see any differences in polyspermy, they didn't see any differences in the asynchrony you might get by fertilizing a couple hours later, and they ended up with similar pregnancy rates and similar negative outcomes. So I thought that was a fascinating paper.

I'm still not sure I'm ready to change my mind, and I'm sure my embryologist is not going to change their mind. In fact, not that I'm breaking her confidence, she might've looked at this paper once or twice. So that's why I brought it up to you guys, because it's a point of discussion, because it's challenging a couple of things that we thought were written in stone, so to speak.

So what do you guys think? For the listener who hasn't read the paper, can you clarify if these were then freshly transferred embryos or embryos that were frozen and then subsequently transferred? Because I know there's a lot of debate about if you rescue ICSI, should you still plow ahead with a fresh transfer on your day five? And just clarify for the listener. Yeah, I'm sorry I said that too quickly, but all these people went ahead with a fresh transfer and then froze the rest of the embryos, and the fresh transfer rate was dissimilar. Again, not every rescue ICSI was transferred fresh because they might've chosen a different embryo, but overall, using this practice for years and thousands of patients, they didn't see a difference in fresh transfer rate or in polyspermy rates.

So I have two thoughts. One is you could use these data, and I'm certainly not arguing for it, but there are programs that do 100% ICSI. And so you could say in a good prognosis population of patients, rather than going through the process of conventional insemination after several hours, and then after several more hours, looking, identifying, and performing rescue ICSI, just do ICSI for all people.

So that's one thought that could be an argument as a result of this paper. The second thought- You're starting the morning off with some controversy, go ahead. Always, always, Pietro.

But they indirectly do answer that question, because they said, don't use it if you have 50% or more of your eggs fertilized. In that case, then doing a non-ICSI normal cycle is better than rescue ICSI. So they're basically saying, don't ICSI everybody.

It's just better to try conventional, and if you don't get 50% fertilization, then rescue the others. Fair, but I still think that you could view it through the lens of, okay, outcomes were equivalent in those that you rescue ICSI versus the other, so why not just ICSI all? I'm not advocating for that, but I'm just sort of seeing how these data could be interpreted, or you would argue, misinterpreted. The second point, and I want to give a shout out to Joan Riley, who's our phenomenal lab director, who's an avid listener of this.

And Joan, I almost texted you yesterday. But I think the lab directors, this would place significant burden on the lab. And as we're talking about trying to ramp up, innovate in the lab, trying to maybe make things more automated, maybe decrease the workload of the IVF laboratory because of the increased volume, this would add significant workload because you then have to look four to six hours after conventional insemination and then perform rescue ICSI.

So if you have an egg retrieval at noon or beyond that, you're doing conventional insemination two hours later, and then rescue ICSI four hours beyond that. I don't think that it's a realistic workflow for most IVF laboratories. But isn't that an interesting debate? We do IVF according to a formula.

Much of it, we thought we did. I don't know what the right adjective is. We did it because we thought it was right, and we've stayed with it.

But what if there are better ways to do it? What if the constraints on the lab saying we have to do it this way because of staffing are wrong? I'm not saying they are. I respect our lab, and they work incredibly hard. I'm just saying we sometimes have to think outside the box that just because we have a formula now doesn't mean that a different formula might be better.

I don't disagree. But I think it is a balance, and you have to look at what is the number needed to treat? How many additional cycles of rescue ICSI are you going to have to do to have one additional live birth? I wish Michael was here because he could whip out those calculations pretty quickly. But I think it's a minimal benefit for a lot of additional work.

I think that our embryologists are humans. Maybe in a day where we get towards more automation or maybe in a day where we have improved staffing, people can work shifts. But this seems to me like a nominal benefit that is going to really increase the workload of the IVF laboratory.

It's going to prevent us from being able to scale up more effectively. Not doubting that, but I am challenging you all. I'd love to hear Kate and Pietro's thinking.

Again, this is this data. I'm not even sure this could be replicated. I'm not advocating this.

But let's just say there was a technique that increased your pregnancy rates from 45% to 65%. You don't think that that would be worth entertaining, that I can increase my pregnancy rate by 20% by changing the way I do things? What's the absolute number of people that stand to benefit from it, right? I feel like rescue ICSI cases at baseline are rare in our center, and we're not a 100% ICSI center, and I suspect they're rare in yours, Kurt, Eve's, and Kate's centers. It's a lot of work for your lab.

You have to look at how are they defining rescue ICSI. So they're defining it as less than 50% fertilization at four to six hours post-conventional insemination. And again, I agree.

I think that in our center, because we carefully choose who is ICSI versus conventional insemination, I do think that the number that we see with fewer than 50% or less than 50% fertilization is low. But I want Kate and Pietro to talk a little bit about this a little more. I'm being tag-teamed here.

I'm in the theoretical here saying that there might be something that could change our value. We should look at it. And they're saying, no, not this one.

This one is just not going to change our practice. So rescue me here. Look, I think that it's fascinating that they found this in this model.

I think that this is actually something that can't be used to change practice because it is, as you say, radical. And this level of evidence is, while fascinating, not enough to convince me. So I mean, I absolutely agree that this would be a ton of extra work.

I also absolutely agree that a 20% increase in pregnancy rates would be well worth it. And we wouldn't need to change the way we did things if we had a well-designed trial that showed this. So I hope more to come from this group or others based on this paper.

That said, I'm not going to have all my embryologists start checking four hours after conventional and some just yet. I agree with you all. I'm just pointing out that this is why I like this paper is that it made me think differently, that it made us challenge what we do because that's the way it should be done.

I was given a book years ago when I was on a board that was entitled Sacred Cows Make the Best Hamburger, that if you really want to change something, you have to go back and say, why do we do it this way? And the answer is because we always do. That's the first thing you should change. So I'm not saying this should be changed, but I'd love the idea that people were thinking outside the box here.

This sounds like a really good article for a embryology slash clinician journal club. If you're looking for something to really stir up some good debate at your center, this has that written all over it. I wonder if it could be done as a simulated trial too.

That's something that we've been talking about a lot is the benefit of that. So anyway, I hope we learn more about this potential technique going forward. Well, listen, from one sacred cow to the next, Kate, you have an equally controversial topic.

Your article is entitled Success Rates with PGT and Good Prognosis Patients Is Dependent on Age. Tell us a little bit more about this paper. Yes.

So this paper is from my friend and colleague, Dr. Ben Harris and his colleagues at Duke. They looked at a SART data set collected from 2016 to 2019 and evaluated 56,500 or so retrievals among patients who are 21 to 40 years old. Notable exclusions, and I really do think this is kind of the most important thing to think about when thinking about how to apply these data, were retrievals that resulted in fewer than five 2PNs, retrievals where PGTM or PGTSR was performed, oocyte thaws, recurrent pregnancy loss, and this is another important one, cycles employing multiple embryo transfer and cycles with more than three transfers.

12% of the total cohort of retrievals had PGTA. And what the authors found was that PGTA was associated with a higher cumulative live birth overall. So 62.5 versus 59.1 in patients who were aged 35 to 37 years and found that they had a significantly higher cumulative live birth per retrieval among those patients who are 38 to 40 years old.

So 51.3% versus 44.8% in those patients. They also found that in these older patients, so we're still talking about 35 and older, there was a lower rate of miscarriage. Conversely, in the young patients, the younger cohort, they found that there was a lower cumulative live birth with PGTA.

So again, just to summarize, in the 12% of these retrievals that used PGTA, they found that it helped patients who are 35 to 37 or 38 to 40 in terms of cumulative live birth, but it hurt patients who were younger than 35 years old. In the younger cohort, they didn't find any differences in their secondary outcomes, including miscarriage. So the benefit in terms of lower miscarriages, they only found in those older patients.

So they used modified Poisson regression modeling to control for race, ethnicity, BMI, parity, smoking status, infertility diagnosis, and the number of blastocysts. They also found that in their total cohort, not segregating by age, overall, there was a 3% increased cumulative live birth among those not using PGTA. So it's a little complex in all of the slicing and dicing of the groups where we're seeing a benefit here.

I did want to return to the exclusion criteria that they used. So when you go to actually the supplemental figure and you look at the way that they, again, removed any patients that had more than three transfers or fewer than five 2PNs, you can imagine that this might have introduced some significant bias here, right? So who are the patients who have more transfers? Who are the patients that have multiple transfers? In the older patient populations, those that don't do PGTA and have multiple transfers, you know, maybe are worse prognosis patients, right, than those that did the PGTA. So I do think that in the exclusions that they used, that may account for why we're seeing higher cumulative live birth rates in the PGTA group in the older patients.

We all know that there's really no way that PGTA can increase cumulative live birth rates, right? If you're transferring all of the embryos, it's really just not, it's not logical that that could be the case. So I think a really interesting paper, I think overall reassuring that probably this isn't hurting that much, at least in this very refined group, but I'm not convinced, frankly, that PGTA can increase anybody's cumulative live birth rates. So wanted to hear a little bit more from the three of you as to whether this would change the way you practice in any of these patient populations, young or old, and also just your overall thoughts on the paper.

Why do you think this is what they found in such a large group of patients? My only thought in terms of how it could impact cumulative live birth is patient dropout, that perhaps patients that know that they have euploid embryos are less likely to quit treatment and more likely to follow through with treatment, whereas patients who have untested embryos may drop out before the entire cohort is transferred. Other than that, I really, it's nonsensical to say that PGT increases the cumulative live birth rate because as everyone who's listening knows, PGT doesn't change the actual embryo, it just changes the order in which we transfer those embryos. And so I'm curious to hear what the others think, but I couldn't wrap my head around it or think of an alternative explanation other than patient dropout, which is not accounted for here.

Yeah, well, I totally agree with that. And also that the patients who don't do PGTA are more likely to have more than three embryos transferred, right? So again, I wasn't completely clear on why the authors implemented that particular criterion. I enjoyed reading this paper, but I really think this paper was a missed opportunity.

I think that it chose a population, and I'm still not convinced why five embryos or five, whatever the criteria was, was chosen. And it just biased it towards people that have a lot of embryos. It had an opportunity to use this art database, call for papers, call for analysis.

We could have done this study with an analysis of what if you didn't restrict it to any blastocysts, or one blastocyst, or two blastocysts, or three blastocysts, and you could have answered that question about does PGTA help in lots of different situations, rather than only the occasional 37 or older patient that has five embryos to begin with. So I think this moved to a very biased suggestion, and I'm glad we're discussing it as such, because I think it doesn't really answer the question. But I don't want to forget, this did say something important.

PGTA lowered the pregnancy rate in young women. So there's no doubt in my mind that the exercise of selecting an embryo is selecting some embryos out. Damage to the embryo, missed call, false positives.

Somehow you're reducing the number of embryos to transfer. In a young woman, the chances are pretty good the embryo is normal. It looks like it doesn't help.

In an older woman with a lot of embryos, finding the one right embryo might make sense. But it doesn't answer the question if you have one embryo, or two embryos, or three embryos, because I personally think that biopsying those embryos is not a good thing. If anything, it only has harm.

So I just don't want people to take away that the title of this that says PGTA should be used in all people greater than 37 years old. I think this is a great example of when you're thinking about your study design, how your inclusion and exclusion criteria could absolutely bias your findings and point you in a very specific direction. And Ben, I know you're a listener of the podcast.

This sounds like another secondary paper, a subgroup analysis, research letter, potentially exploring some of these more nuanced subgroups that you may see slightly different findings from. Yeah, shout out to Ben. He's a CREST scholar as well.

So maybe he can use this same data set for yet another analysis and publish it to let us all know what the answer is for the total cohort. So I'm going to bring up one methodologic issue on PGTA, because I hope we do more studies like this, and we use the SART database and other databases and hopefully even do a randomized trial. I think we've come to a consensus that cumulative live birth is the right outcome in the perfect world, but we all recognize that that's not a perfect world.

So we have to come up with a way of saying, what is a good cumulative pregnancy rate? Is it three transfers? Is it a year? Because subjecting someone to say you have to use all of your embryos is maybe it's not ethically bad, but it's just impractical. So I think our field needs to somehow come up with a consensus on what we think the right outcome would be here, because it's certainly not embryo per transfer in my mind. It really does have cumulative pregnancy rate is logical.

It's just a question of how you define it. Yeah, it's a really hard study design question every time we try to decide how to look at cumulative live birth, because you bias your sample as well if you remove all those patients that have embryos remaining untransferred. Yeah, and again, this data set doesn't say how many people.

The problem with the SART database, for those of you now are going to design your own study, is it doesn't often say who intended to have PGTA. So it's going to be hard to use this data set to have that, because really what you should include is everybody with that intent and include the people that got no embryos, no embryos that were normal, no embryos to transfer, because those have to be included as well. You can't just say, well, those that got a normal embryo that we transferred is our population.

And just for the listener who maybe doesn't go to the supplemental figure, they had an initial data set of 256,000 retrieval cycles that they whittled down to 56,000. So again, it's definitely a refined population that we're looking at here. I have a slightly easier paper to wrap our head around moving away from complex statistics and methodologic questions.

This is a really nice paper by first author Tingting He, entitled Embryo Retention and Live Birth in Frozen Embryo Transfer Cycles, a Cohort Study. So generally, the embryo retention rate in the literature is reported between 1.4 to 2.8%. For me, it was actually 100% after my first transfer as an attending physician. My very first transfer as an attending was retained embryo.

And I was like, this can't be good. This is not a good omen. Subsequently, the rate has gone down to 1.4 to 2.8. But studies suggest that the occurrence of embryo retention is related to many factors, contamination with blood and mucus, number of embryos transferred, even things as subtle as the volume and the type of transfer media.

But it appears that blood and mucus contamination are the most significant recurring themes in the literature. When it happens, the typical practice is to go ahead and attempt to retransfer. And the data on outcomes of this retransferred embryo are a little bit all over the place.

It's pretty heterogeneous data that includes fresh embryos, frozen embryos, day 3 and day 5 embryos, as well as embryos that have been biopsied or hatched. This study did a nice job in that they tried to whittle down the population to only those transferring frozen embryos, and then went a step further and used propensity score matching to help manage some of the variables that might be at play here when we're looking at incidence of embryo retention. This is, again, a single center paper from China from 2016 to 2022, where 39,000 transfers were available.

And these were frozen embryo transfers that included both hormone replacement and non-hormone replacement cycles. The transfer procedure was pretty standard, very similar to how I think I do it in the United States. Cotton swab soaked in culture media to clean the cervix, and then afterload of the embryo transfer catheter with 20 microliters of media and an embryologist forming the plunge.

Primary study outcome here was live birth, and the secondary outcomes were biochemical pregnancy, miscarriage, and ectopic pregnancy rate. The propensity score matching matched for the things that you think would be important, so age, BMI, infertility duration, the endometrial thickness, as well as the number of transfer cycles, the type of endometrial preparation, and then, importantly, embryo stage number and embryo quality. So of 39,000 FETs available, only 185 retained embryos were recorded.

These were matched three to one for a total 740 patients that were also analyzed without embryo retention. The high-level finding is pretty straightforward. The results demonstrated that embryo retention in the transfer catheter significantly reduced the chance of biochemical pregnancy, clinical pregnancy, and live birth.

However, there were no significant differences observed in terms of miscarriage or ectopic pregnancy. That stands in contrast to some of the literature. Some of the literature does suggest that there's no difference in live birth, and I think that's usually what we tell patients at the time of transfer, since you want to be a bit more optimistic, but I think the study did a nice job including a very homogeneous group of people undergoing just frozen embryo transfer cycle.

Now, in the discussion section, the authors postulated the potential reason for such a low embryo retention rate. They were well under the 1.4 to 2.8 percent reported in the literature. One technique item that they talked about was that they specifically rotated the catheter after the embryo was transferred, so they performed a kind of a half turn or a full turn of the embryo catheter, and the thought was that this would reduce negative pressure on the catheter and facilitate contact between the catheter tip and the endometrium.

It's not something historically that I have done at the time of transfer, but curious to see, Eve, Kurt, and Kate, if you have any special tips or tricks that you think are voodoo and may help with embryo retention. I don't love that twisting voodoo, to be honest, because if the embryo is retained or, you know, didn't go to the place that I wanted it to at the time that we, you know, transferred it, I want to know about that, so I'd rather have it be retained and put it back than, you know, twist it, you know, into the cervix or something of that nature. The voodoo I do is to hold the plunger as I withdraw, although I suppose you could make the same argument there, but I think the voodoo word is highly important here because we really just don't know, unfortunately.

Yeah, I do the same voodoo, and it might have to do with having trained in the same place, Kate, but I also don't twist. I had a sort of an embarrassing situation this summer where I had a patient who had a retained embryo, not once, not twice, but three times, and she's pregnant, so I was very fearful. I've never seen that happen before.

I've, you know, maybe had one retained embryo every other year. Like, I would say the rate is incredibly low. I've kept an eye on it in my own practice, haven't really gone into our data to see, but my gut sense with my own transfers is that it has not impacted the pregnancy rate, and I was, again, very fearful this summer with a thrice retained embryo, and much to everybody's surprise and happiness, she is pregnant, so I think it's interesting.

I don't know what accounts for the difference between this study and previous studies. I suspect there may be some laboratory factors, some operator factors, but I really do commend the authors with their methodology and the rigor of this particular study and the rigor of this methodology. It may make me counsel patients a little bit differently, saying some studies have actually shown more of a decrease than we will anticipate, but I agree I'm not one to rotate the catheter.

I don't think that the negative aspiration pressure that they talk about really impacts the likelihood of retention. Voodoo, I was taught was to leave the catheter in for, someone told me, a minute. I was like, there's no way I'm leaving the catheter there for a minute, but I've had embryologists come back, don't take it out yet, don't take it out yet, you know, pause, and I'm not sure if that makes a difference either.

I mean, again, the theory is the negative pressure, but I think, I agree with Kate, if that were the case, I think I would just be pulling the embryo to the lower uterine segment, not that I would be pulling it back into the catheter, but I don't know, hard thing to study, but it does happen. We do all have retained embryos. Eve, can you, for the listener, tell us what you did differently between transfer 1 and 2 and transfer 2 and 3 for that patient with a thrice retained embryo? We had different embryologists load the catheter, and it still kept.

Ah, blame the embryologist, I like that. It still kept sticking to the catheter. That's the child that never leaves home, never goes to college, boomerangs back again.

I will say I was so happy when this patient had a positive beta. I was actually in Paris for the mobile phone, and I saw it was actually Roland Garros for tennis, being like the biggest nerd that I am, and I stepped away to call the patient and let her know she was pregnant. I was very concerned.

I had never seen a three-time embryo retention, but I was thrilled when this patient became pregnant. It's a win for the good, guys. Kate, we're going to go back to you.

You have an article in the fertility preservation section. Tell us a little bit more about long-term safety of what we do for fertility preservation. Yeah, so I really enjoyed reading this paper, and it was a little bit of a feel-good one as well in terms of reassurance, so I certainly recommend it to our readership.

Shapira and co-authors out of Israel evaluated in another research paper, a retrospective cohort study, 213 women who were 18 to 43 at the time of a stage 1 to 3 breast cancer diagnosis and were treated with systemic chemotherapy, so the time of diagnosis in 2015 to 2019 with a follow-up time of at least two years. So a third of these patients approximately did ovarian stimulation for fertility preservation, could have been egg or embryo freezing, and they had all of them an antagonist protocol, Lupron trigger, and random starts were employed as needed in terms of treatment timing. And so what they looked at was whether those patients who opted to undergo fertility preservation and ovarian stimulation had an association with their disease-free survival.

So multivariate Cox regression analysis was used, and they took a different approach than the last paper that we discussed. They didn't evaluate their covariates or potential confounders based on what they identified a priori. Rather, they created their model using only those variables that were statistically significantly associated with the outcome.

So they adjusted for HER2 positivity and age, which were positive prognosticators, as well as K67 status, greater than or equal to 30%, and lymph node involvement, which obviously are negative prognosticators. Thankfully, and this is the feel-good part for our patients and for what we do in long-term survival, is the authors found no statistically significant difference in disease-free survival, nor in the extent of disease upon recurrence among the two groups. So those who did FertPres and those who didn't.

In terms of some other factors, just in thinking about these data and their applicability, the patients doing FertPres were younger, more likely to be single, more likely to be nulliparous, all this making perfect sense. They were also more likely to have a BRCA mutation and larger tumors. And they were followed for five fewer months on average, but the difference in follow-up time was not significant.

And so overall, 25% of the patients who did FertPres had a recurrence versus 16% in the control group. So there was a numerical difference there, but not statistically significant in their model. They also, and this, you know, I really liked that they did this as well, did a subgroup analysis of those patients who we might worry about the most in terms of their probability of having a recurrence attributable to ovarian stimulation.

And that was the patients who had an estrogen receptor positive cancer. And for those patients, or for that analysis, rather, they adjusted for BRCA status. And they, again, found no difference in any of their outcomes of interest, including their disease-free survival or extent of disease.

The patients that had an estrogen receptor positive tumor did receive Tamoxifen co-administered during their ovarian stimulation. So I think this is a great paper. It's a small cohort.

And so that needs to be acknowledged as a weakness. And as much as it is a long follow-up, it's, you know, we might want it even longer than this. That said, overall, more data to counsel with in these patients who are considering preserving their fertility prior to undergoing chemotherapy.

I'm interested to hear this group's take on both the outcomes in these patients in terms of their probability of recurrence, and also what you thought about the differences in the groups. You know, is this what you see in your patient population that those with kind of worst prognosis disease are more likely to do FertPres? And, you know, sometimes I find the opposite. So interested in everybody's thoughts here.

I agree with you. I also see the inverse of this. A lot of patients with DCIS that often doesn't require chemotherapy, doesn't require radiation, more extensive surgery, and it's just two to five years of letrozole.

Those are the patients that I really feel like are coming to us in droves. And I'm happy that anyone is coming for Fertility Preservation Consult. I think a win is a win.

I'm more curious about how they stimulated the ovaries. I'd love to kind of pull this small audience. They started tamoxifen 20 milligrams once a rise in estradiol levels were detected.

Is that how everyone generally practices in patients with breast cancer? Are there different medications you use? Do you use them for longer periods of time? I'll tell you what I do. And this is informed from fellowship at Cornell, where we saw lots of fertility preservation from Sloan Kettering and now co-directing the Onco Fertility Program at Boston IVF. I use letrozole 2.5 milligrams daily.

Started with cycle day one of medications. I continue it through retrieval and continue it for seven days after the retrieval to try to maximize keeping estradiol levels as low as feasible during the cycle. I don't titrate.

I don't wait for an estradiol rise. I just started at the beginning. It does mean I trigger around the slightly larger size.

I believe that data from Octay that you probably do need a trigger in the 20 millimeter plus range to maximize maturity. But that's what I do. Eve, Kate, Kurt, what do you all do? Yeah, we do the same with letrozole.

And we don't continue it for seven days after retrieval, but we trigger and typically we'll use a Lupron trigger to have more immediate luteolysis. We do always in breast cancer patients add a small dose of HCG co-trigger, like a thousand, just to make sure that we're not failing a Lupron trigger and further delaying treatment. But I think, you know, I really like this study.

It is a small number of patients and the follow-up duration was five years and not 20 years. And I know that while recurrence is most likely to occur within the first five years, I would be much more reassured. And I am overall reassured, but I think that the oncologist would probably be much more reassured having longer term data in a larger cohort of patients.

But I really liked this study and I think it's a nice addition to the literature. Yeah, I agree that we're still learning on this. It's hard to protocolize this with such little information and such variety of what we get and how people present in aqua fertility.

So good addition to literature. All right, let's keep it going. We have a little bit more data to cover today.

Lots of really interesting and diverse set of articles. I have the next one. This is, again, moving away from some of the heavy-hitting science that we have in F&S to something that I think is really practical and on our minds and patients' minds.

This is a study by my old intern on Dr. Anna Vanderhoff and Liz Ginsburg, current president of the ASRM, entitled Similar Accuracy in Patient Experience with Different One-Step Ovulation Predictor Kits. So here's a fun fact. The WHO was actually involved in the development of the urine LH assay in the early 1980s.

And these ovulation predictor kits have been commercially available since 1984. Data from women who are trying to conceive suggest that over 50 percent of women are using ovulation predictor kits during their trying-to-conceive window. And there are a lot of diverse sets of products on the market.

There are at least 20 commercially available OPKs, but not a ton of data exists on their efficacy. And there's a pretty significant range in pricing and sophistication. Some of them have Bluetooth connectivity in an app.

Some of them are just a smiley face, pretty broad range. So what these authors decided to do was assess the five most popular ovulation predictor kits for accuracy and understand the patient experience of using these kits. So how did they do it? They took patients from Brigham and Women's Hospital who are undergoing either natural frozen embryo transfer cycles or IUI cycles and who are also undergoing daily LH levels from the serum and had them use ovulation predictor kits starting right around cycle day 10.

Of note, these patients had normal menstrual cycles, BMI is under 40, and were not taking Clomid or Letrozole for ovulation induction. They used five commercially available ovulation predictor kits, the Premom EZ, the Wandfo, the Pregmate, Clearblue EZ, and Clinical Guard. That's a mouthful.

All of these LH kits had sensitivities ranging from 25 to 40 milli IUs per ml. Now all patients were asked to take all five ovulation predictor kits with the first urination starting on cycle day 10 and had their LH levels checked within two hours of their home urine LH level measuring. They did this for five days, so days 10, 11, 12, 13, 14.

After that they no longer were asked to continue the LH kits. So in total they had 23 patients participate. Only 13 of these patients or 56 actually had a blood LH surge during the testing window of cycle day 10 to 14.

So they did not have 23 patients worth of data to analyze. They had a smaller number, 13. The day of LH surge the mean level was 54 and the range was 29 to 105.

And when testing all five ovulation predictor kits together they all did really stinking good, no surprise there. The accuracy ranged from 91.75 percent on the low end to 95.88 percent on the high end. Patient experience was generally good.

The instructions were clear to follow. There were no kind of mishaps. And probably the most important thing and the takeaway for me from this study is that more expensive ovulation predictor kits did not perform better than the other more affordable kits.

And there was a decent range in pricing in the ovulation predictor kits that were tested. I think this harkens back to how I tell patients to buy ovulation predictor kits. I tell them to go to the dollar store, Dollar General.

They have the most affordable ovulation predictor kits. And if you're looking for something in the 90 percent accuracy range that's going to do a good job and not break the bank, you don't need one that's connected via Bluetooth to your app that has charging station. You could just get the old-fashioned ones and they're going to do a pretty darn good job.

So a nice paper, something that I think is on the top of patients' minds and just a little bit more data to help us guide patients on making affordable options with at-home testing devices. And, you know, this isn't the only at-home testing device that we're going to be talking about. Kurt, you have kind of on the flip side today.

You're going to be talking about old sperm concentration testing, but we'll get to that in a sec. Any thoughts on this paper, guys? I remember that this technology was so novel and so earth-shattering, you know, I don't know, decades ago, right? Not that long ago, actually. But right now the technology is not novel.

And I would think that you can get generic devices, that this is the way many devices go. So I guess these results don't surprise me, but I'm glad they're published so people can see that. You don't have to necessarily pay for bells and whistles for a technology that's been around for a really long time.

My take on it, though, was it still missed. If you detect a surge, there's a really good probability that you're really having a surge. But I think it missed a significant number of patients who were having a surge.

And so therefore, my take-home on this, and we don't do ovulation monitoring with an LH surge alone for frozen embryo transfer cycles, but for the programs that solely rely on call us with a surge, and then we'll check your progesterone levels a few days later, you may have more canceled cycles or missed opportunities if you actually miss your surge. And I felt like those numbers were a little bit higher than I would have liked to see. I just think it's amazing that they got patients to use five different ovulation predictor kits every morning for five days in a row.

In this population of patients, the negative predictive value was actually pretty good still. That said, I would love to see a paper looking at these tests among patients that have more intermittent ovulations. That's the much more challenging population.

I'm not surprised, and I'm very reassured that these work so well. And I tell my patients the same thing, Pietro, is buy the ones that you can get 100 of them for 20 bucks on Amazon. That said, when I have a patient that has, for example, PCOS, I worry a lot about false positive ovulation predictor kits, right? Because they have high baseline LHs, and all of these tests tout themselves as being ultra sensitive and accuracy down to 12 milli IU per ml.

I tell my PCO patients to look for the test that has the highest threshold, the least sensitive one to avoid the false positive. So great paper. Do you guys have any voodoo that you tell your specific patient populations in terms of which kits to buy for which patients? No, I say the cheapest as well.

The least complicated. I don't want people misinterpreting what's positive and what's negative. For sure.

This is no different than my counseling for prenatal vitamins. I tell them if it's on Instagram, stay away. Try to get the Costco brand ones.

As long as it's got folic acid, you're going to be fine. All the other stuff is fluff. And I think that's more and more true when we talk about accoutrement that can happen for fertility patients.

Yeah, I agree. I'm curious, though, for each of you, if you're doing a natural cycle frozen embryo transfer, how do you monitor patients? Kurt, I know we're going to actually talk about this with your article, but just for our listeners, we typically will have patients come in on either cycle day 10 or 12, depending on their natural cycle length. And we'll have them do ovulation predictor kits and call us if they get a surge and they need to come in sooner than their scheduled monitoring date.

But typically, we'll have patients come in on cycle day 10 or 12. We usually trigger. We try to do more modified natural cycles in our patients.

And then we trigger when we have a lead follicle that's appropriate and aligning that looks good. But I'm curious how you guys do it. For natural cycle FETs, we do something similar to you.

We have them come in usually around their day 8 to 10, or if we know they have shorter cycles, maybe a little bit earlier than that. And similarly, we trigger. I always trigger.

Even if we have a surge, I always trigger. I feel like it's just additional luteal phase support. And then we do the transfer a week after the trigger or one day earlier if their progesterone has risen.

For natural cycle IUIs, we use simply home ovulation predictor kits unless they can't detect it, in which case then, of course, we have them come into the office. Yeah, and I think the stakes are lower with IUI, but it's interesting because my understanding, and Pietro, you can speak to this, but my understanding is the center where this study was conducted solely uses OPKs to time frozen embryo transfers. So they rely on OPKs and then monitor blood levels post ovulation.

Here's the dirty little secret. Their pregnancy rates are just as good as everyone else's. So I think there's a lot of wiggle room in when you place that embryo back that we're probably missing.

Right, but I think what the data doesn't show us is how many patients had to skip a cycle because of an improperly detected surge. So I agree that if you get the surge and you time it appropriately and you do the transfer, fantastic, and it doesn't matter what OPK you use, but how maddening is it if you miss your surge? Yeah, that'd be a good question. Maybe we'll have Liz Ginsburg on the podcast and we can ask her.

To answer your question, Eve, about how I do the natural frozen embryo transfer monitoring, I use the Cornell approach where patients come in on cycle day 10 and they'll get an ultrasound every day or every other day until their lining is 7 millimeters and a follicle is 13 millimeters. Once that's done, then no more ultrasounds and it's just blood work every day until we detect a surge or blood work until you decide you want to trigger someone. So there's a couple of different ways to do it and I think a lot of it just depends on how easy it is for patients to get to your center, how expensive it is for them to monitor.

I think there's a bunch of really good ways to do it. I'd love to get to the stage where I can do at-home monitoring and just do one ultrasound for a quick lining check. That would be my dream.

I know there's a bunch of different companies that do urine monitoring of all of the serum hormones, progesterone, LH, estradiol, but I haven't gotten there yet. Something I'm working on intellectually. Just add in the home ultrasound and, you know, really good to go there.

They just come in with the... Next we'll have mobile embryo transfers and we'll go to their house. See, we are thinking outside of the box. Kurt, in the interest of staying on topic, we're going to actually jump to your paper, which is another at-home monitoring, but on the male side, before we go back to Eve's very, very interesting article.

Kurt, tell us a little bit about at-home sperm concentration testing. Sure, this is a nice bookend to this. So LH kits have been around forever and what people are working on now is what's going to be needed, which is an at-home sperm test.

So this is, again, we've talked about this in FNS before, there's an NIH-sponsored male contraceptive unit that's progressing very, very well with wonderful data that uses cegestrone acetate, which is a potent progestin, and testosterone as a hormonal male contraceptive. So they have to use the male contraceptive for months to suppress spermatogenesis, and then they need a sperm test to show that the sperm test is zero before you can go into the quote-unquote efficacy phase. You can use it.

So getting an assay in a laboratory is cumbersome, and so they've developed an at-home sperm test that uses a threshold of less than 0.2 million. And this is a confirmation that that test works well in the participants in this study, which basically showed that if they did an at-home sperm test, with the gold standard being they also did an assay at the same time, that they were about 90% in terms of predicting that this at-home sperm test was negative. I always get confused in these tests.

In this case, negative means good, that negative means there's low sperm. So interestingly, it's a very short paper. It's a research letter.

There's one little caveat on it, and I agree with it, which is that there was about a 10% false negative rate. That might be alarming, but there was never two false negative tests in a row, and the criteria is that you need to have two negative sperm counts to be able to use an efficacy. So this study is going a long way to maybe making male contraceptive a reality, because I think we need some sort of test to show that it's working because of the long-term compliance necessary for a man to do this.

So I'm glad F&S published this paper. It's straightforward, but the new concept that I'm getting across in the podcast is that we are moving towards male contraception, and things like this are necessary in terms of meaning things like this. Yes, male contraceptive necessary, but so is an at-home sperm test.

So I hope that the technology moves forward. And have one without the other. Eve, you probably have one of my more interesting articles of the month, the association between sleep quality and ovarian reserve.

Is this just another burden that we're going to be putting on our reproductive age patients? Like you're not sleeping enough, that's why your AMH is what it is. Tell us more. Yeah, this is interesting.

So the title of this paper is Association Between Sleep Quality and Ovarian Reserve in Women of Reproductive Age, a Cross-Sectional Study. And this was by Yaoxiang Lin and others from Hangzhou Normal University in China. So I think as a bit of background, I think we can all appreciate that we spend about a third of our lives sleeping, or maybe a quarter of our lives if you sleep like I do.

Sleep duration is decreased in modern society, and the percentage of adults sleeping six hours or less is estimated to be about 31%. Poor sleep has been associated with diabetes, cancer, and all-cause mortality. But the relationship between sleep and infertility is poorly understood.

And just a plug for our center, we are currently analyzing our sleep data from our Aura study, and we're going to be hopefully submitting that to ASRM in the spring and presenting it in the fall. And a shout out to our fabulous fellow, Sarah Cromack, who's done a tremendously phenomenal job spearheading that sleep study. But the objective of this study was to evaluate the association between sleep quality and ovarian reserve among women of reproductive age.

There were a total of 1,070 female participants aged 20 to 40. They all presented to the infertility clinic. They excluded women who had known diseases that were associated with decreased ovarian reserve, such as endometriosis or those who previously received chemo or radiation therapy.

They also excluded women with PCOS because of the high ovarian reserve. They used a validated sleep measure, the Pittsburgh Sleep Quality Index, or the PSQI. They gave the PSQI to all patients at their first visit to subsequently measure sleep quality.

The PSQI is a self-reported index, so it's obviously reliant upon self-report. We know that self-report for sleep is okay, but it's not the most accurate. And so I think that's a huge limitation of this study.

But it's a self-reported index. It asks the patients about subjective sleep quality, what's called sleep latency or how long it takes to fall asleep, sleep disturbances, the use of sleeping medications, and sleep disorder. The PSQI is scored from 0 to 21, and higher scores are associated with worse sleep.

Demographic information was collected on each patient as well as lifestyle factors. Patients underwent standard measurements of ovarian reserve using antral follicle count, AMH, day 3 FSH levels, LH, testosterone, and prolactin levels. Their definition of DOR was AMH less than 1.1, FSH greater than or equal to 10, and antral follicle count less than 7. They then looked at the relationship between PSQI and ovarian reserve, and they looked at subgroup analyses in young patients as defined as those under 35 and older patients older than 35.

And they looked at the impact of BMI in an underweight normal and overweight and obese groups. And interestingly, the BMI subgroup analysis didn't show statistically significant interaction between BMI, PSQI, and DOR. So I think the most interesting findings of this study was that the incidence of DOR in the poor sleep group was significantly higher than that in the good sleep group.

So it was 41% versus 15%. And this was true both for patients who were under 35 and patients who were older than 35. They did univariate and multivariate logistic regressions.

And in the univariate model, they looked at AMH, AFC, FSH as the dependent variable, and the results showed that age, PSQI score, BMI, and salponjectomy were associated with diminished ovarian reserve. So for every one point increase in PSQI, the odds of having diminished ovarian reserve increased by 27%. In the multivariate model, they took the PSQI as the independent variable, and then they adjusted the model for age, salponjectomy, and interestingly, age of menarche.

So for every per unit increase in PSQI score, the odds of having DOR increased. So the PSQI greater than 5 group had an increased odds of DOR with an adjusted odds ratio of 5 for AMH level, 5.3 for AFC, and 3.14 for FSH. So really in both groups, you saw this increase in PSQI, or you saw this association with worse sleep in patients who have diminished ovarian reserve.

And so I think it's a really interesting study. I think the largest limitation is self-reported sleep, and it's not very accurate. And with newer wearable technologies, such as the Whoop or the Aura or the Apple Watch, I think we can, and we should, and we are doing much more accurate sleep research.

The question that I have is really chicken versus the egg. Does poor sleep cause early loss of ovarian function, or do subtle changes in ovarian reserve lead to lower estrogen levels that can interfere with sleep, similar to sleep disturbances and perimenopause? I think it's interesting. I actually think it is the latter, and I'm curious what you all think, but the authors don't hypothesize the latter.

They discuss theories on the relationship of sleep and infertility, such as alterations in the hypothalamic pituitary axis, increase in cortisol levels, alteration in other reproductive hormones, or through compromising immunity. But to me, the most simple explanation is low estrogen levels impact sleep, and patients who have DOR probably have lower estrogen levels at certain points in their menstrual cycles that really impact sleep. So I'm going to open it up for discussion, and I'm curious what you all think.

Yeah, so I agree that this is a totally fascinating paper, and I had the same exact reaction about whether this is a chicken and egg problem, which one came first. So another thing that I think we need to kind of really consider weightily here is our patients that are going through fertility treatment are super stressed out already, right? And so they're always coming to us asking us, what can I do to improve my outcomes, my egg quantity, my egg quality? The last thing that they want to hear is that they should get perfect sleep because we don't have perfect control over that. So while I think this paper is really, really interesting, I hope my patients don't read it.

Yeah, I agree. I think it's going to be really interesting to see. So our sleep study, we took 150 patients who have euploid embryos, had them wear Oura rings during their prep cycle for FET, and we're analyzing whether or not sleep parameters were associated with either positive or negative pregnancy tests.

So it's a highly controlled population of patients with euploid embryos who are undergoing FET. So it's an analysis, just to plug, it's Sarah Cromack and Jesse Walters, our senior author. And I'm really curious to see where that data goes.

I can't wait for that. That's going to be great. So this next paper is prediction of menstrual cycle phase using cross-sectional measurements of reproductive hormones.

And this is by Iris Lee from the University of Pennsylvania with a great team of authors, including Sunni Mumford and our very own Kurt Barnhart. The study aimed to develop thresholds for serum estradiol, luteinizing hormone, and progesterone at a single time point to classify the menstrual cycle phase as early follicular, periovulatory, or luteal. And the goal was to accurately predict menstrual cycle phase at a single point in time without the use of serial monitoring or pelvic imaging.

This was a retrospective cohort study of ovulatory females who underwent serial ultrasound and blood monitoring visits prior to natural cycle FET from 2015 to 2019. So at Penn, they do visualization of follicle collapse, which verifies ovulation. And that is how they time their frozen embryo transfers.

And this is considered day zero. Early follicular is onset of menses three days prior to ovulation. Periovulatory is two days prior to ovulation until day of ovulation.

And luteal is day after ovulation to the onset of menses. They use clinical expertise to propose an initial set of mutually exclusive laboratory values for each phase. They came up with early follicular was an estradiol of less than 150, LH less than 15, and progesterone less than 1.5. Periovulatory was an E2 greater than 150, LH greater than 15, and still low progesterone.

And luteal was defined by a progesterone level of greater than 1.5. They divided their data into training and validation sets. They use some fancy lowest curves for each hormone. And these were used to identify the inflection points, bi-cycle phase, and iteratively revise the cutoffs to maximize the accuracy.

The final algorithm resulted in high accuracy within the training set. And then they applied final rules to the validation set to fulfill predetermined, predefined acceptability criteria. So the final algorithm actually changed the cutoff.

So it used an estrogen threshold value of 400 in the follicular and periovulatory phase with an LH cutoff of 15 in the periovulatory phase. And luteal phase progesterone threshold was moved from 1.5 to 1.75, meaning it had to be above this to be considered in the luteal phase. And so overall, I think it's a really nicely done piece of work.

It can be used as a snapshot into a woman's menstrual cycle phases. I think it's very simple, but very elegant in that these phases have never been defined in this way before. Yeah.

Novel study, great way of thinking about it. Yeah. Nicely done, Kurt.

All right, guys. That's a lot of bouncing around topic-wise, but we covered some hard-hitting science, some controversial topics, and then some stuff that we both want patients to know. And as Kate said, we don't want patients to know with regard to their sleep.

Micah, you're missed here, but we'll see you next month at our next recording. And that's we have for you this month at F&S On Air. This is another wonderful podcast.

Thank you, everybody. I hope that you'll continue listening, and I'll see you all at an upcoming meeting. And thank you again.

Until we meet again. Bye-bye. Bye, everyone.

Go birds again. Bye, everybody. 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 and Dr. Adriana Wong. 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 hosts, 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.