Friday, October 30, 2015
In a nutshell, not much.
You need a lining of at least 8mm (which I have always had) to do a cycle at every clinic I’ve looked at.
I have talked to several REs who have all been supportive / encouraging of acupuncture. We’ve done it for every cycle but one (I was taking a break from all of the peripheral stuff last time), but I will definitely do it for our remaining cycles.
My first (and only fully successful) cycle, I did two days of bedrest. Since then my clinic has said only one day is needed, and I have read things suggesting two days are unnecessary. That being said, CCRM still does two days of bed rest, so I’ll do that in my next cycle.
Other things I have read about, and don’t have any evidence to support them for help—eat pineapple, wear warm socks…. They can’t hurt, so I’ll do it.
I did read an interesting article recently. It suggested that “social isolation”—specifically, isolation from men other than the father—for three days after transfer can increase success rates:
INTERESTING. Next time I’m taking a three-day hiatus from men. Working from home!
Tuesday, October 27, 2015
I skipped acupuncture for my last cycle. I just did not have the emotional energy to deal with it. I regret it—everyone agrees acupuncture can actually help success rates in IVF. (Although I had three failed cycles with acupuncture, so….) So I started up with my acupuncturist today. She was pretty unhappy that I only came to see her three weeks before my transfer. (I was busy! She was booked!) She said she wants to see patients at least a month before they start their cycle. She was also not super happy that I did not take a “break” between my last cycle and this one. She probed to see if I would just agree to move my cycle back. When I did not seem receptive to that suggestion (we’ve already started, I just want to be done with this), she sighed and was like, “I’ll do what we can, and you have two other embryos if this does not work out.” Nice vote of confidence!
I had not seen her since right before my anencephaly diagnosis, so we discussed that briefly. And of course that started the waterworks.
Fuck I hate this.
Monday, October 26, 2015
We’ve all done it—sometime during the IVF period, we figure out when our “due date” would be if everything works out. Will I have a summer maternity leave? Will my kid be the oldest or youngest in their class? Maybe you even count backwards and figure out when you’ll tell family and friends. I’ll be 12 weeks around Thanksgiving, I’ll announce it to the family then. I’ll be 18 weeks in December, far enough along to let people know in my Christmas letter.
I always figure out my due date when I know when my transfer date is going to be. (Here’s a good one to use to figure out a due date for a 5-day transfer: http://www.ivf.ca/fet5dayduedate.php) I’ve had 6 transfers. Six theoretical due dates. If I get a positive pregnancy result and my numbers look good, I might even put a little star on my calendar. (Three times I’ve had “good” numbers: (1) my son; (2) my blighted ovum; and (3) my anencephaly pregnancy. All of those got stars on the calendar. Twice the stars were later erased.)
Today would have been my due date. If things had worked out, maybe she would have been born already. Maybe I’d be exhausted and covered in spit-up and I’d be able to be happy for everything I have been through because it had to work out in exactly that way for her to be my child. Or maybe I’d still be pregnant, swollen and uncomfortable and bursting with excitement to meet her, hoping she was not born on Halloween.
But things did not work out, so here I am. Starting another cycle, without any of the optimism I once brought to this process. Except I did calculate my due date… just in case….
Wednesday, October 21, 2015
As I mentioned, I made calls to “my team” to see if anyone had any reasons why I should / should not take inositol during my next FET cycle to try to reduce the risk of a NTD.
I heard back from my OBGYN’s office. She was unfamiliar with the studies on inositol for prevention of NTDs, so she could not recommend it as a supplement (no surprise). She did say that she knows the body produces it naturally so probably a little is not harmful. Ringing endorsement!
I also heard back from someone involved with the Duke NTD study. She was aware of the mice studies and the PONTI study on humans with respect to NTDs and inositol, but noted that there is no conclusive evidence yet that inositol supplementation in humans reduced the risk of NTDs and therefore no recommendation (in the US) for women to take it. She was aware of some women who chose to take it. Another ringing endorsement!
Finally, I heard back from my RE’s office. They said it was fine, and sent me to a specific lab to order it (they have other patients use it for ovarian health and function):
Ovasitol: 50mg d-chiro-inositol, 2000mg myo-inositol in a powder form, taken morning and evening in water. A 3-month supply with a doctor’s code is $78.
My RE suggested that most studies suggest folic acid alone is fine. But he did not try to convince me not to take inositol on top of it. Inositol, here I come!
Monday, October 19, 2015
One of the best things about this blog has been getting feedback from others. Recently, a commenter from the UK (thanks Emily!) pointed me to the PONTI (Prevention Of Neural Tube defects by Inositol) study. I’d never even heard of inositol before! Apparently some researchers think that inositol supplementation (on top of folic acid) may help to prevent neural tube defects.
As we’ve already discussed, folic acid is really powerful in reducing the number of NTD-affected pregnancies, but it does not eliminate them. One article suggests that “30–50 % of NTDs are not folate preventable. . . .”
Apparently, scientists have known for a while that inositol (here myo-inositol) prevents folate-resistant neural tube defects in mice:
They theorized this would be true in humans as well. A 2002 article reported that a woman with two nueral tube defect pregnancies (even with folic acid supplementation, ie. FA-resistant) used 500mg inositol with her third pregnancy, and had a healthy baby without any side effects to mom or baby:
Here’s another study noting no side effects to mom or baby with inositol:
And here’s one that suggests myo-inositol might be helpful in avoiding gestational diabetes:
In 2006, the PONTI study researchers noted that inositol helped to prevent NTDs in mice that were “folic acid resistant”: “We found that inositol prevents NTDs in a FA-resistant mouse model. Moreover, serum inositol is lower in mothers and children with NTDs. Pre-clinical animal testing, and limited testing in humans, suggest that inositol therapy is safe in pregnancy.”
Here’s the information about the PONTI study (which has been completed). Women with a history of a neural-tube affected pregnancy and were planning to become pregnant were given 5mg of folic acid (the standard UK supplement for pregnancies at high risk of NTD) and either 1 g inositol or a placebo.
Another study out of the Washington University has also found that, in mice, there is a link between inositol metabolism and NTDs:
Okay, before we go any further, what the hell is inositol? There are actually nine forms of inositol, although only two forms were discussed in any of the literature I reviewed: myo-inositol [the most widely-occurring in nature] and D-chiro-inositol.
Inositol was once considered a member of the vitamin B complex (formerly B8), but that’s no longer true.
Myo-inositol and D-chiro-inositol are chiral epimers of one another—they have the same chemical formula and weight, but different chemical structure. (Like your right and left hand, they are mirror images of one another but they do not have the same structure. Hmm, all that high school and college chemistry is coming in handy.) Some scientists think that your body makes D-chiro-inositol from myo-inositol. SO, if you are unable to convert D-chiro-inositol from myo-inositol, a D-chiro-inositol supplementation may help you. Other people who make the conversion, but with less than optimal efficiency, may benefit from large doses of myo-inositol. People in the middle may benefit from some of each. At the end of the day, though, people who need inositol are likely to see positive results from either one:
It can be purchased as an over the counter supplement in the US (not regulated by the FDA):
http://www.amazon.com/Jarrow-Formulas-Inositol-Powder-227g/dp/B0013OUKPC/ref=sr_1_1?s=hpc&ie=UTF8&qid=1445270219&sr=1-1&keywords=Inositol (226g powder of Myo-inositol for $15)
http://www.amazon.com/D-Chiro-Inositol-30-Caps/dp/B00HS41DSY/ref=sr_1_3?s=hpc&ie=UTF8&qid=1445270300&sr=1-3&keywords=D-chiro-inositol#customerReviews(D-chiro-inositol – expensive! 30 300mg tablets are $15, which means 3 mos of 900mg (just under 1g) would be $126)
http://www.amazon.com/Solgar-Inositol-Vegetable-Capsules-Count/dp/B00129AI6O/ref=sr_1_3?ie=UTF8&qid=1445270138&sr=8-3&keywords=Inositol+500+mg+Vegetable+Capsules+solgar (vegetarian, unclear what form)
Inositol has been studied as a treatment for PCOS, with findings that myo-inositol alone and myo-inositol along with D-chiro-inositol were both helpful, with the combination being particularly good.
Some amazing woman went through in amazing detail the use of inositol for PCOS:
It appears there are no results for the PONTI study yet:
I sent them an email to see if they would share their early results, but I’m not holding my breath. (email@example.com) But there are a number of blogs (mostly from women in the UK, it appears) that suggest their doctors are proscribing inositol after a pregnancy has been affected with an NTD.
The dosage recommendation appears to be 1g of inositol (along with 5mg folic acid) for the first 12 weeks.
One study suggests that D-chiro-inositol is more effective than myo-inositol in preventing folate-resistant mouse neural tube defects:
http://www.google.com/url?sa=t&rct=j&q=&esrc=s&frm=1&source=web&cd=19&cad=rja&uact=8&ved=0CEwQFjAIOApqFQoTCJ_cnba0z8gCFQSSDQod1ucCGw&url=http%3A%2F%2Fhumrep.oxfordjournals.org%2Fcontent%2F17%2F9%2F2451.full.pdf&usg=AFQjCNFCQD_zGqY7MM2YVzzPvPf7Pzx_Bg (link to full article)
So, am I going to take inositol? Hell yes I am. I have calls in to both my fertility doctor and my regular OB before I start it, but unless they give me some really damn convincing arguments why I should not take this, I am going to do it.
Friday, October 16, 2015
One of the measurements fertility doctors look at during an IVF cycle is progesterone.
It’s well-settled that low progesterone is a problem and can be a strong indicator of a pregnancy that is likely to fail, depending on when it’s measured.
For women undergoing IVF, and thus receiving some support (shots or suppositories), higher progesterone measurements 14 days after embryo retrieval were associated with pregnancy success:
115 women (26%) had a viable intra-uterine pregnancy at 8 weeks gestation, 80 (18.1%) had an abnormal pregnancy (biochemical, ectopic, miscarriage) and 247 (55.9%) failed to conceive. Women with on-going pregnancies had significantly higher serum progesterone levels (median: 430, 95%CI: 390-500 nmol/l) compared to those who had either an abnormal pregnancy (72, 48-96 nmol/l; P < 0.001) or failed to conceive (33, 28-37 nmol/l; P < 0.001). Receiver-operator curve analysis demonstrated that a single serum progesterone on day 14 post-oocyte retrieval, could highly differentiate between normal and abnormal pregnancies (area under the curve = 0.927, 95%CI = 0.89-0.96; P < 0.0001).
The same thing was shown for women who conceived naturally (it’s easy to forget that women can get pregnant without years and years of invasive medical treatments). This article say for women WITH miscarriage symptoms (i.e. bleeding), low progesterone (below 10) strongly correlated with loss, but HIGHER thresholds (15-20) were not as strong:
For women with symptoms alone, the progesterone test had a higher specificity using a threshold of 10 ng/mL (nine studies with 4689 participants18 20 21 24 26 29 30 3132), rather than higher thresholds at 15 and 20 ng/mL, and predicted a non-viable pregnancy with pooled sensitivity of 66.5% (53.6% to 77.4%), specificity of 96.3% (91.1% to 98.5%), positive likelihood ratio of 18 (7.2 to 45), and negative likelihood ratio of 0.35 (0.24 to 0.50).
Here’s some more information about progesterone (and it’s drop around week 7):
In other words, in early pregnancy, high progesterone levels are good and low progesterone levels are bad:
Viable intrauterine pregnancies can be diagnosed with 97.5% sensitivity if the serum progesterone levels are greater than 25 ng/mL a few days after being late on your period. Conversely, finding serum progesterone levels of less than 5 ng/mL can aid in the diagnosis of a nonviable pregnancy with 100% sensitivity
So, can your progesterone be too high? At least one study suggests that if your progesterone is too high on the day of egg retrieval, pregnancy can be (much) less likely:
Progesterone levels at the time of egg retrieval only were associated with pregnancy outcome. Progesterone levels on the day of egg retrieval were, on average, significantly lower in women who achieved pregnancy (7.8 ng/mL) than in women who did not (10.2 ng/mL). Implantation rates of those with progesterone levels below 12 ng/mL on the day of egg retrieval were 43.9% versus 31.6% in those with levels above 12 ng/mL. Clinical pregnancy rates of those with progesterone levels below 12 ng/mL on the day of egg retrieval were 38.6% versus 20% in those with levels above 12 ng/mL.
Of the women who achieved pregnancy, 75% had progesterone levels less than 10.6 ng/mL. None of the women with progesterone levels greater than 18.1 ng/mL achieved pregnancy. As progesterone levels increased, pregnancy rates decreased. In particular, there appeared to be a steeper decline in pregnancy rates once progesterone levels were above 12 ng/mL. This may suggest that this is a clinically important level beyond which pregnancy is less likely.
These people even offer a handy chart with normal ranges on it:
For day 3 (ie before egg retrieval) you want a progesterone measurement below < 1.5 ng/ml. “An elevated level may indicate a lower pregnancy rate.”
For 7 days post ovulation (or 7 days after egg retrieval) you want a measurement above 15 ng/ml. It explains that “most doctors want to see a level over 10 on a natural cycle, and a level over 15 on a medicated cycle. There is no mid-luteal level that predicts pregnancy. Some say the test may be more accurate if done first thing in the morning after fasting.”
It also says that in the first trimester, a normal range is 10-90 ng/ml, with “Average is about 20 at 4 weeks LMP, and 40 at 14 weeks LMP. It is important to note that while a higher progesterone level corresponds with higher pregnancy success rates, one cannot fully predict outcome based on progesterone levels. Progesterone supplementation is unlikely to help if started after a positive pregnancy test.”
Tuesday, October 13, 2015
After a number of failed cycles, many women (smartly) switch fertility clinics. If we had nothing but failures at my clinic, it would be a no-brainer. We would have switched for our last fresh cycle. BUT my clinic has gotten me pregnant in all of our cycles but one (5/6) and has actually gotten us pregnant with “viable” pregnancies twice (2/6). So I would not say I have no confidence in them.
Still, I did cheat and get a second opinion with CCRM. I was impressed, but I wanted to see what my doctor had to say after our most recent failure. It was interesting and reassuring.
First, he reiterated the fertility doctor mantra—for recurrent pregnancy loss, the biggest reason (70%?) is due to genetic causes. Those losses tend to be earlier in pregnancy (first trimester). The second biggest reason for recurrent pregnancy loss is due to uterine abnormalities (ie polyps, fibroids, scar tissue, etc.). Those losses tend to be later in the first trimester. The third biggest reason relates to “systemic” causes—basically, are you sickly (ie diabetes, thyroid conditions, infections, autoimmune disorders like lupus or rheumatoid arthritis)? These losses also tend be later (10-12 weeks). In this bucket he also placed immune issues. He basically said what the docs at CCRM said—nobody knows if immune issues play a part in recurrent loss, there’s debate but nothing has been proven. The theory is, much like the way the body can reject a transplanted organ, the body can reject a pregnancy as invasive. He said some doctors will treat patients with steroids (such as prednisone) or blood thinners (heparin, aspirin.
With respect to the “systemic” causes—I have none of the known things that would cause concern. Also, all of my losses have been very early, so they are likely not systemic. With respect to the uterine abnormalities—they have been repeatedly ruled out after the doctor has done saline sonograms. (I just had another one that confirmed—my uterus has no issues.) Plus, they also tend to be later losses, not earlier losses.
Which leaves us with genetic issues. This one is confusing, too, as we have now failed with chromosomally normal embryos (ie. the right number of chromosomes). But it might be our genes (ie. the question of whether the chromosomally normal embryo develops normally) that are the issue.
I had three pregnancy losses before I even saw a fertility doctor. One was definitely ectopic, and at least one of the other two was also likely ectopic (we saw further scarring of my tube). SO, we have to put those in a different bucket because they may have been caused by my tubal issue. (Which itself may have been caused by hernia surgery I had as a baby. My whole life my mom worried I would be infertile because the doctor told her, just after operating on a month old baby, that my ovaries were “swollen” and I might have trouble conceiving children. Fast forward 30 odd years later, and it turns out that abdominal surgeries are thought to potentially increase the likelihood of tubal pregnancies.) Anyway, we can’t really say for sure, but we won’t “count” those in the recurrent pregnancy loss bucket we’re trying to solve for now because they may have been related to a tubal issue that IVF all but solves.
Okay, my second “bucket” of losses are the two failed pregnancies I had with chromosomally untested embryos after my second IVF cycle. One was a blighted ovum, so it was likely a genetic issue. The other one was a chemical pregnancy, and those are also generally due to genetic issues.
My third “bucket” of losses was with chromosomally normal embryos after my third IVF cycle. As it related to the anencephaly pregnancy, that embryo turned out to be chromosomally normal. (We did not know that when we put it in, but we had it tested at 12 weeks.) While the “chromosomes” were normal, there was a genetic issue, as anencephaly is, as we have previously discussed, some mixture of genetic and environmental. So there was a genetic issue. My FET after that was with a chromosomally normal embryo, but that also ended in a chemical pregnancy. It too was likely related to genetic issue, even though the chromosomes were normal.
In other words, our genes might be a problem.
And how do you solve for a “genes” issue when all you can do is test the embryos for chromosomes? Well, you just keep putting chromosomally normal embryos back in and hope that one of them is genetically normal as well.
Here are two decent overviews of causes of recurrent pregnancy loss:
And here’s one that says that for women with recurrent pregnancy loss, they are losing chromosomally normal pregnancies at a higher rate:
We talked about whether, with our history, we should just bite the bullet and put in two embryos in our next cycle. This process is just NOT FUN. But our doctor (like the CCRM docs) is anti-twin. As he said, even the best twin pregnancy has more risk than a singleton pregnancy. Twin pregnancies are hard on moms (higher blood pressure, more likely to go on bed rest, more likely to get gestational diabetes, more likely to need a C-section) and hard on the babies too (more likely to be preemies, more likely to suffer from health issues). He was like, if you want one healthy baby, but not twins, put one embryo in at a time.
We also discussed whether it was ethically appropriate to use a B3 girl instead of a B2 boy. He said their rating system (B1-B2-B3) was not strongly correlated with success (it’s as much art as science to rate those little suckers) and once they are tested to be chromosomally normal, the ratings of the embryos matter even less. So he was like, go ahead and use your B3s if you’d like to have a daughter.
I had a whole list of questions for him, so I’ll just run through them now.
First I asked, is it possible we have a translocation? He said no, both my husband’s blood and my blood had been tested for translocations, and we were both normal (I was 46xx, hubby was 46xy). He said that he did not do a “skit test” to look for DNA damage because we had good luck getting embryos to the blastocyst stage. (If there is DNA damage, the hubby can go on folic acid in an attempt to improve sperm quality.) So, it’s not a translocation. We’ve ruled that out.
Second, I asked, is it possible it’s thrombophilia (clotting issue). He said probably not, as those tend to cause late first trimester / early second trimester losses. But, just to be sure, we had my blood tested to confirm. (Factor 5 test, factor 2 test, protein C test, and protein S test.) If that was an issue, I would go on baby aspirin / lovenox or heparin (blood thinners). But the tests came back normal. We’ve ruled that out.
Third, I asked if it was possible I had structure abnormalities. He said unlikely—we’ve had saline sonograms that have said things are normal, and confirmed after each of our losses. He assured me that if there was a structural abnormality, the saline sonogram would catch it. We did another saline sonogram. Normal. We’ve ruled that out.
Fourth, we discussed the “immune response” issue. He basically said nothing was proven and he has never treated a patient with steroids (such as prednisone) and / or antihistamines just for the hell of it. (In other words, he poo-poo’s CCRM’s hail Mary approach.) My husband was very uncomfortable with us doing any protocol that had no scientific support—especially with a drug as potentially dangerous as prednisone. So, we decided that we were comfortable not using a “hail Mary” approach… for now.
(The theory behind the use of a steroid such as prednisone is that embryos might be exposed to bacteria or leukocyte infiltration if the protective coating of the zona pellucida is breached and that immunosuppression via steroids would help combat that. But a study by did not find any beneficial effect of adding low dose progesterone during the luteal phase:
Fifth, I asked if we should use inter-muscular progesterone next time. (Keep in mind I’m the one that’s been pushing NOT to use IM P4 in oil this whole time.) He said, yes, let’s do it. Again, there’s no scientific proof the shots are better than the suppositories, but he said they might be so let’s do it. Big needles, here I come.
So, where does this leave us? CCRM was very impressive, but our doctor said basically all the same things. The big difference in protocol is the “hail Mary” approach that would include the use of prednisone. My doc is against it, CCRM is for it. At the end of the day, my husband is against anything that has not been shown to improve our chances of success, so he’s against the unproven “hail Mary.” From what I’ve read, I’m comfortable with that approach… for now.
I was not convinced that transferring our embryos would be a good decision. If we were considering doing another fresh cycle, I think we would switch. But there did not appear to be much of a benefit to us to transfer the frozen embryos to a new lab. Another consideration is the fact that (a) we would have to use our boy first and (b) CCRM might not even accept our girls. Neither of those things make us want to switch.
Finally, I DO still have confidence in my doctor. He gave us our son. He got us pregnant a bunch of times, twice legitimately, and it’s probably true that those generally failed due to genetic causes or other causes outside of their control. So let’s just blow through the rest of these embryos and see if we’re lucky enough to stumble onto a good one.
We’re staying with our current horse.
Monday, October 12, 2015
If you’re reading this, it means you’re the kind of person (my kind of person!) who looks for answers to fertility issues online. And if that’s the case, you’ve likely run across the Colorado Center for Reproductive Medicine. They have really impressive statistics and are generally recognized as being a leader in the field of fertility treatments. So, after our FOURTH failed cycle from our clinic (I don’t count my cycle where we got pregnant but terminated after our anencephaly diagnosis a “failure” on my clinic), we did what many couples have done before us—we got a second opinion.
I have to admit, the doctors (two of them) I met with were VERY impressive.
I’ve complained that we’ve never had an official diagnosis of what exactly our problem was. In other words, why am I infertile? We discussed my health history and the doctors suggested that a hernia surgery I had when I was a newborn might actually have had an impact on my fertility. They suggested that they have seen other examples of women coming in with tubal issues after having abdominal surgery, and that maybe my first three pregnancy complications / losses could have been related to that issue. (My first pregnancy was an ectopic, and there was further scarring of my tube after my second one, so it was also likely ectopic.)
They also suggested that my three failed IVF cycles last year—on genetically untested embryos—could have been because of genetic abnormalities. (That’s the unexplained failed IVF gut reaction.) Certainly the blighted ovum was likely a genetic issue.
And with our last failed cycle with a genetically normal embryo—well, that signals that there’s either a potentially serious issue or I’m just unlucky.
Anyway, CCRM suggested that with an extensive history of IVF failure—yes, that’s the bucket I’m in now—we should do a recurrent pregnancy loss workup.
There are three things they would like to rule out with that work-up:
(1) A genetic translocation. They said it’s rare (1/500 people carries a balanced translocation), and in 3-5% of couples with recurrent miscarriage, one partner has a balanced translocation. These tend to be early first trimester losses. (Like ours.) They suggested that they could test our blood to see if we have it, and if we do the embryos can be tested to see if they carry it. (Our frozen ones would have to be thawed and re-biopsied. Apparently there is little risk to the embryo. Amazing!)
(2) Thrombophilia. They said the non-genetic form thrombophilia (acquired)—a clotting disorder, and more specifically a tendency to form blood clots—has been shown to cause early first trimester losses. They test for it with a blood test. If you have it they can treat you with Lovenox (a blood thinner) for the first 10 weeks of pregnancy. As the CCRM doctor said, there is a risk to the mom because if you’re in a really serious accident, well, you don’t want to be on a blood thinner. In other words, it’s not something to mess around with.
(3) Structural abnormalities of the uterus (such as scar tissue). These tend to cause later first trimester losses, and are unlikely to be our problem considering we’ve been monitored for such things.
We also talked about our fresh IVF protocol (even though we’re very unlikely to do another fresh cycle). Every fresh cycle we’ve done, we have done a luteal Lupron protocol (also called “long Lupron” or agonist “down regulation”). I generally responded well to those cycles, and we got a number of fair quality embryos.
CCRM claims that that’s a “traditional” cycle. And they are “cutting edge.” CCRM says 95% of the time they do an antagonist protocol. (That works with normal menstruation, instead of putting patients on birth control. Instead of using Lupron on the front end they stim harder later.) CCRM claims an antagonist cycle allows for harder stimming and therefore more eggs without the risk for ovarian hyper stimulation syndrome. For a minority of their patients, they use a microdose flare (when patients have a diminished ovarian reserve and concerns about stimming too hard are not there).
Here’s a more detailed discussion of the different protocols:
I confirmed that at the end of the day, the egg QUALITY is the same no matter the cycle—that is, one protocol might get you more eggs, but none of them will get you better eggs.
For frozen cycles (the most relevant question for us), they first confirmed that they will take frozen embryos from other labs—with some caveats. (They also noted that the embryos have to be SHIPPED and there is a risk (small) that something could happen to them.) First, the lab that froze the embryo has to be good enough quality. (They want good quality vitrification [freezing procedures]. They also might have to actually specially order the medium.) I know our lab just updated its freezing methodology, so I am certain they would meet that criteria. Second, the embryo has to be good quality. Apparently CCRM does not freeze crap embryos, and will not accept low-quality embryos. Third, if an embryo is genetically tested, the testing lab has to have a low error rate. CCRM claims that its in-house testing lab has a very low error rate—less than 4%. So they would want an equally quality lab. Our embryos were tested by Natera, so I’m sure it’s fine. (Although I do not know what their error rate is. It’s scary that there is an error rate and that it’s so high!) Finally, and this was the most interesting, CCRM is VERY open about the fact that its success rates are highly important. (Indeed, the first, second, and third rules are directly related to success rates.) Anyway, CCRM does NOT tell patients the gender of the embryo (one of the options when testing is done in-house) and they do not allow gender selection. Again, that’s not about morally being against gender selection, but about picking the absolutely best embryo regardless of gender to maximize for the highest chance of success.
That raised a really interesting issue for us. We did not do genetic testing with our first five transfers, so the gender was as much a mystery to us as it would be for anyone. But with our last transfer, we had two equally rated B2s. (Who knows if an embryologist could have said one was slightly better than the other.) One was a boy and one was a girl. Because we have a son we said, heck, put the girl in. That cycle did not work. NOW we have a B2 boy and two B3 girls—that is, the boy is a better looking embryo. Would we want to pick the girls over the boy, even though they would be less likely to work? Well, if we did transfer our embryos to CCRM, they would not give us that option—we would have to go with the boy. And it’s not clear from their rules that they would even accept our “crappy” girl embryos.
When I told my husband that they might reject our embryos if we wanted to transfer them, he was completely turned off. And, of course, I would NEVER transfer my B2 if they would not accept the others—what if I went through a whole cycle and then my B2 did not thaw? The idea that I would not have my back-ups to use… well, no way.
But I’m getting ahead of myself. Is there even a benefit to transferring my embryos if we’re just going to do frozen cycles? Unclear.
First we talked about FET protocol. They said for patients with recurrent IVF failure (again, my bucket), they have a “hail Mary” protocol. Most of it is the same as what we have done on our other cycles, but with some new stuff.
CCRM’s hail Mary FET protocol:
(1) 3x a day progesterone suppository (what we always do) PLUS every other day IM progesterone. (No more avoiding shots for me.) When I confessed that I have avoided shots in every cycle, the CCRM doctors acknowledged that there was no data suggesting shots are better than suppositories, but with their hail Mary they just do it.
(2) Vivel patches. (I’ve done vivel patches in the past, but have been using estrace more recently.) Again, they indicated that there was no study that suggested one was better than the other, although the patches are easier on the liver. (I completely forgot how hard this is on the woman’s body!)
(3) Prednisone (steroid) and antihistamine for 10 weeks. This is the “hail” part of it. They acknowledged that there was a controversial idea that there was an immune system response, and although there was nothing concrete for their “hail Mary” patients they go for it. (Again, anyone googling infertility extensively has probably run across Dr. Sher’s office. http://haveababy.com/fertility-information/ivf-authority/recurrent-pregnancy-loss-immune-therapy When I mentioned his name they were like, “oh, we don’t go that far!” I should also note that he does not actually offer any suggested treatment regiments online, at least that I could easily find. http://haveababy.com/fertility-information/ivf-authority/recurrent-unexplained-ivf-failure-with-good-quality-embryos)
That’s it. The hail Mary. But I can do all of those things at my lab. So I pushed, is there any benefit in transferring my embryos to your clinic as it relates to the actual transfer? It seems like not much. They two things they suggested were: (1) Good quality control, including the fact that the embryo is literally in an incubator in the room, so it spends almost no time out of the incubator / mom. (2) They use “embryo glue” in the transfer (acid) (literally—it’s called embryo glue http://www.vitrolife.com/en/Products/G-SeriesTM-media/EmbryoGlue/).
Those are benefits, but I’m not sure it’s worth the risk that the embryos might get destroyed in the move. I asked, “would you move your embryos if you were me?” They did not answer yes or no as it relates to me, although one of the two docs suggested she had done IVF and she HAD transferred her own frozen embryos to CCRM.
We also discussed my prior pregnancy with anencephaly. I was worried that my remaining embryos were all created during that time and thus all might be bad. They were reassuring—the folic acid is most important during the time the embryo is developing, not when the egg is developing, so it’s not certain that all of my remaining forties are doomed.
I have an appointment with my doctor next week. I think we’re going to have some hard questions for him.
Sunday, October 11, 2015
For my first pregnancy, I did not take a home pregnancy test (HPT). I waited for the blood test to be taken at the end of the two-week wait, and was legitimately surprised (although I suspected) when I got the call from the doctor’s office that it worked.
Sometime after that, I heard / read that you can take HPTs days before the blood test at the doctor’s office and get an accurate result. So for every cycle since then, I have taken a home pregnancy test two days before the blood test. And they have always been right.
Recently, I read that some pregnancy tests can give results FIVE days before a missed period (or five days before the clinic blood test at my doctor’s office). So I bought the (allegedly) most sensitive ones and started testing way earlier than normal for this cycle.
The allegedly most accurate drugstore ones are Clearblue Easy Earliest Result Pregnancy Test (25 mIU/ml) and First Response Early Result Pregnancy Test (25 mIU/ml):
Bad idea. Either it’s positive, but you know there’s a risk that things could go south any way, or it’s negative and you’re devastated but hopeful anyway. Either way it sucks. The blood test at the doc’s office is best because it tells you both if you’re pregnant and how healthy the pregnancy is.
All three of my HPTs this time were negative. At least I knew what result to expect at the doc’s office—negative. The blood test confirmed it—HCG level of 2 which means implanted but going nowhere, or “not pregnant.” Fuck.