Ask Our Doctors – Archive
Our Medical Directors are outstanding physicians that you will find to be very personable and compassionate, who take care to ensure that you have the most cutting-edge fertility treatments at your disposal. This is your outlet to ask your questions to the doctors.
Hi Dr Sher, I have already sent a similar question but missed some details out regarding NK cells, apologies.
Hi Dr Sher,
I have just turned 37. My husband, (42) & I have been trying for a baby since Jan 2013 (naturally) followed in 2015 by a year of unsuccessful fertility treatment – 3x clomid cycles & 3xiui cycles.
During this time I have also had a HSG X-ray & the results all came back normal, I have also had a Lap & Dye, again all results normal.
My husband’s sperm results : progressive motility 54million (m)/ml, non progressive motility 1m/ml, immotile 9.7m/ml, sperm number 64.7m/ml, total sperm number 129.4m/ml. Morphology 5%. & all doctors have been happy with these results.
We were diagnosed with unexplained infertility in Jan 2016.
I had these results in Jan 2016 before I started my 1st IVF cycle: My FSH 6.6, LH 5.8 AFC 28, progesterone levels 55, prolactin 249, TSH 2.35. I don’t have NK cells.
Since March 2016 I have had 3 unsuccessful IVF cycles,
The first was a short Cetrocide protocol. I took BCP for 10 days, followed by a break & bleed & then had 11 days of 150iu menopur (with Cetrocide added in part way through) I had the HCG on day 12.
7 eggs were collected but only 3 were mature, these fertilised with ICSI but was told from the offset that they were developing too fast/slow. These however turned into day 5 blastocysts & I had 1 x grade 3 (Grade 1 = best) transferred. Progesterone support, however this cycle was unsuccessful.
In July I started my 2nd round at a new clinic & was advised to try a long protocol & change of drugs. I down reg’d for 18 days using Buserilin, had a bleed but with continued Buserilin, a scan confirmed that I had down reg’d & everything was ‘quiet’. I then had 12 days of 225iu Gonal f & 10,000iu pregnyl trigger. I had 13 eggs collected & was devastated when I got the call the next day saying none were mature.
In our follow up meeting, our consultant said that in his 25 years of practicing he’d only come across a handful of people with response like this. He spoke about upping the drugs, changing the stims, & leaving ER until 39 hours to help with maturity. He also recommended taking extra supplements of COQ10, myo-inositol & melatonin for the 3 months before my next cycle.
In Novemeber I started my 3rd cycle, same dose all the way through of Buserilin (as previous cycle) 300iu of menopur, then 15,000iu of pregnyl for the trigger shot but also a 300iu of menopur & Buserilin at the same time to boost the effects on my follicles/eggs. All the way through my scans there only seemed to be 6 decent sized follicles & then on ER (39 hours later) 11 eggs were collected. 6 mature, 5 fertilised normally, but by day 2, two had arrested. On day 3 we received a call from the clinic stating we had 1x 8 cell (they were pleased with) 1x 5 cell & 1x 3 cell. We opted for day 3 ET & when we got to the clinic the 2 slower embryos were now both 6 cell. We had the best 6 cell & 8 cell transferred. My endometrium was triple layer & 9mm & I had progesterone support.
This cycle has just failed. Can you please give me some advice on a protocol that might be more successful for me? & also how long to wait in between cycles? I am very conscious of my age..
Many thanks
Kate
There are many reasons for repeat IVF failure, but in my opinion, your situation strongly suggests a stimulation protocol issue.
Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
1.Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
2.Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3.The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
4.Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
a.A“ thin uterine lining”
b.A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c.Immunologic implantation dysfunction (IID)
d.Endocrine/molecular endometrial receptivity issues
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•The Fundamental Requirements For Achieving Optimal IVF Success
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
•Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Blastocyst Embryo Transfers Should be the Standard of Care in IVF
•IVF: How Many Attempts should be considered before Stopping?
•“Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
•IVF Failure and Implantation Dysfunction:
•The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
•Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
•Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
•Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
•Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
•Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•A personalized, stepwise approach to IVF
•How Many Embryos should be transferred: A Critical Decision in IVF.
•The Role of Nutritional Supplements in Preparing for IVF
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
So I am currently waiting for my period to start so I can do another FET… I have gained weight because they upped my metformin ER and my Synthyroid and now my Appetite is crazy.. I could just eat and then be hungry 5 minutes later. I was wondering can I take prescription Diet pills while I am waiting for my period? would I need to stop them once I started Lupron for my FET?
You need to discuss this with your treating RE.
Geoff Sher
Hi Dr Sher, thanks for your response below. Do you still advocate PGS for older women if the error rate is 25%? If so why? It seems quite a high risk, why not just give the embryos a chance rather than potentially disposing of viable embryos?
Because, in spite of the shortfalls I enumerated, identifying those embryos that are most likely to propagate a viable pregnancy in older women and those with diminished ovarian reserve markedly improving the chance of a healthy pregnancy without having to resort to egg donation. This is especially beneficial when PGS is combined with Embryo banking By way of a tangible example, the selective transfer of one such “competent” embryo to the uterus of a women of 43Y could improve success per embryo transferred, by a factor of X 4-6. In addition, the repeated transfer of PGS-normal embryos without resulting in a pregnancy strongly highlights the need to seriously consider an anatomical or immunologic implantation dysfunction as the root cause.This again highlights the important diagnostrtic benefit of PGS testing.
Having said this, I am very much against discarding embryos where a single chromosomal irregularity is detected because of the ever present risk of mosaicism and the inability to accurately recognize its present in the clinical setting. Such embryos should in my opinion be considered for transfer to the uterus , but only after full disclosure as to potential risk, and after informed consent and an expressed willingness to do prenatal genetic testing in the 1st or 2nd trimester and consider termination of pregnancy if this reveals a grossly abnormal conceptus. The reason for my attitude is that mosaic pregnancies can ans sometimes do autocorrect in the uterus.
Geoff Sher
Geoff Sher
Hi Dr Sher, I have a question regarding functional cysts. My FS does not aspirate functional cysts and I have read that if you don’t, any FSH taken will be eaten up by the cyst. Is that really what happens? Should a smaller functional cyst just be ignored as they generally settle over time?
An ovarian cyst is any collection of fluid, surrounded by a very thin wall, within an ovary. An ovarian follicle that is larger than 22mm is termed a functional follicular cyst. They are non-malignant (benign) and harmless and in most cases, don’t even cause symptoms, however, in some cases, rapid distention of the cyst , or rupture with bleeding , can lead to sudden and severe pain and in some cases, a disruption in hormone balance leads to vaginal bleeding.
There are 2 varieties of “functional ovarian cysts:
1.Follicle Cysts: In menstruating women, a follicle containing the unfertilized egg will rupture during ovulation. If this does not occur, a follicular cyst of more than 2.5 cm diameter may result. These cysts develop in response to stimulation with follicle stimulating hormone that is either self-produced (by the woman’s own pituitary gland (endogenous) or is induced by agonists (e.g. Lupron/Decapeptyl/Buserelin) that sometimes propagate increased and sustained pituitary FSH release.
2.Corpus luteum cysts: These appear after ovulation or egg retrieval. The corpus luteum is the remnant of the follicle after the ovum has moved to the fallopian tubes. It usually degrades within 5-9 days. A corpus luteum of > 3 cm is regarded as being cystic.
A:Follicular cysts: These lesions have special relevance in women about to undergo controlled ovarian stimulation (COS) with gonadotropins for IVF where they can literally, “throw a spanner in the works”, causing a delay, postponement and sometimes even cancellation of the cycle of treatment.
Functional Ovarian cysts must be distinguished from “non-functional or cystic ovarian tumors”. By definition, “tumors are capable of independent growth. Thus “cystic ovarian tumors do not develop as a result of exposure to gonadotropin stimulation and it is this feature that distinguishes them from “functional” ovarian cysts.
Aside from sometimes causing pain and dysfunctional uterine bleeding, unruptured follicular cysts are usually relatively non-problematic. As stated above, in some cases, functional “cysts” undergo rapid distention (often as a result of a minor degree of bleeding inside the cyst itself). In such cases the woman will often experience a sharp or aching pain on one or other side of her lower abdomen and/or deep seated pain during intercourse. The cysts may even rupture, causing sudden lower abdominal pain that exacerbates and may even simulate an attack of acute appendicitis or a ruptured ectopic (tubular) pregnancy. While very unpleasant, a ruptured “functional cyst” seldom produces a degree of internal bleeding that warrants surgical intervention. The pain, typically is made worse by movement. It stabilizes within a number of days but subsides progressively to disappear within about four to seven days.
Whenever an ovarian cyst is detected (usually by ultrasound examination), the first consideration should be to determine whether it is a “functional cyst or a “cystic ovarian tumor”. The reason for this is that tumors are subject to a variety of complications such as twisting (torsion), hemorrhage, infection and even malignant change, all of which usually will require surgical intervention.
Gonadotropin releasing hormone agonists (GnRHa) such as Lupron, Buserelin, Nafarelin and Synarel, administered daily, starting a few days prior to menstruation, all elicit an initial and rapid, out-pouring (“surge”) in pituitary LH and FSH release. This “surge” lasts for a day or two. Then as the pituitary reservoir of FSH and LH becomes depleted, the blood FSH and LH levels fall rapidly reaching near undetectable blood levels within a day or two. At the same time, the declining FSH result in a drop in blood E2 concentration leading to a withdrawal bleed (menstruation). The progressive exhaustion of Pituitary FSH/LH along with the decline in blood E2, is referred to as ” down-regulation” The continued daily administration of GnRHa or its replacement (supplanting) with a GnRH antagonist (e.g. Ganirelix, Cetrotide or Orgalutron) results in blood LH concentrations being sustained at a very low level throughout the ensuing cycle of controlled ovarian hyperstimulation (COH) with gonadotropins, thereby optimizing follicular maturation and promoting E2 induced endometrial proliferation.
Functional follicular cysts resulting from controlled ovarian stimulation (COS), can occur regardless of whether down regulation with GnRHa (Lupron/Buserelin/Decapeptyl) is initiated in cases where the cycle of stimulation is launched with the woman coming off a BCP or when the agonist is initiated on day 20-23 (the mid luteal phase) of a natural cycle. When this happens it is due to the initial agonist-induced FSH “surge” sometimes so accelerating follicular growth that it leads to the development of one or more “functional follicular cysts”. These cysts release E2 and cause the blood E2 often to remain elevated (>70pg/ml). Depending on the extent of this effect, it sometimes leads to a delay in the onset of menstruation and thus also to deferment in the initiation of COS.
Failure of menstruation to commence within 4-7 days of initiating treatment with GnRHa suggestive of an underlying “functional ovarian cyst” and calls for an ultrasound examination to make the diagnosis. Once diagnosed, depending upon the number and size of cysts detected. There are two therapeutic options:
1)Wait for the cyst to absorb spontaneously and for menstruation to ensue: While it at first might seem that this approach of continuing GnRHa therapy in order to cause absorption of the cyst(s) within a week or two might be a good approach , it often has unintended consequences. First there is the real possibility that prolonged uninterrupted GnRHa therapy might blunt subsequent ovarian follicular response to gonadotropin therapy and second, if menstruation does not follow within 10-14 days, the cycle will usually need to be cancelled.
2)Immediate needle aspiration of the cyst(s) under local anesthesia. I personally favor needle aspiration, sooner rather than later in such cases. Menstruation will usually follow a successful aspiration within 2-4 days. Upon menstruation a blood E2 level is measured and as soon as it drops below 70pg/ml COS can be initiated.
B. Corpus Luteum cysts: As with follicular cysts, so at times do Corpus Luteum cysts also bleed, distend and cause fain. They often delay onset of spontaneous menstruation by a week or longer (Halban syndrome”.). In isolated cases, internal bleeding within the cyst substance causes pain, rapid enlargement of the lesion and by ultrasound examination reveals local areas of absorption causing it to appear as a “complex” cystic lesion that simulates a tumor, prompting surgical intervention. Sadly, there are countless cases where women have had an entire ovary removed due to this happening.
“Functional ovarian cysts” rarely present as a serious health hazard. In the vast majority of cases they spontaneously resolve within 2-4 weeks while “cystic tumors” will not. Accordingly, the persistence of any ovarian cyst that persists for longer than 4 weeks should raise suspicion of it being a tumor rather than with a “functional cyst”. Since ovarian tumors can be (or become) malignant, all ovarian cysts that persist for longer than 6 weeks (whether occurring in non-pregnant or pregnant women), should be considered for surgical removal and this should be followed by pathological analysis.
I hope this answers your questions fully!
Geoff Sher
Hello doctor
I am doing a frozen embryo transfer with doneated embryo i have been offered a 3 day transfer with 2 embryo or a 5 day transfer with 1 embryo i am 28 and have unexplained infertility i have have mild pcos and have never been pregnant after have 3 iui and have decided for my own health to go for embryo adoption would like to know which embryo has the more chance sin live birth would it be 2x 3 day or 1x 5 day a tein pregnancy is an option we have considered and are willing to take the risk
I would go with the day day 5 blastocyst!
With IVF, embryos may be transferred at the cleaved stage, 2 days following fertilization (2-4 cell stage) or 3 days post-fertilization (5-10 cell stage or alternatively, 5-6 days following fertilization, at the blastocyst stage (>100 cells). Blastocyst embryo transfer thus requires extending the embryo culturing duration for an additional 2-3 days.
With blastocyst transfer, the chance of pregnancy is significantly higher than with cleaved embryo transfers. This is because many numerically chromosomally abnormal (aneuploid) embryos arrest in development before they reach the blastocyst stage.
Previously (and to a large extent even today), IVF doctors and embryologists have intuitively believed that the uterus provides a more “natural” and favorable environment for embryo development, than the petri dish and incubator and accordingly have held that the sooner an embryo is transferred to the uterus, the better off it would be. By this belief an embryo transferred as on day 2 -3 post-fertilization rather than as a blastocyst (on day 5 or 6) would have a better chance of resulting in a live birth. We now know this to be erroneous.
Background information: Before the freshly fertilized egg, starts to cleave (divide), it is called a zygote. After the first 24 hours, (Day 1) the embryo has divided into 2 cells. By Day 2 the embryo has 4 cells blastomeres and by the third day, there should be between 6 and 9 cells. Up to that point, embryonic development is under the control of maternal genes in the egg. Around the 8 cell stage, the embryo’s own genes (embryonic genome) begin to take over control of development. By the fourth day, the embryo has between 16 and 32 cells. At this point it looks like a mulberry and is called a morula. Until the morula stage, all of the embryo’s cells are the same and are “totipotential” (i.e. they have the ability to ultimately develop into any tissue or organ type). By day 5 post-fertilization, differentiation of the embryo begins. A fluid-filled cavity blastocoel forms in the center of the conglomerate of blastomeres. This blastocoel will eventually become the amniotic sac and the fluid surrounding the conceptus in the uterus.
The cells around the outside of the morula develop into the trophectoderm, which will eventually form the placenta and fetal membranes, while the cells on the inside of the morula aggregate and group together to form the inner cell mass, which ultimately develops into the fetus. This complex creation is now called a blastocyst. By this stage the embryo comprises more than 100 cells. As the blastocoel fills with fluid, the blastocyst expands, its walls thin out and it eventually breaks through (hatches) its envelopment zona pellucida. The trophectoderm then begins to invade the uterine lining (implantation) by the 6th to 8th day after ovulation (or egg retrieval in the case of IVF treatment).
Human embryos are very fickle. They have specific metabolic requirements in order to survive. The earliest type of artificial embryo culture media developed for IVF purposes was relatively simple in composition and could only support limited embryonic development in the Petri dish and incubator. Thus, the majority of embryos cultured in such media could only survive to the third day, whereupon their development would usually arrest. Subsequent improvements in media composition allowed for more reliable embryo development to the third day…which became and remained the standard time at which embryos were transferred for more than two decades.
In the mid-1990s, researchers in Australia, Scandinavia and the USA simultaneously developed a new generation of culture media that could support the growth of embryos to the fifth or sixth day. This development was based on a clearer appreciation of the metabolic needs of the early embryo. Now, contingent upon the age of the egg provider, approximately 30-40% of morphologically “good quality” day 3 embryos (comprising 5-9 cells with minimal/no fragmentation) can be grown to the blastocyst stage using such advanced culturing methods.
A few years ago I and my research partner, Levent Keskintepe PhD, reported on the fact that embryos that failed to develop into blastocysts were almost always aneuploid and incapable of propagating a viable pregnancy (i.e. “incompetent”). However, not all embryos that developed into expanded blastocyst were chromosomally normal and “competent”. As such, embryos that fail to develop in the laboratory to the expanded blastocyst (advanced preimplantation) stage by day 5-6 post-fertilization, would not have developed into a viable pregnancy had they been transferred to the uterus earlier on in the cleaved stage (day 2-4 post-fertilization). Accordingly, there is in my opinion, little justification for transferring embryos that have not developed into fully expanded blastocysts by day 5-6 post-fertilization. Since many aneuploid (“incompetent” embryos are culled out during the developmental stage, it follows that blastocysts are much more likely to be “competent” than are cleaved, earlier stage embryos. Thus blastocyst transfer reduces the incentive on the part of IVF doctors to transfer multiple embryos in order to bolster their success rates, and the process this reduces the risk of high order multiple pregnancies (triplets or greater) with its incumbent risks to both mother and babies.
As mentioned earlier on, the older the egg provider, the lower the chance that her fertilized eggs with develop into blastocysts. In fact, in spite of the introduction of specialized culture systems and other new techniques, at best (even in younger women) 40% of “good quality” day 3 embryos (those that are 6-9 cells and have little fragmentation) will develop into expanded blastocysts by day 5-6 post-fertilization in younger women. And the blastocyst conversion rate declines rapidly as the woman ages beyond 35 years, such that by age 40 years, the conversion rate is about 15-20% and by 43 years of age it is <10-15%. Since blastocysts are much more likely than cleaved embryos to implant following embryo transfer (ET), the transfer of 1-2 good quality blastocysts will in any age category, proportionately yield a far better IVF success rate
The new found ability to safely freeze blastocysts using a new ultra-rapid process known as vitrification which does not compromise their subsequent (post-thaw) ability to propagate a viable pregnancy, has led to many IVF programs to preferentially cryobank vitrified blastocysts for transfer in one or more subsequent frozen embryo transfer (FET) cycles. Also, the introduction of Preimplantation genetic sampling (PGS) with full numerical chromosomal assessment (full karyotyping) using methods such as comparative genomic hybridization (CGH) and next generation gene sequencing or (NGS) now permits the identification and selective transfer of only the most competent blastocysts, thereby improving IVF outcome substantially. This allows many older women and those with diminished ovarian reserve(DOR) who are averse to doing egg donation-IVF, to have their embryos biopsied and then bank (stockpile) their embryos over several cycles, in the hope of subsequently transferring only those that are determined through PGS to be the most “competent” ones
For all these reasons (and there are probably many others) most IVF centers of excellence have graduated from transferring cleaved embryos to blastocyst transfers.
Other than patient preference and easing pressure on doctor and/or patient, there is in my view seldom a justification for transferring embryos on day 2 or day 3. In light of the aforementioned revelations and developments I therefore hold that blastocyst transfer should be the embryo transfer method of choice.
Geoff Sher