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.
I just posted this on your other website then I saw a post to post it again here.
I have a question about egg quality, advanced age, and obesity. I have read some of your articles that indicate that a different protocol may be better but I haven’t seen specific information related to weight factors.
I completed an egg retrieval cycle in Bilbao, Spain in May. This was my first cycle and it was done in Bilbao because I have been teaching English here for the last few years. I am 42, around 270-275 lbs. and about 5′ 7.5? (I am large boned and active but obviously also obese, and my weight is up after various problems in the last few years.) I am single and I have never tried to get pregnant with a partner.
I had an Anti-mullarian hormone level of 2.52 (so it was a good reserve for 42) and I responded to the medicine more or less well even though weight was a factor.
Unfortnately these were the results of the retrieval.
TYPE OF CYCLE: Antagonist Protocol
o Number of oocytes retrieved: 11 cumulus oophorus complexes (COCs)
o Quality of the oocytes: 7 MI, that don’t reach MII stage in the laboratory.
o Number of mature oocytes valid for vitrification : 0
May 17 — Elonva 150
May 23 – Orgalutron 0.25
May 24 – 300 Puregon
Orgalutron 0.25
suero ESTRADIOL…………….. 2117.0
May 25 – Orgalutron 0.25
suero ESTRADIOL…………….. 2489.0
May 25 – Ovitrelle 250 (about 9:10pm) (I was told 9pm but 9:10pm was needed to find place where I could do the injection and it was discussed with the doctor when I was given the time).
The clexane was only done for 8 days ending on May 26 (morning) because of a prescription error.
The retrieval was done at 9am on Friday May 27.
Clexane was required because I had a DVT and PE following ankle surgery last year. I tested negative for clotting factors.
retrieval from my left ovary was difficult because rather than moving downwards with follicle growth it moved up further into the abdominal cavity, but there was retrieval.
– 17/05/2016: Baseline Pelvic Ultrasound
Right ovary: 10 antral follicles.
Left ovary: Poor visibility, antral follicles cannot be seen. Absence of cysts.
– 21/05/2016: 1st control
Transvaginal ultrasound:
Right ovary: 1 follicle of 11mm, 1 follicle of 10mm, 4 follicles < 10mm.
Left ovary: 1 follicle of 11mm, 1 follicle < 10mm.
– 23/05/2016: 2d control
Transvaginal ultrasound:
Endometrium: 8,8mm
Right ovary: 1 follicle of 14mm, 2 follicles of 13mm, 2 follicles of 10mm, 1 follicle < 10mm.
Left ovary: Poor visibility.
– 25/05/2016: 3rd control
Transvaginal ultrasound:
Endometrium: 11,8mm
Right ovary: 1 follicle of 19mm, 1 follicle of 16, 2 follicles of 15mm, 1 follicle of 12mm, 1 follicle
of 11mm, 2 follicles < 10mm.
Abdominal ultrasound:
Left ovary: 1 follicle of 20mm, 2 follicles of 17mm, 1 follicle of 16mm, 1 follicle of 13mm.
Left ovary in abdominal cavity.
Following the retrieval at my next appointment I was told that I should not continue with further cycles. My egg quality is too low and that even if I obtain a MII egg it will never fertilize.
I realize that I am 42 and quality may very well be the issue, but I keep finding references to changes in the protocol and medicine as being possibilities as well. The clinic I used said that there were no deformities, merely immature eggs but insist that the only reason for this is egg quality.
I am looking for a second opinion because I have read changes to medicine and treatment can affect this, but I am not sure what to think.
There is no doubt that advancing age negatively impacts egg “competency”. However so does a suboptimal stimulation (I do not personally approve of antagonist protocols starting on day 6-7 of stimulation in ollder women and of using 250mg Ovidrel/Ovitrelle as a trigger dosage. You would in ,my opinion need 500mcg in my opinion or 10,000U hCGu to effect optimal egg maturational division (meiosis).
The prevalence of obesity in Western societies is on the rise. This has a profound effect on the reproductive performance of women who are trying to have a baby. Recent evidence suggests obesity in women of the reproductive age is associated with decreased birth rates, increased miscarriage rates, higher rates of premature delivery and a marked increase in pregnancy complications. We use two parameters to measure height-weight relationship. The first is Body Mass Index (BMI) (the ratio of height to weight that is calculated by taking body weight in kg and dividing this by the square of height in meters. The second is the percentage contribution made by fat to overall body mass
BMI: A BMI of <20 is regarded as underweight; 20 - 25 is ideal/normal. A BMI of >30 is definitively indicative of being overweight. A BMI of 30-40 is obese and > 40 is morbidly (dangerously) obese. The “ideal BMI” for fertility is 20-25. A BMI of<20 increases the risk of miscarriage. Women with a BMI of > 30 fertility often have a reduction in response to ovarian stimulation. BMI significantly impacts male fertility as well. Men with an increased BMI often experience significant sperm dysfunction.
Percentage Fat: The contribution of fat to body weight is also important. The normal contribution of fat to body mass in adult women is about 28%. Anything under 22% can result in dysfunctional or absent ovulation. Both diet and exercise modification can help regulate the percentage of body fat and BMI.
Simply stated, being overweight with a significantly elevated BMI and or having a high percentage of body fat has a decidedly adverse effect on overall reproductive performance. And when it comes to IVF in specific, while the results of several studies have in some cases have been discordant the general trend strongly suggests that women who are moderately overweight (BMI>25-30) and those who are obese (BMI>30) have poorer IVF outcomes than do controls with a BMI <25. As alluded to above, it would appear that women with a BMI of >25 and especially those with a BMI of >30 exhibit a poorer ovarian response to fertility drugs (impaired follicle and embryo development with fewer blastocysts becoming available for transfer). They also tend to have a reduced ability to implant transferred embryos into their uterine linings (perhaps due to reduced endometrial receptivity).
Women with polycystic ovary syndrome (PCOS) often usually have BMI’s of >30. In such women, the hormonal environment in the ovaries is known to adversely affect follicle and egg development. Given that there is often no clear cut distinction between PCOS and other overweight women, it is possible that many of the factors that are believed to affect egg/embryo quality in PCOS might similarly affect egg development and endometrial receptivity in overweight women. Such factors could include increased production of luteinizing hormone (LH), hyperinsulinemia and increased production of ovarian male hormones (androgens such as testosterone). The link between increased LH and resulting increased production of ovarian androgens (mainly testosterone) and poor follicle and egg development is well established. It is also well known that such hormonal changes can be transmitted to the adjacent uterus thereby adversely affecting endometrial development.
Clearly the question arises as to whether the negative effect of an elevated BMI (>25) on general fertility potential and IVF outcome is due to compromised egg development, endometrial receptivity to the implanting embryo or both. In my opinion, while a direct ovarian influence probably predominates, there is also likely to be an adverse influence on endometrial development. This endometrial affect is commonly seen in PCOS women who, when they develop severe ovarian hyperstimulation on fertility drugs often have a very thin (< 8mm endometrium). Then there is the reality that it is often technically more difficult to perform a “smooth” and “flawless) embryo transfer in women who are overweight. This is especially true when it comes to those with a BMI of >30. Visualizing the cervix is much more difficult and the introduction of the embryo transfer catheter through the cervix, often difficult. Given that the efficiency by which ET is conducted, represents a rate-limiting determinant of IVF outcome, kit follows that obese women tend to have poorer overall IVF outcomes.
Finally, it is important to emphasize that overweight women are at far greater risk during pregnancy than are women of normal body weight. As previously mentioned, the miscarriage rate is much higher. So is the incidence of diabetes, high blood pressure, preeclampsia, premature labor, surgically assisted deliveries, stillbirth and neonatal death. Maternal complications that occur after birth of the baby (i.e., infection, uterine post partum hemorrhage, etc. are also much more common. Babies born to such mothers, are also at great risk of developing respiratory distress syndrome (RDS). This condition which ordinarily only occurs in preterm babies can also occur in the absence of prematurity in such cases. RDS is the commonest reason for the newborn having to be admitted to a neonatal intensive care unit and also the commonest cause of death in the first week of life.
The clinical significance of a growing population of overweight women is enormous because not only can this compromise their overall reproductive performance but it also compounds the risk of chronic medical conditions such as diabetes, coronary/cerebral/peripheral vascular disease and thus compromises life expectancy as well as the quality of life. As such, being overweight represents an overall life hazard that should be addressed by the medical profession as well as by society as a whole. The answer is surely not a simple one but the solution does not lie in dieting alone (which rarely is of sustained benefit). Instead it requires an overall modification in lifestyle.
Older women as well as those who (regardless of age) have diminished ovarian reserve (DOR) tend to produce fewer and less “competent” eggs, the main reason for reduced IVF success in such cases. The compromised outcome is largely due to the fact that such women tend to have increased LH biological activity which often results in excessive LH-induced ovarian testosterone production which in turn can have a deleterious effect on egg/embryo “competency”.
Certain ovarian stimulation regimes either promote excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), augment LH/hCG delivered through additional administration (e.g. high dosage menotropins such as Menopur), or fail to protect against body’s own/self-produced LH (e.g. late antagonist protocols where drugs such as Ganirelix/Cetrotide/Orgalutron that are first administered 6-7 days after ovarian stimulation has commenced).
I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of a modified, long pituitary down-regulation protocol (the agonist/antagonist conversion protocol-A/ACP) augmented by adding supplementary human growth hormone (HGH). I further recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing/NGS)-normal blastocysts in such cases. This type of approach will in my opinion, optimize the chance of a viable pregnancy per embryo transfer procedure and provide an opportunity to capitalize on whatever residual ovarian reserve and egg quality still exists, allowing the chance to “make hay while the sun still shines”.
The prevalence of obesity in Western societies is on the rise. This has a profound effect on the reproductive performance of women who are trying to have a baby. Recent evidence suggests obesity in women of the reproductive age is associated with decreased birth rates, increased miscarriage rates, higher rates of premature delivery and a marked increase in pregnancy complications. We use two parameters to measure height-weight relationship. The first is Body Mass Index (BMI) (the ratio of height to weight that is calculated by taking body weight in kg and dividing this by the square of height in meters. The second is the percentage contribution made by fat to overall body mass
BMI: A BMI of <20 is regarded as underweight; 20 - 25 is ideal/normal. A BMI of >30 is definitively indicative of being overweight. A BMI of 30-40 is obese and > 40 is morbidly (dangerously) obese. The “ideal BMI” for fertility is 20-25. A BMI of<20 increases the risk of miscarriage. Women with a BMI of > 30 fertility often have a reduction in response to ovarian stimulation. BMI significantly impacts male fertility as well. Men with an increased BMI often experience significant sperm dysfunction.
Percentage Fat: The contribution of fat to body weight is also important. The normal contribution of fat to body mass in adult women is about 28%. Anything under 22% can result in dysfunctional or absent ovulation. Both diet and exercise modification can help regulate the percentage of body fat and BMI.
Simply stated, being overweight with a significantly elevated BMI and or having a high percentage of body fat has a decidedly adverse effect on overall reproductive performance. And when it comes to IVF in specific, while the results of several studies have in some cases have been discordant the general trend strongly suggests that women who are moderately overweight (BMI>25-30) and those who are obese (BMI>30) have poorer IVF outcomes than do controls with a BMI <25. As alluded to above, it would appear that women with a BMI of >25 and especially those with a BMI of >30 exhibit a poorer ovarian response to fertility drugs (impaired follicle and embryo development with fewer blastocysts becoming available for transfer). They also tend to have a reduced ability to implant transferred embryos into their uterine linings (perhaps due to reduced endometrial receptivity).
Women with polycystic ovary syndrome (PCOS) often usually have BMI’s of >30. In such women, the hormonal environment in the ovaries is known to adversely affect follicle and egg development. Given that there is often no clear cut distinction between PCOS and other overweight women, it is possible that many of the factors that are believed to affect egg/embryo quality in PCOS might similarly affect egg development and endometrial receptivity in overweight women. Such factors could include increased production of luteinizing hormone (LH), hyperinsulinemia and increased production of ovarian male hormones (androgens such as testosterone). The link between increased LH and resulting increased production of ovarian androgens (mainly testosterone) and poor follicle and egg development is well established. It is also well known that such hormonal changes can be transmitted to the adjacent uterus thereby adversely affecting endometrial development.
Clearly the question arises as to whether the negative effect of an elevated BMI (>25) on general fertility potential and IVF outcome is due to compromised egg development, endometrial receptivity to the implanting embryo or both. In my opinion, while a direct ovarian influence probably predominates, there is also likely to be an adverse influence on endometrial development. This endometrial affect is commonly seen in PCOS women who, when they develop severe ovarian hyperstimulation on fertility drugs often have a very thin (< 8mm endometrium). Then there is the reality that it is often technically more difficult to perform a “smooth” and “flawless) embryo transfer in women who are overweight. This is especially true when it comes to those with a BMI of >30. Visualizing the cervix is much more difficult and the introduction of the embryo transfer catheter through the cervix, often difficult. Given that the efficiency by which ET is conducted, represents a rate-limiting determinant of IVF outcome, kit follows that obese women tend to have poorer overall IVF outcomes.
Finally, it is important to emphasize that overweight women are at far greater risk during pregnancy than are women of normal body weight. As previously mentioned, the miscarriage rate is much higher. So is the incidence of diabetes, high blood pressure, preeclampsia, premature labor, surgically assisted deliveries, stillbirth and neonatal death. Maternal complications that occur after birth of the baby (i.e., infection, uterine post partum hemorrhage, etc. are also much more common. Babies born to such mothers, are also at great risk of developing respiratory distress syndrome (RDS). This condition which ordinarily only occurs in preterm babies can also occur in the absence of prematurity in such cases. RDS is the commonest reason for the newborn having to be admitted to a neonatal intensive care unit and also the commonest cause of death in the first week of life.
The clinical significance of a growing population of overweight women is enormous because not only can this compromise their overall reproductive performance but it also compounds the risk of chronic medical conditions such as diabetes, coronary/cerebral/peripheral vascular disease and thus compromises life expectancy as well as the quality of life. As such, being overweight represents an overall life hazard that should be addressed by the medical profession as well as by society as a whole. The answer is surely not a simple one but the solution does not lie in dieting alone (which rarely is of sustained benefit). Instead it requires an overall modification in lifestyle.
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.
•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 Aproach
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
•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?
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
•Preimplantation Genetic Testing (PGS) in IVF: It Should be Used Selectively and NOT be Routine.
•Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
•PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
•Implications of “Empty Follicle Syndrome and “Premature Luteinization”
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
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.
Geoff Sher
Dear Dr.Sher.
we have had 2 failed IVF now.
im 33 years old and my amh is 19 and my fsh is 6. Healthy in general.
My husband is 45 and revised his sterilization 1,5 years ago.
His sperm test shows 11 millions sperm per ml and 40% mobility.
last IVF they retrived 8 mature eggs and 2 immature but none fertilized with normal IVF.
i had a short protocol with menopur.
what is your thoughts to this?
Do you think we should consider ICSI next time?
All the best
gunn
Respectfully, I do not use Menopur in >75U a day dosages for IVF. It contains hCG/LH and in too large a dosage, can in my opinion have a deleterious effect on egg quality. We do100% ICSI in my practice.
Intracytoplasmic Sperm Injection ICSI which began in 1992 as a treatment for severe male factor infertility, involves the direct injection of a single sperm into each egg under direct microscopic vision.
Soon after the turn of the 20th century it was reported that while the diagnosis of a male factor infertility had remained static, the use of ICSI had markedly increased and that indications for ICSI had expanded from solely male infertility (for which it had primarily been developed) to a wide variety of other indications such as “unexplained infertility, unexplained IVF failure, polycystic Ovarian Syndrome (PCOS) and cases where the woman’s eggs had become more resistant to conventional fertilization. ICSI was also being used in cases where sperm was absent (or virtually absent) from the ejaculate due to congenital or traumatic or medically acquired obstruction of the main collecting ducts (vasa deferentia), testicular failure and in cases where for traumatic, neurologic, or psychologi reasons (impotency) no semen/sperm was being ejaculated. In such cases, sperm obtained through Testicular Sperm Extraction (TESE), or aspiration (TESA) was being successfully used for ICSI. Today in the United states more than 70% of all IVF fertilizations are being conducted using ICSI with high fertilization and pregnancy rates being reported, regardless of sperm concentration, motility or morphology.
Clearly ICSI is increasingly replacing conventional insemination due to its many benefits and lack of definable drawbacks. In fact, pregnancy rates achieved by this method of fertilization are at least as high as those of conventional IVF performed in cases of non-male-factor infertility. Indeed, ICSI is associated with high fertilization and pregnancy rates regardless of sperm concentration, motility or morphology.
Notwithstanding, the above, the proposition that ICSI be preferentially used as the routine method for fertilizing eggs in IVF continues to meet with resistance. Die hards argue that about 1-3% of pregnancies resulting from ICS are associated with congenital developmental and genetic defects that affect the offspring. They cite conditions such as *Beckwith-Wiedemann syndrome, *Angelman syndrome, *hypospadias, sex chromosome abnormalities, a slightly increased miscarriage rate and the fact that male offspring resulting fom ICSI pregnancies are themselves at risk of subsequently developing male infertility in later life.
What you do not often hear from nay-sayers is that those studies that site the above mentioned risks do not distinguish between cases where ICSI is/was mandated for male infertility )and cases where ICSI is/was done for other (non-male infertility) reasons. If this was done, what in my opinion would emerge is that the above mentioned birth defects and developmental conditions are largely confined to the underlying male factor for which ICSI was indicated and are not due to the ICSI process itself. In fact a relatively recent study performed in Sweden demostrated this well. Here 542 children who were conceived naturally were compared with 941 children conceived through IVF (440 by conventional IVF & 541via ICSI) The babies/children were assessed at birth and during the first 5 years of life: The findings revealed that while the incidence of birth and developmental defects was indeed higher in ICSI babies, this only applied to cases where ICSI had been done for male infertility. It did not apply to cases where ICSI was done in the absence of male factor infertility.
Another very important consideration that supports the routine fertilization of eggs by ICSI is the fact that good quality IVF relies heavily on an ability to adequately assess egg maturation immediately following egg retrieval. To do this requires removal of layers of cumulus oophoris (CO) cells that cover the egg envelopment (zona pellucida). Only after the CO is stripped can the 1st polar body (PB-1) which is located immediately under the zona pellucida be identified and it is the presence of PB-1 signifies that indicates that the egg has gone through meiosis (reproductive division) and is thus mature (M2) and overwhelmingly, successful fertilzation and viable embryo development requires that the fertilized egg was mature (M2). This assessment for the presence of PB-1 cannot be reliably done without first removing the cumulus oophoris cells attached to the outer surface of the zona pellucida. The problem is that stripping the cumulus oophoris cells away, markedly reduces natural fertilization potential, leaving ICSI as the only alternative by which to subsequently achieve viable embryo propagation. The only way by which to avoid fertilization by ICSI would be to bypass the important step of assessing egg maturation and this in my opinion would compromize IVF outcome significantly. Thus optimization of the entire IVF process virtually mandates routine ICSI in IVF.
For the above reasons, I proudly count myself among a growing majority of IVF practitioners who support the routine use of ICSI for all IVF patients
*Angelman syndrome is a complex genetic disorder characterized by delayed development, intellectual disability, speech impairment, and problems with movement and balance (ataxia). Most cases are not inherited, particularly those caused by a deletion in the maternal chromosome 15 or by paternal uniparental disomy. These genetic changes are random events that take place during the formation of reproductive cells (eggs and sperm) or in early embryonic development.
*Beckwith-Wiedemann syndrome is a congenital growth disorder that causes large body size, large organs, and other symptoms. t results from a defect in the genes on chromosome 11. About 10% of cases can be passed down through families.
*Hypospadias: Hypospadias is a condition where the opening isn’t at the tip of the penis. Instead, it is located any place along the underside of the penis.
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.
•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 Aproach
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to 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.
Hello Dr. Sher,
We are currently nearing the end of out third cycle; one full IVF fresh in which we transferred one embryo and it ended in a chemical, the second being and FET which was a complete failure and this final time was another FET again transferring two embryos. My first beta was 31, the second 48 hours later was 81- so we were optimistic, although low our numbers were doubling as they should. Yesterday, however my third beta (a week after the second) came back at 68. I am devastated, but more than that I am frustrated. I have “no issues”, at least none that have been identified, my husband has low count and decent motility. My lining was where it should be at the first ultrasound, and my embryos were expanding right before the transfer. My clinic doesn’t grade our embryos, or at least they don’t tell me what it is if they do, they simply tell me we had good embryos- all made it to blast. This last FET was the last of our embryos, we would have to do another full cycle for our fourth attempt. Any input? Thoughts? Suggestions? My Dr. isn’t very personable, or easy to talk to and chalked the last two failures up to “flukes”. I understand it is far from an exact science, but I need more to go on than simply “flukes.” I’m considering getting another opinion from another RE, maybe a set of fresh eyes or a different approach would be helpful? I am 31 and my Husband is 37, I’m not ready to give up. Thank you.
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.
•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 Aproach
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•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)
•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:
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to 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.
Hello Dr. Sher,
I have PCOS and have been trying for #2 for over two years now. I am on my first cycle of letrozole 5mg days 4-8. I went in for a second ultrasound today (CD14) and have one 20mm follicle and another 15mm. They grew from 15 and 12mm (CD12). My RE triggered me this AM and I am scheduled for an IUI tomorrow morning. My question is what are the chances that 15mm will also release and mature? Do follicles continue to grow after trigger? Thank you.
It is not likely that the 15mm follicle3 will ovulate.
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.
•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 Aproach
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & Con’s!
•Micro-IVF: Often Preferable to Ovarian Stimulation with or Without IUI
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.
Geoff Sher
How is immunologic implantation dysfunction treated?
I had 3 IVF failure with an egg donor.
stage 1 endometriosis
Right Salpingectomy due to rupture ectopic pregnancy.
Treatment: aspirin, multivitamins, prednisone, levotiroxine, estradiol gel, progesterone 200mg, and clexane 40mg.
Hi Morena,
Please read the articles below.Place emphasis on the articles on endometriosis and thyroid disease and its link to immunologic implantation dysfunction (IID). Thereupon read the other articles on IID below and this will address your questions. Clearly we need to talk!
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.
•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
•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)
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•Endometriosis and Infertily
•Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
•Treating Ovarian Endometriomas with Sclerotherapy.
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.