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.
In 2010 I was 34 had ivf with 17 eggs retrieved with 8 making it to blasts. Fresh cycle 2 embryos BFN. FET two months later 1 didn’t survive thaw & 3 transferred. Got pregnant with twins but one had no heartbeat shortly after hearing heartbeat. We had two remaining blasts & transferred in April 2016, bfn.
Ivf in November 2016. 13 embryos, 12 fertilizer 9 9 made to three Day & 5 to day 5.
4 sent for PGS. Two came back normal. We did an shg & mock transfer & FET in December, BFN.
Then final PGS tested blast transferred early January, BFN.
Lining was 13 triple layer, we did endo scratch.
I felt like prior to 2nd PGS tested blast we should’ve done some additional
Testing but doc thought since I’ve previously had child it is not immune issue.
I would love to continue until success but not if there is no hope.
Is there any hope?
The fact that you had a child does not totally rule out an immunologic implantation dysfunction. In fact it is quite common to see this min cases of alloimmune implantation dysfunction.
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.
Dr. Sher-
I’m in the middle of an FET cycle. I’ve had 1 successful pregnancy 16 months ago after IVF. I just started freaking out, out of no where about having a child with a disability, such as autism. Are there any studies linking IVF to Autism? Do you think this is a valid fear? Do you know the statistics of having a child with an issue using ART vs natural conception?
Thank you
Autism Spectrum Disorder (ASD) encompasses a range of conditions that most commonly affect males and are characterized by lifelong neurodevelopmental derangements manifesting as deficiencies in social interaction, verbal and nonverbal communication, and dysfunctional interests and behavioral pattern that range from social isolation, delayed speech, and repetitious movement, to Asperger’s syndrome, characterized by higher levels of cognition and social behavior.
Over a period of less than 2 decades, the incidence of diagnosed (ASD) has increased from about 1:1000 to more than 1:100. And the incidence continues to increase year by year. In fact, according to the most recent Centers for Disease Control and Prevention estimates, 1 in 68 children in the United States has ASD. This represents a significant increase from the prior estimate of 1:88, in released in 2012. The question arises as to whether this dramatic change is due increased awareness of the condition leading to over-testing and over-diagnosis and/or whether it represents a true epidemiologic phenomenon. Regardless, it is an undeniable fact that we who are actively involved in medically promoting reproduction are commonly confronted by prospective parents who are concerned that their age and reproductive performance could be associated with an increased risk that their offspring could be affected by ASD….
The relationship between infertility treatments and ASD remain a subject of heated debate. Factors such as the effects of fertility medications, fertility procedures performed, a relationship to the cause of the infertility, maternal obesity (BMI), maternal and paternal age, genetics and hormonal factors linked to fetal testosterone have all cited as possible contributing factors to the occurrence of ASD in patients seeking infertility treatment. Of interest is the emergence of evidence to suggest a possible etiologic role of the immune system in ASD. This having been said, it is as yet not possible to establish a clear relationship between infertility, its treatments, and ASD. Infertility diagnoses and treatments.
The question arises as to how/whether IVF itself increases the risk of ASD in the offspring. A relatively recent large study analyzed the birth records of 2.5 million children born in Sweden between 1982 and 2007, and after correcting for confounding variables, found there to be a very small increase in the incidence risk of intellectual impairment in the resulting children (about 4% of IVF children had physical or mental problems at birth compared with 3% of those conceived A naturally) but no link between in vitro fertilization (IVF) and ASD. This having been said, the study was somewhat flawed in the fact that the IVF births reported dated back more than 30 years when IVF technology was still in its infancy. Overall, the main message was a positive and reassuring one for patients undergoing IVF treatment
Here are a few relatively established facts regarding the occurrence of ASD.
1.Gender: ASD is more common in male offspring.
2.Obstetrical History: ASD is more common in first born babies, in multiple births, in premature and small-for-gestational-age babies, following intrauterine bleeding and fetal distress, as well as following birth asphyxia or trauma
3.Age
1.The mother’s age: The incidence of ASD increases with advancing age of the mother In fact, women over age 40Y are 51% more likely than women aged 25-29 to have a child with ASD.
2.The father’s age: Traditionally, the negative effects of the advancing “biological clock” on reproduction have been linked to women, while the question of the effect of the man’s advancing age has been largely ignored. But now, a recent study published in the magazine Nature suggests that the risk of ASD (and perhaps schizophrenia too) increases as the age of the father progresses. When the man siring the child is under 35 years of age, the risk of ASD is about 1:100, while when the man is over 50, the incidence doubles to 1:50. Consider the fact that about 1:88 children born develop ASD.
Several recent studies have shown that certain genetic mutations implicated in ASD are four times more likely to originate in the sperm than in the egg. This is probably explained by the fact that unlike women, who are born with a lifelong component of eggs, a man’s sperm are in a constant state of being generated. During the process of sperm generation, dividing precursor cells are easily susceptible to acquiring new mutations with each successive division. The finding that conditions such as ASD (and schizophrenia) can be influenced by a man’s age is likely to change the reproductive conversation, pushing it more into the mainstream. It is about time that men start to realize that it is not only women that should be worried about unduly putting off parenting. Hopefully, it will also prompt physicians to recommend to their married male patients that they begin considering their “reproductive options” sooner rather than later and that the topic be taught in medical school.
1.Genetics/Epigenetics: With identical twins, when one has ASD, the other is about 90% likely to also be so affected. In non-identical twins, the concordance rate is twenty times lower. This points strongly to a genetic link. There is new evidence that defects in epigenetic regulatory genes and in certain gene regions on chromosomes likely play a role in the development of autism. About 10% of ASD cases have definite links to genetic disorders such as Fragile X, neurofibromatosis and tuberous sclerosis which can often (although not easily) be detected through meticulous parental clinical history taking and can be diagnosed pre- and postnatal using genetic testing, ultrasound examination and by sophisticated chromosomal and DNA testing.
2.Predicting/Diagnosing ASD: It is as yet not possible to diagnose ASD through preimplantation genetic diagnosis (PGD) or through prenatal testing. Unfortunately, only a few specific gene mutations known to be linked to autism have, as yet, been identified. But this could all change in the next few years with the rapid advancement in genetic research. Recent reports have emerged of a newly found ability to isolate fetal cells from the mother’s blood, even early in pregnancy. Once sophisticated genetic testing for specific mutations evolves, it is likely that it will become possible to draw blood from the pregnant woman, isolate fetal cells, and thereby gain access to the entire fetal genome for genetic testing.
3.Preventing ASD: The risk of ASD in the offspring can sometimes be reduced by the taking of folic acid supplements (4-6mg daily) for several months prior to conception. This is especially true in cases where the mother has a form of thrombophilia (a hereditary clotting disorder) associated with MTHFR pleomorphic (most particularly those associated with the C677T variant) where such pre-conceptual folic acid supplementation could be especially beneficial.
Hope this helps!
Geoff Sher
PH: 800-780-7437
Hi Dr. Sher,
my wife (32) and me (38) have just started the eigth icsi. My wife had a raise of hcg in the first, fourth, fifth and sixth try. They were all biochemical pregnencies and the highest hcg was around 110 on day 10 after transfer. After that the hcg dropped (or it was already dropping). We are now treating with granocyte for the second time and hope this will help as it must be some kind of immunologic problem.
What are your thoughts on our situation? I habe oat 3 and my wife has no known problems. We have done all available tests for common known issues. Is there any suggestion you would give us? Should we try it wirh donor sperm maybe or is there a reasonable chance that granocyte will be the holy grail we habe been looking for? Thank you so much in advance for your thoughts on this.
Hello Dr Sher,
I was on long Lupron protocol but it turns out that during my egg retrieval I had ovulated 3 eggs based on the ultrasound appearance. Oddly my LH was only 0.4 the day of retrieval so it doesn’t look like I surged. How is it possible to ovulate then?
We should talk!
Geoff Sher
800-780-7437
Dr Sher,
What are your thoughts of fresh vs frozen embryo transfer. My RE is pushing hard for a frozen saying there’s 5-7% increased success rates.
Until about 15 years we believed that the best and safest way to cryopreserve embryos was by using a slow freezing method. What we subsequently learned was that the slow freezing process caused the formation of intracellular ice and that this, by damaging embryos and compromised their post-thaw survival as well as IVF outcome, significantly. The introduction of ultra-rapid embryo freezing (vitrification) has changed all that. With vitrification, embryos are frozen so fast that ice cannot form and as a result embryos are hardly damaged. In fact, about 90% of pre-vitrified embryos survive the freeze thaw in at least the same state of health as the day they were frozen and upon being transferred to a receptive uterus, have at the very least the same ability to propagate a viable pregnancy as they would have done, had they been transferred fresh. In fact there are many who believe that the post-FET pregnancy rate is now, perhaps even better than with fresh transfers. This is probably due to the fact that optimal hormonal preparation for FET provides the opportunity to better prepare the uterine lining for implantation than when fresh embryo transfers are done where unpredictably erratic levels of steroid hormones along with other potentially harmful byproducts of ovarian stimulation endometrial development might compromise endometrial development and receptivity. Against this background, and in the absence of prejudice, more and more IVF practitioners are freezing embryos for subsequent dispensation in FET cycles.
There are different ways to prepare the uterus for FET. Some authorities favor the use of commercially available oral estradiol products (e.g. Estrace, Progynova), while others recommend transdermal, transvaginal, or subcutaneous/intramuscular estradiol injections. The problem with oral estradiol administration is firstly that anything taken orally will upon gastrointestinal absorption, first pass through the liver (via the venous portal system) before being delivered into the systemic circulation and to the uterus. It is processed in the liver so what reaches the uterus is an altered substance and is substantially watered down. Secondly, the most commonly used form of estradiol, namely Estrace, readily metabolizes into both estradiol and estrone which could be prejudicial to optimal endometrial development. Trans-vaginal (suppositories) and trans-dermal (skin patches) administration also have drawn-backs that relate to erratic and unpredictable absorption issues. In my opinion, the optimal way to administer estrogen for endometrial development in preparation for embryo reception (FET), egg donor-IVF and gestational surrogacy) is through the twice weekly intramuscular administration of (slow release) estradiol (e.g. Delestrogen). This method of estradiol delivery allows for even absorption and is delivered directly to the uterus via the systemic circulation without having first to pass through the liver. I have advocated the use of
Delestrogen for uterine preparation exclusively for more than 20 years. Results are excellent and I see s no reason to change. Here is how I implement the treatment:
It starts with administering an oral contraceptive (OC) to the recipient. This is later overlapped with Lupron daily for 5-6 days. The oral contraceptive is then withdrawn, but the daily Lupron injections are continued until the onset of menstruation at which point the Lupron dosage is reduced and intramuscular (IM) estradiol valerate (Delestrogen) is administered every 3 days. The objective of the estradiol is to achieve and sustain an optimal plasma E2 concentration of 500pg/ml-1,000pg/ml and a 9mm endometrial lining as assessed by ultrasound examination. Intramuscular and/or intravaginal progesterone is administered daily starting about 6 days prior to the FET and continued along with twice weekly IM Delestrogen until the 10th week of pregnancy or until it has been confirmed that the patient is not pregnant.
Daily oral dexamethasone commences with the Lupron start and continues until a negative pregnancy test or until the completion of the 8th week of pregnancy. Then it is tapered down and discontinued. The recipient also receives prophylactic oral antibiotics starting with the initiation of Progesterone therapy, until the day after ET. Usually we would thaw vitrified blastocysts with the objective of having 1, 2 or 3 for transfer; depending on a couple’s stated preference. Commencing on the day following the ET, the patient inserts a vaginal progesterone suppository daily and this is continued until the completion of the 8th week of pregnancy or until a negative pregnancy test.
As an alternative regimen for women who cannot tolerate intramuscular Progesterone (PIO), we prescribe either Crinone vaginal gel or Endometrin vaginal inserts according to protocol. If you’d like to explore one of these options, talk to your physician. For blastocyst FET’s, the blood pregnancy tests are performed 13 days and 15 days after the first progesterone administration is commenced.
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
•Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting 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.