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 was scheduled to start my IVF cycle May 2016. My RE put me on BC on March 24th to control the cycle. From then until present, I have been experiencing break through bleeding and most recently, (while on the pill) started bleeding. Throughout the time, my RE had me double my dose several times to try and stop the bleeding. I have recently stopped the pill and now my RE tells me that my body is basically is in suppression from the birth control pill. My LSH level was 0. He warned that now even with injectables, I will likely not make eggs. What does this birth control suppression mean? I do not understand what is meant by “my body is producing no hormones”.
Respectfully Kayla, I do not believe that would happen. The suppressed FSH is due to the pill suppressing your hypothalamo-pituitary axis, but that in no way is a measure of how you would respond to ovarian stimulation…in my opinion.
Geoff Sher
Hi,
I just had a chemical pregnancy with my second FET cycle. My first FET also ended in a miscarriage at 7 weeks due to a faint heart beat. All of my embryos have been tested genetically, so I am not understanding why this may be occurring. My doctor told me I would have to move on to a gestational carrier and I am not ready to do this. My treatment plan was very similar both times around, so I am wondering if we are not doing enough for the baby to stick. I still have 2 embryos left, but I do not want to go through the same protocol with the same result. Have you had any experience with 2 FET miscarriages and then seeing success with the third? I am wondering if those embryos had low mitochondria? The only thing I have been diagnosed with is a low AMH, so everything else seems normal. Any advice on what protocols you would change or look at again?
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
•Recurrent Pregnancy Loss (RPL): Why do I keep losing my Pregnancies?
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting 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
•Traveling for IVF from Out of State/Country–
•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
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.
How to increase uterine lining naturally . Is there any food intake which help to increase uterine lining
Not really!
Sorry!
Geoff Sher
Sorry, I posted this on an old forum of yours and then saw a message that this was the right one to use. Here is my question:
I’m a former patient of yours who had success in my first IVF cycle. I have wonderful 2 year old twins now. Thank you!
I may be interested in a FET with one of my frozen embryos, no sooner than Summer 2017. In the meantime I am considering different born control options than the one I am using no now (progesterone-only pill, as my IVF testing by revealed MTHFR and Factor V Leiden so a combo pill is not recommended) and am wondering if the Mirena IUD would be appropriate. I am specifically concerned with 1) the details of time-frame for removal before a FET cycle – how far in advance would I have to plan for, and is having used it likely to impede my success? And 2) How likely is it to cause endometrial lining or other uterine problems? Specifically during my IVF cycle I had a very thin endometrial lining which you treated with Viagra suppositories. Will using Mirena for about a year before a FET make this problem worse?
Thanks for any advice you can give on this!
The Mirena would be fine. Just remove it one cycle before doung the FET. That should do fine!Great hearing from you.
Fondest regards.
Geoff Sher
If you had to advise between a fresh or frozen embryo transfer what would you recommend? Are the success rates the same or is one better than the other?
FET’s are at leastas successful as fresh transfers. There are circumstances where FET’s are required a (e.g. when PGS is done and time is needed to get results of genetic tets before selecting embryos for transfer) and others where FET is preferable because that is the only way to avoid hormonal compromise of the endometrium due to response to ovarian stimulation (e.g. ovarian hyperstimulation).
It is not that freezing enhances the embryo’s competency in any way. That is absurd, but rather that hormonal preparation for implantation can be better controlled in hormone replacement cycles. That implantation potential can be enhanced in FET cycles.
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.
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.