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Ask Dr. Sher- Open Forum

by Dr. Geoffrey Sher on December 1, 2015

You are not alone. Dr. Sher is here to answer your questions and support you.

If you would like to schedule a one on one Skype, telephone, or in person consultation with Dr. Sher, please fill out the form on the right and our team will get you scheduled right away.

Dear Patients,

I created this forum to welcome any questions you have on the topic of infertility, IVF, conception, testing, evaluation, or any related topics. I do my best to answer all questions in less than 24 hours. I know your question is important and, in many cases, I will answer within just a few hours. Thank you for taking the time to trust me with your concern.

– Geoffrey Sher, MD

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  • Tunde - November 19, 2017 reply

    Hello Dr Sher

    I am hoping you can provide some answers and advice on the likely cause of empty follicles on egg retrieval. I am 43 going on 44 and recently had my first IVF treatment with a short antagonist cycle starting with the birth control pill for 52 days and five days after stopping starting gonal f (Follitropin alpha) and day 6 on gonal f starting ganirelix befor triggering with Ovitrelle (HCG) 250mcg after 12 days of stimulation. I hade six follicles on egg retrieval but only two eggs were retrieved both of which fertilized but arrested on day 4.
    My RE is now recommending that I repeat the exact same cycle but without BCP, is this a good plan given the previous poor response?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 19, 2017 reply

    Frequently, when following vigorous and often repeated flushing of follicles at egg retrieval they fail to yield eggs, it is ascribed to “Empty Follicle Syndrome.” This is a gross misnomer, because all follicles contain eggs. So why were no eggs retrieved from the follicles? Most likely it was because they would/could not yield the eggs they harbored.

    This situation is most commonly seen in older women, women who have severely diminished ovarian reserve, and in women with polycystic ovarian syndrome (PCOS). In my opinion it is often preventable when an optimal, individualized and strategic protocol for controlled ovarian stimulation (COS) is employed and the correct timing and dosage is applied to the “hCG trigger shot.”

    Normally, following optimal ovarian stimulation, the hCG “trigger shot” is given for the purpose of it triggering meiosis (reproductive division) that is intended to halve the number of chromosomes from 46 to 23 within 32-36 hours. The hCG trigger also enables the egg to signal the “cumulus cells” that bind it firmly to the inner wall of the follicle (through enzymatic activity), to loosen or disperse, so that the egg can detach and readily be captured at egg retrieval (ER).

    Ordinarily, normal eggs (and even those with only one or two chromosomal irregularities) will readily detach and be captured with the very first attempt to empty a follicle. Eggs that have several chromosomal numerical abnormalities (i.e., are “complex aneuploid”) are often unable to facilitate this process. This explains why when the egg is complex aneuploid, its follicle will not yield an egg…and why, when it requires repeated flushing of a follicle to harvest an egg, it is highly suggestive of it being aneuploid and thus “incompetent” (i.e., incapable of subsequently propagating a normal embryo).

    Older women, women with diminished ovarian reserve, and those with polycystic ovarian syndrome, tend to have more biologically active LH in circulation. LH causes production of male hormone (androgens, predominantly testosterone), by ovarian connective tissue (stroma/theca). A little testosterone is needed for optimal follicle development and for FSH-induced ovogenesis (egg development). Too much LH activity compromises the latter, and eggs so affected are far more likely to be aneuploid following meiosis.

    Women with the above conditions have increased LH activity and are thus more likely to produce excessive ovarian testosterone. It follows that sustained, premature elevations in LH or premature luteinization (often referred to as a “premature LH surge”) will prejudice egg development. Such compromised eggs are much more likely to end up being complex aneuploid following the administration of the hCG trigger, leading to fruitless attempts at retrieval and the so called “empty follicle syndrome.”

    The developing eggs of women who have increased LH activity (older women, women with diminished ovarian reserve, and those with PCOS) are inordinately vulnerable to the effects of protracted exposure to LH-induced ovarian testosterone. Because of this, the administration of medications that provoke further pituitary LH release (e.g., clomiphene and Letrozole), drugs that contain LH or hCG (e.g., Menopur), or protocols of ovarian stimulation that provoke increased exposure to the woman’s own pituitary LH (e.g., “flare-agonist protocols”) and the use of “late pituitary blockade” (antagonist) protocols can be prejudicial.

    The importance of individualizing COS protocol selection, precision with regard to the dosage and type of hCG trigger used, and the timing of its administration in such cases cannot be overstated. The ideal dosage of urinary-derived hCG (hCG-u) such as Novarel, Pregnyl and Profasi is 10,000U. When recombinant DNA-derived hCG (hCG-r) such as Ovidrel is used, the optimal dosage is 500mcg. A lower dosage of hCG can, by compromising meiosis, increase the risk of egg aneuploidy, and thus of IVF outcome.

    There is in my opinion no such condition as “Empty Follicle Syndrome.” All follicles contain eggs. Failure to access those eggs at ER can often be a result of the protocol used for controlled ovarian stimulation.

    In my opinion, the protocol used for ovarian stimulation, against the backdrop of age, and ovarian reserve are the drivers of egg quality and egg quality is the most important factor affecting embryo “competency”.

    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”.

    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
    • Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.

    If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .

    *FYI
    The 4th edition of my book,”In Vitro Fertilization, the ART of Making Babies” is now available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

    Geoffrey Sher MD

  • Tahlia - November 19, 2017 reply

    Dr Sher, what is your live birth rate for women aged 40-41 using A/ACP (not A/ACEP)? And do you have a refund program?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 19, 2017 reply

    The success rate without PGS is probably around 20% and with PGS at least double that! we have a variety of plans…some (I believe, but am not certain) do include a refund. Please call 7020892-9696 and ask the administrative people.

    Geoff Sher

  • Tahlia - November 19, 2017 reply

    Hi Dr Sher, I know you like to use BCP with an agonist overlap, but what is your personal opinion with the mid-luteal Lupron cycle where you inject lupron on day 21 of your cycle and then start stimulation on day 1 or 2 of menstrual cycle? What, in your view, are the disadvantages of this cycle, which does not use BCP and does not reduce the dose of lupron? Do you use this at all?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 19, 2017 reply

    I think it is another good way to go!

    Geoff Sher

  • Tonya B - November 19, 2017 reply

    Dr. sher,
    My 28 year old daughter and husband have used donor sperm. 11 blastocysts
    Fresh transfer, 2 put back=bfn
    1st fet, 2 put back=bfn
    2nd fet, 2 put back= chemical
    3rd fet scheduled for Wed.
    RE said baby aspirin won’t hurt. Do you agree?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 19, 2017 reply

    Respectfully, I do not prescribe BA to my IVF patients. It increases the bleeding time such that with the embryo transfer and insertion of the transfer catheter into the uterus, local endometrial abrasion can lead to concealed bleeding , thereby reducing implantation potential.Bedsides, there is no proven evidence of efficacy.

    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
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • 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

    If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .

    *FYI
    The 4th edition of my newest book ,”In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

    Geoffrey Sher MD

  • Lyndsey Sheehan - November 18, 2017 reply

    Hello Dr. Sher
    I just did my 7th embryo transfer, an FET. My fifth transfer ended in a loss at 18w5d due to potters syndrome. My next transfer ended in an early MC, now for this one; my betas are rising but on by a little bit. 11/14 beta was 75, 11/16 beta was 105 and on 11/18 beta is now 135.
    Should I be preparing for another Miscarriage? watching for ectopic?
    We’ve done so much testing.. I have PCOS and the husband is all good. I’ve had an HSG, SIS, Family prep genetic screening, hysteroscopy– any suggestions for other tests?
    All of our embryos are great quality, PGS tested and usually hatching by transfer day.
    Please help!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 19, 2017 reply

    Don’t be misled into believing that because you went to 18 weeks (due to “Potter Syndrome”) that this is purely an egg/embryo quality 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
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • 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

    If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .

    *FYI
    The 4th edition of my newest book ,”In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

    Geoffrey Sher MD

    .

  • Darleen - November 18, 2017 reply

    Hi Dr Sher, can 5iu of lupron really prevent an LH surge and potentially early ovulation on an IVF cycle? I see you recommend starting with 10iu then sropping to 5iu. I showed my RE and she said 5iu was very risky as she disn’t think it could prevent a surge. Have you had any patients who gave surged through 5iu of lupron when you halved the dose?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 19, 2017 reply

    Yes, it can and does prevent premature ovulation…all other measures taken being optimal. But remember, when it comes to patients with DOR (who are the ones most likely to experience premature luteinization I use the agonist/antagonist conversion protocol (A/ACP) where I switch from 10U Lupron at the on set of bleeding, to an antagonist (Ganirelix or Cetrotide)….see below.

    GnRH antagonists (e.g. Ganirelix, Cetrotide, and Orgalutron) are currently used with many controlled ovarian stimulation (COS) protocols. The conventional approach is to administer 250mcg antagonist, daily starting from the 6th-8th day after commencing ovarian stimulation with gonadotropins. This traditional approach is in my opinion, best suited to younger patients who have normal ovarian reserve (AMH>2.0ng/ml or 15pmol/L) and are “good responders” to COS, provided that the stimulation cycle is launched with a spontaneous menstrual cycle and is not launched coming off a birth control pill (BCP) or following prolonged premenstrual hormonal suppression (see Use of BCP in IVF”, elsewhere on this blog). However, this approach can in my opinion be decidedly disadvantageous when used in older women (>39y), women with diminished ovarian reserve (DOR) or women with polycystic ovarian syndrome (PCOS) who all tend to have increased LH bioactivity.
    Background information: An important role of LH is to promote male androgen hormone (testosterone, androstenedione and DHEA) production by ovarian connective tissue (stroma or theca) that surrounds follicles. While androgens (predominantly testosterone) represent the building blocks from which follicle granulosa cells manufacture estrogen and are thus essential for optimal follicular growth and egg development, too much LH activity can lead to over-production/exposure to ovarian androgens which might compromise follicular/egg development. Accordingly, when it comes to older women and those DOR and PCOS who tend to have excessive LH-induced ovarian testosterone, it is (in my opinion) essential to maintain LH activity at a subliminal level. Thus LH suppression needs to be in place from the very start of COS…not much later as when antagonist suppression is commenced 6-8 days into the COS process. Accordingly, I believe that GnRH antagonist treatment should be commenced from the very initiation of ovarian stimulation…and that is the concept upon which the agonist/antagonist conversion protocol (A/ACP) is based….see below.
    Bear in mind that the main reason for using antagonist suppression is to avoid the “Premature LH Surge”. This is a condition where high ovarian LH activity propagates androgen-induced “follicular exhaustion” and egg dysmaturity. The term “premature LH surge” is a misnomer since it does not involve a sudden “surge” or sporadic rise in LH. In actuality it occurs as a steady rise in LH activity (a “staircase effect”) which elicits a progressive increase in ovarian stromal androgens that ultimately exhausts follicle development and compromises egg “competency”. A more accurate term might be “premature luteinization.” Such poorly developed eggs will often respond to the hCG trigger by becoming aneuploid (a numerical chromosomal abnormality
    Thus, trying to avoid “premature luteinization” by administering GnRH antagonist 6-8 days into the COS cycle, is like” shutting the gate after the horse has already left the stable”.
    The long pituitary down-regulation COS protocol:
    Here, administration of a GnRH-agonist (Lupron, Superfact, and Buserelin) several days before COS is initiated, expunges all LH from the pituitary gland, exhausting it of reservoired LH. Thereupon, agonist administration is continued until the hCG “trigger”. In this way, developing follicles and eggs are protected throughout COS, from over-exposure to LH-induced androgens…thereby avoiding “premature luteinization”. In my opinion, this approach is ideally suited to younger women who have normal LH, normal or increased ovarian reserve (e.g. those with PCOS) and those who have DOR. The downside of this approach is that the GnRHa (Lupron/Buserelin) can competitively bind with ovarian follicle stimulating hormone (FSH) receptors and suppress ovarian response to gonadotropins, something that is more likely to occur with older women and those who have DOR. I introduced the Agonist/Antagonist Conversion Protocol (A/ACP) more than 15 years ago to try and counter this effect.
    The agonist/antagonist conversion protocol (A/ACP):
    With the A/ACP, GnRH antagonist (Ganirelix, Cetrotide, and Orgalutron) is administered by daily injection from the onset of COS. The A/ACP COS-cycle is launched with the woman coming off a monophasic birth control pill that was administered starting in the 1st 5 days of the preceding cycle and continued for at least 10 days. The BCP is then overlapped with an agonist (e.g. Lupron/buserelin) for three days, whereupon the BCP is stopped and the agonist (Lupron/buserelin) is continued until the onset of menstruation. At or around this point, the agonist (Lupron/Buserelin) is supplanted by an antagonist (Cetrotide/Ganirelix/Orgalutron) and concurrently COS is initiated using an FSH-dominant bias (mainly Follistim/Gonal-F/ Puregon + a small dosage of a menotropins such as Menopur). The combined antagonist/gonadotropin therapy is continued until the hCG trigger. For the reasons cited above, I prescribe some form of the A/ACP for my older IVF patients and those with DOR. ]
    A/ACP with estrogen priming: The A/ACP can be modified for women with very severe DOR through incorporation of “estrogen priming”. We have reported on the fact that the administration of intramuscular estradiol starting about a week prior to commencement of COS. This often markedly enhances ovarian response (presumably by “estrogen priming” enhancing the sensitivity of ovarian FSH-receptors).
    There is one draw-back to the use of the A/ACP. This is the fact that prolonged administration of GnRH antagonist throughout the stimulation phase of the COS cycle compromises the predictive use of serial plasma estradiol measurements as an indication of ovarian response to COH. The blood estradiol levels tend to be much lower in comparison with cases where GnRHa alone is used.The reason for the lower blood concentration of estradiol seen with prolonged exposure to GnRH-antagonist might be due to the result of subtle, antagonist-induced alterations in the configuration of the estradiol molecule, such that currently available commercial test used to measure estradiol levels are rendered less sensitive/specific. Accordingly, when the A/ACP protocols are employed, we rely much more heavily on the measurement of follicle growth by ultrasound than on the estradiol levels. Because of this downside, I refrain from using this approach in “high responders” who may be at risk of developing of severe ovarian hyperstimulation syndrome (OHSS) and in whom the accurate measurement of plasma estradiol plays a very important role in the safe management of their COS cycles.

    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.
    • 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

    If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .

    *FYI
    The 4th edition of my newest book ,”In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

    Geoffrey Sher MD

    zt

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 19, 2017 reply

    Yes, it can and does prevent premature ovulation…all other measures taken being optimal. But remember, when it comes to patients with DOR (who are the ones most likely to experience premature luteinization I use the agonist/antagonist conversion protocol (A/ACP) where I switch from 10U Lupron at the on set of bleeding, to an antagonist (Ganirelix or Cetrotide)….see below.

    GnRH antagonists (e.g. Ganirelix, Cetrotide, and Orgalutron) are currently used with many controlled ovarian stimulation (COS) protocols. The conventional approach is to administer 250mcg antagonist, daily starting from the 6th-8th day after commencing ovarian stimulation with gonadotropins. This traditional approach is in my opinion, best suited to younger patients who have normal ovarian reserve (AMH>2.0ng/ml or 15pmol/L) and are “good responders” to COS, provided that the stimulation cycle is launched with a spontaneous menstrual cycle and is not launched coming off a birth control pill (BCP) or following prolonged premenstrual hormonal suppression (see Use of BCP in IVF”, elsewhere on this blog). However, this approach can in my opinion be decidedly disadvantageous when used in older women (>39y), women with diminished ovarian reserve (DOR) or women with polycystic ovarian syndrome (PCOS) who all tend to have increased LH bioactivity.
    Background information: An important role of LH is to promote male androgen hormone (testosterone, androstenedione and DHEA) production by ovarian connective tissue (stroma or theca) that surrounds follicles. While androgens (predominantly testosterone) represent the building blocks from which follicle granulosa cells manufacture estrogen and are thus essential for optimal follicular growth and egg development, too much LH activity can lead to over-production/exposure to ovarian androgens which might compromise follicular/egg development. Accordingly, when it comes to older women and those DOR and PCOS who tend to have excessive LH-induced ovarian testosterone, it is (in my opinion) essential to maintain LH activity at a subliminal level. Thus LH suppression needs to be in place from the very start of COS…not much later as when antagonist suppression is commenced 6-8 days into the COS process. Accordingly, I believe that GnRH antagonist treatment should be commenced from the very initiation of ovarian stimulation…and that is the concept upon which the agonist/antagonist conversion protocol (A/ACP) is based….see below.
    Bear in mind that the main reason for using antagonist suppression is to avoid the “Premature LH Surge”. This is a condition where high ovarian LH activity propagates androgen-induced “follicular exhaustion” and egg dysmaturity. The term “premature LH surge” is a misnomer since it does not involve a sudden “surge” or sporadic rise in LH. In actuality it occurs as a steady rise in LH activity (a “staircase effect”) which elicits a progressive increase in ovarian stromal androgens that ultimately exhausts follicle development and compromises egg “competency”. A more accurate term might be “premature luteinization.” Such poorly developed eggs will often respond to the hCG trigger by becoming aneuploid (a numerical chromosomal abnormality
    Thus, trying to avoid “premature luteinization” by administering GnRH antagonist 6-8 days into the COS cycle, is like” shutting the gate after the horse has already left the stable”.
    The long pituitary down-regulation COS protocol:
    Here, administration of a GnRH-agonist (Lupron, Superfact, and Buserelin) several days before COS is initiated, expunges all LH from the pituitary gland, exhausting it of reservoired LH. Thereupon, agonist administration is continued until the hCG “trigger”. In this way, developing follicles and eggs are protected throughout COS, from over-exposure to LH-induced androgens…thereby avoiding “premature luteinization”. In my opinion, this approach is ideally suited to younger women who have normal LH, normal or increased ovarian reserve (e.g. those with PCOS) and those who have DOR. The downside of this approach is that the GnRHa (Lupron/Buserelin) can competitively bind with ovarian follicle stimulating hormone (FSH) receptors and suppress ovarian response to gonadotropins, something that is more likely to occur with older women and those who have DOR. I introduced the Agonist/Antagonist Conversion Protocol (A/ACP) more than 15 years ago to try and counter this effect.
    The agonist/antagonist conversion protocol (A/ACP):
    With the A/ACP, GnRH antagonist (Ganirelix, Cetrotide, and Orgalutron) is administered by daily injection from the onset of COS. The A/ACP COS-cycle is launched with the woman coming off a monophasic birth control pill that was administered starting in the 1st 5 days of the preceding cycle and continued for at least 10 days. The BCP is then overlapped with an agonist (e.g. Lupron/buserelin) for three days, whereupon the BCP is stopped and the agonist (Lupron/buserelin) is continued until the onset of menstruation. At or around this point, the agonist (Lupron/Buserelin) is supplanted by an antagonist (Cetrotide/Ganirelix/Orgalutron) and concurrently COS is initiated using an FSH-dominant bias (mainly Follistim/Gonal-F/ Puregon + a small dosage of a menotropins such as Menopur). The combined antagonist/gonadotropin therapy is continued until the hCG trigger. For the reasons cited above, I prescribe some form of the A/ACP for my older IVF patients and those with DOR. ]
    A/ACP with estrogen priming: The A/ACP can be modified for women with very severe DOR through incorporation of “estrogen priming”. We have reported on the fact that the administration of intramuscular estradiol starting about a week prior to commencement of COS. This often markedly enhances ovarian response (presumably by “estrogen priming” enhancing the sensitivity of ovarian FSH-receptors).
    There is one draw-back to the use of the A/ACP. This is the fact that prolonged administration of GnRH antagonist throughout the stimulation phase of the COS cycle compromises the predictive use of serial plasma estradiol measurements as an indication of ovarian response to COH. The blood estradiol levels tend to be much lower in comparison with cases where GnRHa alone is used.The reason for the lower blood concentration of estradiol seen with prolonged exposure to GnRH-antagonist might be due to the result of subtle, antagonist-induced alterations in the configuration of the estradiol molecule, such that currently available commercial test used to measure estradiol levels are rendered less sensitive/specific. Accordingly, when the A/ACP protocols are employed, we rely much more heavily on the measurement of follicle growth by ultrasound than on the estradiol levels. Because of this downside, I refrain from using this approach in “high responders” who may be at risk of developing of severe ovarian hyperstimulation syndrome (OHSS) and in whom the accurate measurement of plasma estradiol plays a very important role in the safe management of their COS cycles.

    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.
    • 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

    If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .

    *FYI
    The 4th edition of my newest book ,”In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

    Geoffrey Sher MD

    zt

  • Amy - November 18, 2017 reply

    Hi doctor,
    I’m 42. My fsh was 25 amh 0.03 and estradiol <5 .i did ovarian rejuvenation recently my amh 2 weeks post prp is 0.36 fsh 1.5 and esteadiol 119 .any idea of what's going on with me.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 19, 2017 reply

    In my opinion, there is no such thing as effective ovarian rejuvenation. I thin k one of the two AMH tests was inaccurate. Hopefully it was the 1st one ().03ng/ml).

    In my opinion, the protocol used for ovarian stimulation, against the backdrop of age, and ovarian reserve are the drivers of egg quality and egg quality is the most important factor affecting embryo “competency”.
    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”.
    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.

    If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .

    *FYI
    The 4th edition of my book,”In Vitro Fertilization, the ART of Making Babies” is now available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

    Geoffrey Sher MD

  • Cybill Morgan - November 18, 2017 reply

    Good morning Dr. Sher.
    I am a 45 yr old , living in PA, who wants to become a GC (gestational carrier) for a married couple in CA. This couple and I have matched with each other and they’ve expressed that they want ME to be their GC. I have 5 children, all born at term. It seems like there are no clinics or RE doctors who’s age limits go that high. I am very healthy, in shape , BMI 24.3, I’ve been cleared psychologically and also by my perinatologist. However, because I’ve been diagnosed with an incompetent cervix (which is due to a laser cone bx) no one will even consider it. My perinatologist, who has taken care of me for the last 22 yrs has cleared me because I have never gone into preterm labor and never had any restrictions while pregnant. They intended parents know everything about my pregnancies and they still want to move forward with me. My perinatologist is willing to send a letter and have a phone consultation with an RE who will consider evaluating me first before turning me away. Would you consider consulting with me. I’m even willing to travel. I really want to help this couple

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 19, 2017 reply

    Age is a factor but not the only consideration. If you have had a LEEP procedure and thereafter nhad a full term pregnancy with or without a cervical cerclage that should not disqualify you either. Each case needs to be evaluated on its own merit. So subject to a thorough medical due diligence as well as a willingness after full medical disclosure of both you and the intended parents to sign off on the potential risks, I would be willing to consider your candidacy.

    If you are interested in, I urge d the intended parents to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You or they, can also reach Julie by phone or via email at 702-533-2691/ Julied@sherivf.com or can also apply online at http://www.SherIVF.com .
    *FYI

    The 4th edition of my newest book ,”In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

    Geoff Sher

    Geoff Sher after f and the intended parents are willing to take the risk

  • Trisha - November 18, 2017 reply

    Hi Dr Sher, today I had a scab which found a 27mm follicle on legt ovary and 17, 20 and 21mm follicles on right ovary. But today is cycle day 5 of a natural cycle. What is going on here? My day 3 estrogen was 131 and LH was 1.1. Sonographer and doctor confirmed none of them are cysts.. is this what happens in women with DOR? What do I makd if this? If I normally ovulate on cd14, these follicles are going to end up being > 30mm.. Surely this is not good?? I’m not on any stimulation at all..

    Trisha - November 18, 2017 reply

    I should add that this cycle follows a failed IVF antagonist cycle.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 18, 2017 reply

    Copy!

    Geoff Sher

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 18, 2017 reply

    Respectfully, this is an hormonally dysfunctional cycle and the large follicles so early on are becoming “cystic”. It might not happen again. It is more common after a prior cycle of stimulation and is one of the reasons I have my patients rest a full cycle after being stimulated, before undergoing another stimulation.

    Geoff Sher

    Trisha - November 18, 2017 reply

    Thanks Dr Sher. Are you saying that those follicles may not contain eggs?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 19, 2017 reply

    Some might do but if so they will be”incompetent”.

    Geoff Sher

  • Kara - November 18, 2017 reply

    Quick question. Do you know of any link between undiagnosed celiac disease and NTD?
    I have not been able to conceive for over 4 years with IVF. Finally got pregnant this summer and baby was diagnosed with anencephaly at 16 weeks. I’m a very healthy eater and took prenatal vitamins with 1000mcg daily. I know I do not absorb B12 well, as I have been on monthly injections for years now. Do you ever test for celiac?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 18, 2017 reply

    I am not aware of such a link…have not heard of it!

    Geoff Sher

  • Talia - November 18, 2017 reply

    Hi Dr Sher, it has been suggested that taking natural progesterone (Prometrium) orally along with vaginal progesterone pressaries during the luteal phase helps avoid early recruitment of follicles. Is this true?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 18, 2017 reply

    Not to my knowledge!

    Geoff Sher

  • Joelle - November 17, 2017 reply

    Hi Dr Sher , I have frozen embryos in a lab in different state from where I live.
    I found out I can transfer them and do the Fet in different clinic close to where I live now , is about 6 hours flight difference, I want to ask you if do you think it is safe to the embryos to do that . Or do you think it’s better to do the fet there ! All I want is to succeed, thank you

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 18, 2017 reply

    Frozen embryos can travel quite safely.

    Geoff Sher

  • Niki - November 17, 2017 reply

    Dear Dr Sher ,
    I have left with 2 frozen embryos, want to ask you if you recommend to transfer both of them together, or to try one embryo at a cycle .
    I’m asking because I don’t want to to have twins . But from the other side I want to do the best to have a child . And in the past I tried one cycle with 2 embryos Fet , it’s didn’t work . Than second time I transferred also 2 embryos fet and I have one child from it ,thanks god .
    Please advice me what to do , I appreciate your time and efforts to answer me

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 18, 2017 reply

    The overall cumulative chance of success is not associated with how many embryos are transferred. It may take longer (>1 try) but in the end it is “embryo competency” that counts. So…you can transfer 1 at a time with the same overal chance of success!

    Good luck!

    Geoff Sher

  • Tiffanie - November 17, 2017 reply

    First off, thank you so much for your invaluable resources to the fertility community. Your blog posts and responses to questions are filled with a plethora of knowledge, so thank you! Also, the question I have is what (if any) detrimental effect could an elevated level of DHEA-S have during a FET? Could it cause implantation failure and/or early loss (i.e., chemical pregnancy)? If pregnancy is achieved, could it have a negative impact on the pregnancy and development of the fetus? Would you recommend the use of Dexmethesone to help address this? Thanks in advance!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 17, 2017 reply

    Elevated DHEAS points to a increased/and possibly excessive male hormone production by the adrenal gland ,,,which could affect both egg development and uterine receptivity.could compromise the uterine lining and I would treat this with steroids regardless of whether for a fresh or frozen cycle.

    Geoff Sher

  • katy - November 17, 2017 reply

    Hi Dr. Sher,

    Why do I always have 10mm follicle during my baseline appointment for IVF. My AMH is 0.36 and FSH 4.5-6.7. I am currently on Famara/Menopur/GonalF and HGH, earlier I was on BCP/GonalF/Menopur and Clomid/Menopur/Follistim. All three time, I had 10mm follicle at baseline and only my one ovary produced 2 eggs. Is there a better protocol for me? Would priming help?

    Thanks
    Katy

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 17, 2017 reply

    The 10mm baseline follicle is irrelevant. You clearly have severely diminished ovarian reserve.

    In my opinion, the protocol used for ovarian stimulation, against the backdrop of age, and ovarian reserve are the drivers of egg quality and egg quality is the most important factor affecting embryo “competency”.
    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”.
    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.

    If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .

    *FYI
    The 4th edition of my book,”In Vitro Fertilization, the ART of Making Babies” is now available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

    Geoffrey Sher MD

  • viktorija mile - November 16, 2017 reply

    my name is viktorija..

    I have hashimoto.. I don’t want this for my kids at any cost…. I am hypothryoid.

    I got this email from another net fertility source.

    I wanted to know the risk for inheretance to my baby. my siblings sisters have hashimoto and mom.

    I can chose PGD for male baby.. but I was told chances are higher than 50%. since 50 of my genes get mixed with 50% of genes from my husband.. I was told chances are high.

    So my second option was donor egg to avoid this. This is more realistic option.

    But I talked to few doctors, i had one say me as a mother my anti bodies pass the placenta and can still have adverse effect.

    I had one endo tell me there is no effect, and another tell me i need to take PTU or MCI to stop the antibodies..

    To give the donor egg baby develop healthy thyroid. Which one is it ?

    I was given your clinic, I want to know the cost for the second option with the donor egg..

    IS the risk the same with donor egg? Is the baby under attack in those 9 months thru the placenta?

    I know I have to have TSH below 2.5, I currently take T3 Eurothyroxin 100mg. I might have to up that during pregnancy..

    But even with TSH controlled What are the risks?

    , do i have to take medicine blockers? how does it work?

    If the risk is the same why do donor egg?

    I had few endocrinologist doctors give me different answers?

    Sincerely,
    Viktorija @ MIle Sambevski

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 16, 2017 reply

    There is no way without doing egg donation to eliminate this risk and it can be genetically transmitted.

    Geoff Sher

  • Gertrude - November 16, 2017 reply

    How would the use of Synarel help with obtaining trilaminar lining?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 16, 2017 reply

    I would not use Synarel!

    Please set up a consultation to discuss!

    Geoff Sher
    800-780-7437

  • Tanya - November 16, 2017 reply

    Dr Sher do you cycle women back to back on your preferred agonist antagonist conversion protocol? Is there any harm in doing this or is it best to wait a month to allow your ovaries to recover after the first stim cycle?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 16, 2017 reply

    I do not do back-to back fresh stimulation cycles. I require at least 1 month rest between.

    Geoff Sher

  • Trisha - November 16, 2017 reply

    Dr Sher, please, I need to understand my day 3 levels after a failed ivf cycle. I had Ovidrel booster during the 2ww and wondering if it’s the Ovidrel that has caused my day 3 FSH to be 5.9, LH is 1.1 and estradiol is 131 pg/ml! Are these normal levels coming off an IVF cycle or should all the meds be out of my system by now to reveal the correct day 3 levels? Just curious as LH is very low and estrogen very high! I know Ovidrel increases estrogen as well as progesterone so wondering if it’s the effect of Ovidrel causing elevated estrogen.. I’m 40 and AMH is 0.95.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 16, 2017 reply

    You need the estradiol to be below 70pg/ml to best interpret the FSH and LH accurately. This having been said, I do not think this has anything to do with a residual Ovidrel effect!

    Good luck!

    Geoff Sher

  • Anne - November 16, 2017 reply

    Hi Dr Sher,
    I have to thank you for your encouraging advice. I reached out to you several months ago about some abnormal embryos I had. They were not mosaic but you said there might be a chance of pregnancy with two of them. So two weeks ago we implanted them and today 13days post ovulation my HCG was 252!! I was dumbfounded. I couldn’t believe they actually stuck let alone there is a possibility of twins. But now I live in utter fear that at any moment for the next 8 months I could miscarry. What miscarriage rates have you seen with abnormal embryos that resulted in a pregnancy. These were not even mosaic. Thank you giving me the courage to do this and all your research.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 16, 2017 reply

    Congratulations Anne! Unfortunately, there is not enough data to provide statistics. All you can do is wait until the 8-12th week and do chorionic villus sampling (CVS). This will be definitive. My hope is that this will turn out to be a healthy pregnancy.Please keep me in the loop!

    Geoff Sher

  • Layla Jameson - November 16, 2017 reply

    Hi Dr. Sher,
    I am 34 years old and just had my egg retrieval on Monday. I am doing A co-IVF cycle so my female partner can carry my eggs. My AMH was considered to be very good according to my doctor and I responded well to the medication. I was on gonal-f 150 and 1 powder of menopur for a few days and then it was increased to 2 powders and 0.25 centrotide for 3 more days (in addition to the gonal-f). I was on the stimms for 8 days total and triggered on day 9 with 40 units of Lupron and 1000 kIU of HCG. My E2 was at 2607 the morning of the trigger. I was told that Lupron was added for fear of hyper stimulation. At retrieval, they retrieved 16 eggs and 15 were mature. We were told that only 4 of the 15 eggs fertilized. We used sperm donor from a reputable bank so I imagine the sperm was not the issue. Can you please advise why we had such a low fertilization rate? At 34 years old and after hearing that 15 eggs were mature, I’m naturally concerned and confused as to the low fertilization rate of 37.5%. Is there hope to achieve a better fertilization rate in the future or does it indicate poor quality eggs? Additionally, could the protocol be changed to increase quality/fertilization rates somehow? I was told all my levels and numbers looked very good. We are awaiting day 6 to see if the embryos progress, but feeling concerned and looking for any expertise.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 16, 2017 reply

    I believe triggering with Lupron to be suboptimal.

    Ideal egg development sets the scene for optimal egg maturation that occurs 36-42h prior to ovulation or egg retrieval. Without prior optimal egg development (ovogenesis), egg maturation will be dysfunctional and most eggs will be rendered “incompetent” and unable upon fertilization to propagate viable embryos. In IVF, optimal ovogenesis requires the selection and implementation of an individualized approach to controlled ovaria stimulation (COS). Thereupon, at the ideal time, maturational division of the egg’s chromosomes (i.e. meiosis) is “triggered” through the administration of hCG or an agonist such as Lupron, which induces an LH surge. The, dosage and timing of the “trigger shot” profoundly affects the efficiency of meiosis, the potential to yield “competent (euploid) mature (M2) eggs, and as such represents a rate limiting step in the IVF process .

    “Triggering meiosis with Urine-derived hCG (Pregnyl/Profasi/Novarel) versus recombinant hCG (Ovidrel): Until quite recently, the standard method used to “trigger” egg maturation was through the administration of 10,000 units of hCGu. Subsequently,, a DNA recombinant form of hCGr (Ovidrel)was introduced and marketed in 250 mcg doses. But clinical experience strongly suggests that 250 mcg of Ovidrel is most likely not equivalent in biological potency to 10,000 units of hCG. It probably only has 50%-70%of the potency of a 10,000U dose of hCGu and as such might not be sufficient to fully promote meiosis, especially in cases where the woman has numerous follicles. For this reason, I firmly believe that when hCGr is selected as the “trigger shot” the dosage should best be doubled to 500 mcg at which dosage it will probably have an equivalent effect on promoting meiosis as would 10,000 units of hCGu. Failure to “trigger” with 10,000U hCGu or 500mcg hCGr, will in my opinion increase the likelihood of disorderly meiosis, “incompetent (aneuploid) eggs” and the risk of follicles not yielding eggs at egg retrieval (“empty follicles”). Having said this, it is my personal opinion that it is unnecessary to supplant hCGu with hCGr since the latter is considerably more expensive and is probably no more biopotent than the latter.

    Some clinicians, when faced with a risk of OHSS developing will deliberately elect to reduce the dosage of hCG administered as a trigger in the hope that by doing so the risk of critical OHSS developing will be lowered. It is my opinion, that such an approach is not optimal because a low dose of hCG (e.g., 5000 units, hCGu or 25omcg hCGr) is likely inadequate to optimize the efficiency of meiosis particularly when it comes to cases such as this where there are numerous follicles. It has been suggested that the preferential use of an “agonist (Lupron) trigger” in women at risk of developing severe ovarian hyperstimulation syndrome could potentially reduce the risk of the condition becoming critical and thereby placing the woman at risk of developing life-endangering complications. It is with this in mind that many RE’s prefer to trigger meiosis by way of an “agonist (Lupron) trigger rather than through the use of hCG. The agonist promptly causes the woman’s pituitary gland to expunge a large amount of LH over a short period of time and it is this LH “surge” that triggers meiosis. The problem with using this approach, in my opinion, is that it is hard to predict how much LH will be released in by the pituitary gland. For this reason, I personally prefer to use hCGu for the trigger, even in cases of ovarian hyperstimulation hyperstimulated, with one important proviso…that being that is she underwent “prolonged coasting” in order to reduce the risk of critical OHSS, prior to the 10,000 unit hCGu “ trigger”.

    The timing of the “trigger shot “to initiate meiosis: This should coincide with the majority of ovarian follicles being >15 mm in mean diameter with several follicles having reached 18-22 mm. Follicles of larger than 22 mm will usually harbor overdeveloped eggs which in turn will usually fail to produce good quality eggs. Conversely, follicles less than 15 mm will usually harbor underdeveloped eggs that are more likely to be aneuploid and incompetent following the “trigger”.

    Here is the protocol I advise for women, <40Y who have adequate ovarian reserve.
    My advice is to use a long pituitary down regulation protocol starting on a BCP, and overlapping it with Lupron 10U daily for three (3) days and then stopping the BCP but continuing on Lupron 10u daily (in my opinion 20U daily is too much) and await a period (which should ensue within 5-7 days of stopping the BCP). At that point an US examination is done along with a baseline measurement of blood estradiol to exclude a functional ovarian cyst and simultaneously, the Lupron dosage is reduced to 5U daily to be continued until the hCG (10,000u) trigger. An FSH-dominant gonadotropin such as Follistim, Puregon or Gonal-f daily is started with the period for 2 days and then the gonadotropin dosage is reduced and a small amount of menotropin (Menopur---no more than 75U daily) is added. This is continued until US and blood estradiol levels indicate that the hCG trigger be given, whereupon an ER is done 36h later. I personally would advise against using Lupron in “flare protocol” arrangement (where the Lupron commences with the onset of gonadotropin administration.
    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.
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas
    • Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
    • A personalized, stepwise approach to IVF
    • “Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
    If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .

    *FYI
    The 4th edition of my newest book ,”In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

    Geoffrey Sher MD

    Layla Jameson - November 16, 2017 reply

    Hi Dr. Sher,
    Thanks for your response. So just to clarify – are you suggesting that despite having mature eggs at retrieval you still believe my low fertilization rate (37.5%) could be a result of having triggered with Lupron?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 16, 2017 reply

    Indeed yes!

    Geoff Sher

  • Kadieva - November 15, 2017 reply

    Hello, dr Sher!
    I would like to introduce you to my sisters’ experiense, who has been conceived unsuccessfully for 7 years.

    After 6 ivf attempts my sister/40 years old now/ has 4 positive bchg tests with value between 20 and 70 and one naturally pregnancy with bchg = 60. Last two attempts were with PGD tested blastocysts – grade 5AB and again biochemical pregnancy.

    The doctors find out that the folopian tubes are passable, the uterine cavity is clear and the uterus is reversed. Endometrium is more than 12mm.
    The following immunological tests were performed:

    NK cells CO3-56+ – 13.93 ref (2-13)
    NK cells activity – 11.2 ref (N<10%)
    Available embryotoxins
    PAI 4G/4G homozygous
    MTHFR (C667T) heterozygous
    Male kariotype – 46 ХУ
    Female kariotype – 46 XX
    AMH – 4.27
    FT4 – 1.190 ref 0.93-1.7
    TSH – 0.794 ref 0.27-4.2

    The threatment is Intralipid before and after positive bchg and Octagam immunoglobulin 3-4days before transfer, prednisolon, aspirin, clexane.

    What is your opinion?
    Thanks in advance

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 16, 2017 reply

    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
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • 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
    If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .

    *The 4th edition of my book,”In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

    Geoffrey Sher MD

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