Dr. Sher Blog

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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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  • Sharon - December 11, 2017 reply

    For my first IVF pregnancy I was on interlipids and steroids I have just found out I am 6 weeks pregnant naturally I can’t believe it… should I get on interlipids and steroids ASAP or is it too late.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 11, 2017 reply

    Probably too late to be of any real value now!

    Geoff Sher

  • Hilary - December 11, 2017 reply

    Dear Dr Sher
    You had advised that I consider staggered IVF and embryo banking and do a Preimplantation genetic screening due to my age(46). I am now considering back to back IVF cycle, freezing the embryos from the first cycle before testing so that the embyros from both cycles can be tested at once in order to manage the cost(The pre implantation screening in my country is actually more expensive than the entire IVF cycle.) Would this be advisable or is Preimplantation genetic screening more viable with fresh embryos?
    Thank you

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 11, 2017 reply

    Thawing embryos to biopsy them …only to refreeze while waiting for the result and then having to thaw again for FET is in my opinion stressful on the embryos and I personally would prefer to avoid this.

    Geoff Sher

  • Sam - December 11, 2017 reply

    Hello Dr. Sher,

    Thanks for taking the time to answer so many questions from everyone!

    I recently have been diagnosed with DOR. (AMH: 0.6, FSH 10, AFC 8)
    We have tried 2 IUI with no success.
    I have high androgens (T – 45 ng/dL (8-48 range) and DHEAS (390 ug/dL (84-378 range)) also have symptoms of hirsutism.
    Before starting IVF i was looking into DHEA as there seems to be a lot of publications behind DHEA for DOR patients. But since it is an androgen precursor now I am thinking i should not as my levels are already high.
    Could the high androgens be effecting my eggs? Could dexamethasone help in reducing the T and DHEAS levels, should I maybe try that before an IVF?

    Thank you!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 11, 2017 reply

    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”.
    Women who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.

    While it is presently not possible by any means, to reverse the effect of DOR, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can in my opinion, make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.I try to avoid using such protocols/regimes (especially) in women with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH). I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy

    Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and 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 Approach
    • 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.
    • A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
    • 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?
    • Blastocyst Embryo Transfers should be the Standard of Care in IVF
    • Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
    • Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
    • 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
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
    • Traveling for IVF from Out of State/Country–
    • A personalized, stepwise approach to IVF
    • How Many Embryos should be transferred: A Critical Decision in IVF.
    • The Role of Nutritional Supplements in Preparing for IVF
    • Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
    • IVF Egg Donation: A Comprehensive Overview

    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

  • anonymous - December 11, 2017 reply

    Can anxiety or fear cause implantation failure / IVF failure?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 11, 2017 reply

    I doubt it!

    Geoff Sher

  • Jessica - December 11, 2017 reply

    Hi Dr Sher,

    I started stimulation on long protocol 4 days ago and there was a discrepancy between the prescription dosage and the stimulation schedule and I made a mistake that I just realised after 3 nights of injecting 300 instead of 225 of gonal f. What should I do? The clinic has said just to continue with 225 dose but will this mistake have an adverse outcome on the cycle? Should I have the scan earlier? What do you think is the best course of action?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 11, 2017 reply

    I really could not say…without knowing details about your ovarian reserve.

    Geoff Sher

  • Abi - December 10, 2017 reply

    Hi Dr Sher, my RE says high dose stims has a deleterious effect on egg quality. I know high dose stims can’t overstimulate a DOR ovary, but can it affect quality?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 11, 2017 reply

    I respectfully disagree with your RE when it comes to DOR.

    Geoff Sher

  • Michelle - December 10, 2017 reply

    Hi Dr. Sher,

    I have a 3 year son that we conceived after 10 months of trying. But last year I was diagnosed with premature ovarian insufficiency (I’m now 35), after having months of hot flashes and no menstruation. My AMH was less than 0.03 and my FSH was 90. I’ve had my FSH checked twice since then, and it’s ranged from 40-60. I recently started on bioidentical hormone therapy to manage the perimenopause symptoms. My doctor told me IVF with my own eggs wouldn’t be a viable option, and that egg donation would be the best choice. Do you agree? I’m really sad about the thought of not having another child biologically related to me, but I also don’t want to “throw away” money if IVF with my eggs has a minimal chance.

    Thank you

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 10, 2017 reply

    I agree with your RE that given the severity of your DOR, egg donation offers by far the best option. However, if you absolutely insist on trying with own eggs in spite of the reduced chance of success then please consider the following:

    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”.
    Women who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.

    While it is presently not possible by any means, to reverse the effect of DOR, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can in my opinion, make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.I try to avoid using such protocols/regimes (especially) in women with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH). I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy

    Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and 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 Approach
    • 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.
    • A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
    • 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?
    • Blastocyst Embryo Transfers should be the Standard of Care in IVF
    • Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
    • Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
    • 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
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
    • Traveling for IVF from Out of State/Country–
    • A personalized, stepwise approach to IVF
    • How Many Embryos should be transferred: A Critical Decision in IVF.
    • The Role of Nutritional Supplements in Preparing for IVF
    • Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
    • IVF Egg Donation: A Comprehensive Overview

    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

  • Maria - December 10, 2017 reply

    I had an egg retrial this past Friday with only two follicles but both follicles contained no eggs and the other issue was that as I’m waiting to go in the ansethiologist refused to give me anesrhis because they didn’t realize that I had an underlying condition and the anesrhiogist wouldn’t do anesrhis without a full blood work up, was i missed off how do u not realize this before the procedure is going to start so they did it by giving me a shot of tegrwtol in my arm and a local in my vagina, idiots but my main concern now is,that I had no eggs

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 10, 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.

    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

  • Hilary - December 10, 2017 reply

    Dear Dr Sher
    Thank you for your prompt response.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 10, 2017 reply

    You are welcome.

    Geoff Sher

  • Stacey - December 10, 2017 reply

    Hi Dr Sher,

    I’m current doing a stim cycle using Gonal f. It is going slower than my precious two cycles because they’ve had me on a lower dose as they were trying to slow me down to aim for egg collection on day 14 rather than day 12 (though previous cycles have gone well and Ive collected 15 and 17 eggs). It appears the dose has been too low this time (275 as opposed to 300 and 325 the previous times), and I’m not responding as they hoped. On day 8 I had 15 follicles on one side and 10 on the other, but they were fairly small, ranging from 5-10mm. They upped my dose to 350 for last two nights. Do I still have time for them to grow sufficiently for a collection? I calculate that if they grow well from now, I could still have a 20mm follicle by day 14, ready for a collection on Day 16? Is day 16 fine for a collection? Does egg quality go down of the collection is too late in the cycle? Is there a cut off day?
    Many thanks in advance for your response. I still have hope for this cycle, I think it is just going much slower because the dose they out me on was too low..
    Many thanks,
    Stacey.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 10, 2017 reply

    The length of time on stimulation , in and of itself, should not be problematic. However, the protocol of implementation is another matter. Obviously without much more information I cannot comment on this.

    Geoff Sher

  • Ellie - December 10, 2017 reply

    Hi Dr Sher, what is your view re starting with 375IU gonal f and dropping down to 225IU on day 3 with the addition of 75IU Luveris. Is that too much of a drop and can it slow down follicle growth? My RE said I can start with 375 and drop to 225+75 luveris or start with 450 and drop to 300+75 luveris, but has left the decision to me.. I can’t decide.. i will be on a long cycle.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 10, 2017 reply

    No! Provided the dosage used for the stimulation is optimal, that drop off seems OK. However, I cannot comment on the starting dosage without much more information about your ovarian reserve and (if applicable) how you responded previously.

    Geoff Sher

  • Robin - December 10, 2017 reply

    Hi there dr Sher, how long should the lupron overlap with BCP for effective results? Is it dependent on the length of time of BCP or does Lupron take a certain number of days to exhaust FSH and LH before dumping it?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 10, 2017 reply

    In my opinion, 3 days…regardless of how long on BCP.

    Geoff Sher

    Robin - December 10, 2017 reply

    Thank you Dr Sher very much! Can overlapping for a bit longer be a problem?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 10, 2017 reply

    Should not pose a problem.

    Geoff Sher

  • Crystal Peshek - December 9, 2017 reply

    I have been trying to concieve for 15 years. I’m 35& I know my time is running out. I so not have funds for fertility treatments at this time. I am at the right weight for my height, I have regular cycles, I eat healthy, I have done a round of Clomid before I lost my insurance that covered fertility treatments. My question is, is there any home remedy ir natural treatment that will help me have the family that I desperately want?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 10, 2017 reply

    Crystal,

    You should undergo a basic fertility evaluation as the very 1st step. Contact your primary gynecologist for starters.
    Good luck!

    Geoff Sher

  • Hilary - December 9, 2017 reply

    Dear Dr Shpreger, seems like my original question was not posted.Am 46 years and just had a failed ivf cycle. AMH is 1.9 and was put on the anatgonist protocol with 450 mg of menopur and growth hormone. Trigger was 10,000 pregnyl and i had 10 eggs retrieved, 8 mature and 2 grade 2-3 blastocyst. but no implantation. Also my uterine lining was 9 mm at the time of transfer. About to start a new cycle but Dr seems to want to use the same protocol.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 9, 2017 reply

    Hi Hillary…This is almost certainly an age factor impacting egg/embryo quality. The chance of any given egg/cleaved embryo being normal at 46y is probably <4%. You need egg donation. However, if you insist upon trying with own eggs then please consider the following very carefully!

    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

  • Hilary - December 9, 2017 reply

    Dear Dr Sher
    Forgot to mention that i used 10,000 Mg of Pregnyl for the trigger and there is no case of MF. Also my uterine lining was about 9mm on the day of the transfer. Of the 10 eggs, collected, 8 were mature, 5 fertlized (ICSI) and only 2 made it to blastocyst. But obviously none implanted.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 9, 2017 reply

    Copy!

    Geoff Sher

  • Ella - December 9, 2017 reply

    I had a biopsy to test my natural killer cells twice, once on day 12 and another on day 16. The results were both normal. Is this the right time to test for natural killer cells or is it best done in the late luteal phase rather than the proliferative phase?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 9, 2017 reply

    It can be done any time.

    Geoff Sher

  • Sammie H - December 9, 2017 reply

    Hello Dr Sher! I just had a question re estradiol. Can too much testosterone cause elevated estradiol levels?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 9, 2017 reply

    Not in my opinion!

    Geoff Sher

  • Norani - December 9, 2017 reply

    It’s so amazing you have given so much of your time to help other women. I am 40.8 years old. I have been TTC naturally now for 2.5 years and it hasn’t worked. I have had a hycosy, a hysterscopy and all is clear. I have been told it’s my age. No male factor infertility either. My AMH is 0.96 ng/ml, what protocol do you recommend for me?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 9, 2017 reply

    Thank you kindly,

    Based upon your AMH you have diminished ovarian reserve (DOR). 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 (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

  • Krishnaveni - December 8, 2017 reply

    Hello Dr.Geoffrey Sher. I’m 32 year old women.My AMH levels are 1.2 ng/ml. I had 4 cycle of IVF, one with agonist and three with antagonist and got pregnant only once. I had oocytes retrived between 9-20 each cycle.I always had LH below 10 after lupron trigger in antagonist cycles. I had ovarian hyperstimulation syndrome with agonist protocol. Could you please let me know why I always have OHSS with HCG trigger even though I have low ovarian reserve.Could you also let me know my chances of getting pregnant.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 8, 2017 reply

    That clearly suggests that the diagnosis of OHSS is not accurate. I would repeat FSH/LH/E2 and AMH in day 3 of your cycle.

    Typically, women with irregular ovulation/menstruation, young women, those with high ovarian reserve (AMH=>6ng/ml) and those who have polycystic ovarian syndrome (PCOS) who undergo ovarian stimulation with fertility drugs are at increased risk of developing severe ovarian hyperstimulation syndrome (OHSS), a life endangering condition. In cases of OHSS egg “competency” (quality) is often severely compromised.
    The fear of OHSS developing often prompts RE’s to trigger egg maturation prematurely with hCG in the hope of arresting the process before ovarian stimulation spirals out of control, increasing physical risk and causing a high percentage of harvested eggs to end up being “incompetent”, (“immature/dysmature).
    Also in an attempt to reduce the risks of OHSS, some RE’s trigger egg maturation using a reduced dosage of hCG or through inducing an outpouring of pituitary LH an agonist such as Lupron or Buserelin. While such approaches indeed reduce the risk and severity of OHSS, they often result in many eggs failing to mature. Thus lowering risk by reducing the dosage of hCG or by using an agonist “trigger”, often comes at the expense of egg “competency”.
    In women with PCOS, poor egg “competency” is also often attributable to high ovarian LH-induced testosterone. Such eggs have reduced fertilization potential, often yielding “poor quality embryos”. While poor egg “competency” in women with PCOS can be due to the fact that such eggs are more prone to having intrinsic quality deficits, it is (in my opinion), more commonly attributable to aberrant intra-ovarian hormonal changes brought about by severe ovarian hyperstimulation. This effect, can be prevented or curtailed through implementation of individualized or customized ovarian stimulation protocols that minimize over-exposure to excessive LH-induced ovarian male hormones (androgens) which can best be accomplished by limiting the use of LH-containing gonadotropins such as Menopur and by using a procedure that I introduced in 1989, known as “prolonged coasting” (see below).
    Approaches to preventing or containing OHSS include:
    1. PROLONGED COASTING: My preferred approach is to use a long pituitary DR protocol coming off up to 2 months on the BCP, overlapped in the last 3 days with the agonist, Lupron. The BCP is intended to lower LH and thereby reduce stromal activation (hyperthecosis) in the hope of controlling ovarian androgen (predominantly, testosterone) production and release. I then stimulate with low dosage recombinant FSF-FSHr (Follistim/Gonal-F/Puregon) to which I add a smidgeon of LH/hCG (Luveris/Menopur) from the 3rd day. Then, starting on day 7 of ovarian stimulation, I perform serial blood estradiol (E2) and ultrasound follicle assessments, watching for the # of follicles and [E2]. If there are > 25 follicles, I keep stimulating (regardless of the [E2] until 50% of all follicles reach 14mm. At this point, provided the [E2] reaches at least >2,500pg/ml, I stop the agonist as well as gonadotropin stimulation and track the blood E2 (without continuing US, follicle measurements) ) daily. The [E2] will almost invariably increase for a few days. I watch the E2 rise (regardless of how high a blood concentration it reaches) and then track it coming down again. As soon as the [E2] drops below 2500pg/ml (and not before then), I administer a “trigger” shot of 10,000U hCGu (Profasi/ Novarel/Pregnyl) or hCGr (Ovidrel/Ovitrel-500mcg) and perform an egg retrieval 36 hours later. ICSI is a MUST because “coasted” eggs usually have no cumulus oophoris envelopment and eggs without a cumulus will not readily fertilize naturally. Moreover, they also tend to have a “hardened” envelopment (zona pellucida), making spontaneous fertilization problematic in many cases. All fertilized eggs are cultured to blastocyst (up to 6 days) and are then either vitrified and preserved for subsequent transfer in later hormone replacement cycles or up to two (2) fresh blastocysts are transferred transvaginal under US guidance.. The success of this approach depends on precise timing of the initiation and conclusion of “prolonged coasting”. If you start too early, follicle growth will stop and the cycle will be lost. If you start too late, you will encounter too many post-mature/cystic follicles (>22mm) that usually harbor abnormally developed eggs. Use of “Coasting” avoids unnecessary cycle cancellation, severe OHSS, and optimizes egg/embryo quality. The worst you will encounter is mild to moderate OHSS and this too is uncommon. The obvious remedy for these adverse effects on egg and endometrial development is to employ stimulation protocols that limit ovarian over-exposure to LH and allowing the time necessary for the follicles/eggs to develop optimally, prior to administering hCG through the judicious implementation of “Prolonged coasting” (PC).
    2. MULTIPLE FOLLICLE ASPIRATION: In some cases, where because of mean follicle size exceeding 16mm or when “coasting” fails to effectively lower the [E2} below 2,500pg/ml within 3 days, the number of developing follicles can effectively and drastically reduced through target transvaginal aspiration, 1-3 PRIOR to planned the hCG trigger. This will almost invariably be accompanied by a rapid and significant drop in the plasma [E2] and in the process will drastically reduce the risk of OHSS occurring without significantly compromising egg/embryo quality. The drawback of this effective approach is the fact that it interjects an additional surgical intervention into an already complex and stressful situation. i
    3. TRIGGERING WITH LOW DOISAGE hCG; Because of the fact that hCG augments the development of OHSS (unless preceded by “coasting”), may RE’s prefer to use a lower dosage of hCG for the “trigger. This is either done by administering 5,000U (half the traditional dosage) or by administering, a 250mcg (rather than 500mcg) of DNA recombinant form of hCGr (Ovidrel/Ovitrel. Some clinicians, when faced with a risk of OHSS developing will deliberately elect to reduce the “trigger” dosage of hCG administered (from 10,000U to 5,000U or 250mcg of recombinant hCG-Ovidrel) in the hope that by doing so the risk of critical OHSS developing will be lowered. While this might indeed be true, it is my opinion, that such a reduced dosage is usually insufficient to optimize the efficiency of egg meiosis, e3specially when there are so many follicles present. While the use of a reduced “trigger” dosage of hCG does indeed reduce the risk and occurrence of OHSS-related life-endangering complications, the price to be paid is reduced egg quality/”competency”.
    4. “TRIGGERING” WITH A GnRH AGONIST (E.G. “LUPRON/BUSERELIN): More recently, an increasing number of RE’s prefer to trigger meiosis by way of an agonist (Lupron/Buserelin/Superfact () “trigger” rather than through the use of hCG. The idea is to mimic what happens in natural cycles to promote egg maturation (meiosis) and ovulation, namely to have the agonist cause a “surge” in the release of body’s own pituitary LH to trigger egg meiosis (maturation) .But the amount of LH released in by the pituitary gland is often insufficient to optimize meiotic egg maturation and thus, while this approach also lowers the risk of OHSS it again comes at the expense of egg quality/competency.

    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:
    • A personalized, stepwise approach to IVF
    • Preventing Severe Ovarian Hyperstimulation Syndrome (OHSS) with “Prolonged Coasting.
    • “Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
    • The “Lupron Trigger” to Prevent Severe OHSS: What are the Pro’s and Con’s?
    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.

    Geoff Sher

  • Deborah - December 8, 2017 reply

    Hi Dr Sher,
    I’m 40 yo and on my third IVF with ICSI cycle. First cycle 2 low grade embryos transferred, negative test. Second cycle 2 blasts transferred, chemical pregnancy. I’m on same protocol as cycle 2 for this cycle, except I’m also taking 200mg of ubiquinol daily. My egg collection is scheduled for Monday. Should I continue taking the ubiquinol after that? Would it do any harm?
    Thanks for taking the time to read and answer my questions. It’s much appreciated.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 8, 2017 reply

    In my opinion, there is no reason to stop taking Ubiquinol.

    Geoff Sher

  • Shelia - December 7, 2017 reply

    Hi,

    I recently transferred a PGS normal embryo and got a BFP. However, I misscarried at 7 weeks. My betas were through the roof. 1st beta 10 post 5 day FET: 798, 13 days post FET: 2,727 and about 20 days post FET: 26, 202. Went in to hear the heartbeat and it was only 81bpm at 6weeks4days. I guess I am looking for answers as to why a PGS normal embryo would fail. I have no known fertility issues other than age, I am 38. This was my 2nd cycle. First cycle was PGS normal but got a BFN, it never implanted. Any suggestions and thank you so much.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 7, 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

  • Anne - December 7, 2017 reply

    Hello Dr. Sher,
    I’m a 41 yo with two natural miscarriages. I recently underwent two rounds of IVF and after retrieval and fertilization of 20 embryos I had 3 that made it to blast and all came back PGS abnormal. These are the results from the 3 embryos:
    1.) 47,XX; +19, 2.) 45,XY; del(1)(pter-p31.1), -18 3.) 44,XX; -19, -21
    Would you consider transferring any of these?
    Thank you for your time.
    Anne

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 7, 2017 reply

    No Anne…I personally would not transfer these.

    Geoff Sher

    Anne - December 7, 2017 reply

    Thank you, Dr. Sher.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 7, 2017 reply

    You are most welcome Anne!

    Geoff Sher

    Martina B. - December 9, 2017

    Would your advice be the same for 45,XY: -22?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 9, 2017

    I would!

    Geoff Sher

    Martina B. - December 9, 2017

    Hi Dr Sher, just to clarify, is your response that you would transfer or not transfer?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 9, 2017

    I would transfer a monosomy 22 blastocyst subject to a full discussion regarding that in the event of success, an amniocentesis/CVS be done to confirm the chromosomal integrity of the pregnancy and the option of terminating it if need be.

    Geoff Sher

    Martina B. - December 10, 2017

    Thank you so very, very much!!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 10, 2017

    You are very welcome!

    Geoff Sher

  • Abi - December 6, 2017 reply

    Hi Dr Sher, I’ve noticed every time I take Chinese herbs my day 3 estrogen is elevated on a natural cycle. In all your years of cycling women on IVF, have you noticed those women taking Chinese herbs have improved their egg quality?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 7, 2017 reply

    No Abi!

    That is new to me!

    Geoff Sher

  • Amy - December 6, 2017 reply

    Hi Dr Sher,
    I had a successful FET some 4 weeks ago but I’m very concerned about my beta levels. They are through the roof while an ultrasound scan at exactly 6wks showed only one gestational sac and one heart.
    -10 days past 4-day embryo transfer (14 dpo) 340
    -12 dpt (16 dpo) 840 — doubling time 36.8 h
    -17 dpt (21 dpo) 6,500 — doubling time 41 h
    -24 dpt (28 dpo) 46,000 — doubling time 60 h
    What could be the reason why the levels are so high? Is there an elevated risk of chromosomal abnormalities or miscarriage? I’m so stressed about it.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 7, 2017 reply

    Looks good to me!

    Remember, after the beta goes over about 6,000, it no longer will double every 48h.

    Good luck!

    Geoff Sher

  • Melissa - December 6, 2017 reply

    I’ve had 2 ICSI cycles already, first 24 eggs retrieved but only 2 embryos came from that. Second cycle (lower meds) 15 eggs retrieved but again only 2 embryos in the end. I was told most eggs were immature. My AMH is 4.6 and I am 33 years old, no male factor. Why are my results so bad? I have a feeling I’m being stimmed wrong, both times Gonal F CD3-4, orgalutran, and no BCP.

    Melissa - December 6, 2017 reply

    I forgot to add that both cycles were antagonist protocols, first cycle I had Gonal f 150 IU CD3-CD12, with 75 IU luveris and 250mg cetrotide started CD5,
    then ovidrelle 250mg trigger.

    Second was Gonal F CD4-10, with orgalutran CD6-8, then ovidrelle 250mg trigger

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 6, 2017 reply

    I absolutely believe that 250mcg of Ovidrel is too low a trigger dosage.

    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”.

    Geoff Sher

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 6, 2017 reply

    In my opinion, the most important consideration should be selection of an ideal protocol for ovarian stimulation.

    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

    Melissa - December 7, 2017 reply

    I’m so sad you’re retiring and I just want to say how much of a difference you made in my life with this very difficult infertility journey, you’ve been such a blessing

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 7, 2017 reply

    Thanks Melissa ..but as things currently stand my departure is likely about 1 year away!

    G-d bless,

    Geoff Sher

    Melissa - December 8, 2017

    That’s great news for us all!!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 9, 2017

    Hopefully!

    Geoff Sher

  • Anne - December 6, 2017 reply

    I had a recent failed IVF for unexplained infertility (I had asked my doc to skip the initial IUI’s because we want a baby sooner than later due to the uncertain health status of my grandmother and father in law). Well the IVF was a dismal failure with only one embryo after ICSI of 5 eggs (I have AMH 0.64). So my doctor asked me to at least go through the usual protocol and give him a shot with 3 IUI’s since I’m 34 and have 2 children (my husband has no bio children). I deep down felt the IUI’s were a waste of time because another RE had told my husband that we couldn’t get pregnant via IUI because he has DNA fragmentation. But, low and behold, the final IUI I became pregnant (I had my husband collect a double sample into the sample cup for the first time and his post wash count went up from his prior counts of 1mil and 3.8mil to 28mil for this double collection!). So now I am 5 weeks and 3 days post IUI. No symptoms of miscarriage, however I am concerned about my betas. 11 days post IUI my beta was 37.5, 5 days later it was 214.9, and then 8 days later (today) it was 1714. So, if I calculated properly, the doubling time is around 64 hours. I can’t find any definitive information online as to whether this doubling time is acceptable, and I was wondering your thoughts. Thank you so much!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 6, 2017 reply

    It is a slowish rise but this can vary. So I would repeat it in 2 days time to see if it doubles and thereupon, about a week later, do an ultrasound to determine what is happening with more confidence.

    Good luck!

    Geoff Sher

  • Angela - December 6, 2017 reply

    Dear Dr Sher,
    Thank you for replying so promptly. May I also please ask what an optimal cycle day 1 LH level would be ? My level was 6.6. I am over 40 and have PCOS. I have been on 1000 Metformin daily.
    Thank you

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 6, 2017 reply

    That is tough because the LH is often elevated in PCOS. 6.6MIU/ml is somewhat elevated. I like to see the LH lower than that.

    Geoff Sher

  • Ashlyn - December 5, 2017 reply

    Hi Dr Sher,
    I am 8dp5dt (1 PGS embryo that was 4AA) and took a hpt this morning and got a very positive! I was very excited until I wiped and saw brown/pink discharge. This type of discharge happens to me the day before I start my period like clockwork. I’m taking 1mg progesterone in oil injections and estradiol pills. Could this be a chemical pregnancy?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 6, 2017 reply

    It is more likely that this would be a viable implanting pregnancy!

    Good luck!

    Geoff Sher

  • Abigail Jackson - December 5, 2017 reply

    Hi Dr Sher! I would appreciate your insight into this issue. In 2015 we did a cycle of IVF with ICSI. We were diagnosed with male infertility, low sperm count, no female issues. At the time I was 29, and put on low stimulation protocol. We ended up with 19 follicles, 17 were good size but none of them fertilized normally. There were 4 that had 2 polar bodies initially, 2 of those continued to grow and were transferred. Amazingly, God blessed us and we now have a healthy boy from that cycle! My question is, in your opinion, how likely are we to experience the same fertilization problems if we tried IVF again? Our physician at the time said she didn’t know where the issue originated but said it was more likely a problem with the sperm. Do you see that patients with fertilization problems tend to continue to have them in subsequent IVF cycles? Thanks for your time!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 6, 2017 reply

    No Abigail. Rather than this being a sperm issue, it is in my opinion more likely to be a stimulation protocol issue.

    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

  • Eleanore - December 5, 2017 reply

    Hello dr. Sher. Thank you for the possibility for asking you for advice from Europe.
    I’m in my fourth ICSI cycle and I had on the 8th of november a Decapeptyl depot 3.75 CR. Since 25th november I stimulate with 150 IU Meriofert and 150 IU Ovaleap.
    4 december I had a blood test and the result is:
    – LH         2.3   IU/L
    – FSH       33.4 IU/L
    – E2          4846 pmol/L
    – Progesteron    1.5 nmol/ L

    The result of my bloodtest of 30th november is:
    – LH     0.9   IU/L
    – FSH       27.5 IU/L
    – E2          648 pmol/L
    – Progesteron        0.3 nmol/ L

    Yesterday I had a 2nd ultrasound and in the right ovary there are 8 follicles ranging from 16 mm till 20 mm and in the left ovary about 5 follicles around 12 mm and 2 of 10 mm.
    I’m told to stimulate tomorrow morning with only the Meriofert and I’ve trigger tomorrow at 22.00pm with 5000IU Pregnyl. Friday morning at 09.00 am I’ve the egg retrieval. My question for you is if it could do harm if I trigger with 10.000IU Pregnyl. My RE said explicietly that I’ve got to trigger with 5000IU, but I don’t know why…
    And do you think that the response of my left ovary has to do with the protocol which is used? I’ve got immature oocytes with my previous cycles so I hope that this time the result will be much better. Fingers crossed….
    Looking forward to read your response. Thank you in advance!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 6, 2017 reply

    I would respectfully differ with your RE. In my opinion, 10,000U Pregnyl is preferred.

    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”.

    Geoff Sher

    Eleanore - December 6, 2017 reply

    Good morning dr. Sher,
    Thank you for your response.
    So with this blood and ultrasound results you would still advice me to trigger with 10000 U Pregnyl? Cause I don’t get any bloodtest or ultrasound anymore till the egg retrieval this friday. I have 10.000U Pregnyl at home so I’ll just use it.
    Wednesday I have the ET, and friday 15 december I’ve booked a bustrip to London from the Netherlands. Should I cancel it or can I join the trip?
    Thank you so much dr. Sher for your time! Kind regards.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 6, 2017 reply

    Whatever you do should be with the knowledge and agreement of your RE. Don’t do anything without this consent.

    Geoff Sher

  • MS Carney - December 5, 2017 reply

    Desperate for advice after 2 failed frozen donor egg cycles. I was told the original issue was me due to poor response/diminished ovarian reserve and after 3 failed iui’s and 6 failed own egg ivf icsi cycles (including 1 miscarriage) we turned to donor eggs. With our 1st donor we had a thaw issue supposedly and ended up doing a 3 day transfer with 2 embryos (1 4cell +1 6cell) that failed. We were told since half of our frozen eggs did not thaw and only 2 out of 3 fertilized that they thought it was an issue with those donor eggs. We then moved on to a second donor who was proven and now had even worse results: all 6 thawed but 1 abnormally fertilized and 4 did not divide at all so we had a 3 day transfer of 1 6cell embryo that failed. We are now being told by the RE office that after looking at only the frozen donor egg cycles that they now think we also have a sperm issue going on. How can this be possible now after 3 years of infertility treatments? Also my husband has a 12 year old child from a previous relationship who was conceived naturally, we have been told that his semen analysis was normal and met the egg bank standards both times but that after they prepped the sperm for icsi they noticed that the count had drastically decreased and this actually happened with both donor egg cycles yet no one notified us about this finding until now. They also said that when embryos do not divide that also usually indicates a sperm issue. At this point we are at a loss we never had fertilization issues or issues with embryos not dividing with my own eggs so why would this happen with donor eggs. To say that we are emotionally and financially drained is an understatement and I cant just trust what we are being told at this point we are not ready to quit or give up and are looking for any advice or guidance!?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 5, 2017 reply

    I am opposed to using frozen eggs from a bank. Results are never as good as when using a fresh donor. Given the history of your husband having fathered a child, I very much doubt this is a MF. This having been said, your past history of failed IUI’s and failure with own egg-IVF, suggests there could be an additional factor such as an implantation dysfunction.

    Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
    It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
    1. Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
    2. Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
    We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
    3. The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
    4. Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
    a. A“ thin uterine lining”
    b. A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
    c. Immunologic implantation dysfunction (IID)
    d. Endocrine/molecular endometrial receptivity issues
    Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.

    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation (COS)
    • The Fundamental Requirements for Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • 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
    . IVF with egg donation

    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.

  • Angela - December 5, 2017 reply

    Dear Dr Sher,
    I am currently on day 1 of my cycle, my period started today and was instructed to start Orgalutran today but half dose and continue on until trigger day but I accidentally took the full dose. I am afraid that I have ruined my cycle. The Orgalutran is to keep my LH in check as I am 42 years old. My LH was tested today and is 6.6. Should I continue on with 1/2 dose tomorrow? I am really worried.
    Thank you so much
    Angela

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 5, 2017 reply

    It wont do any harm!

    Good luck!

    Geoff Sher

  • Caroline - December 5, 2017 reply

    Hello Dr Sher
    My husband and I have recently discovered that we are likely both carriers for autosomal recessive polycycstic kidney disease. This is caused by mutation in the PKHD1 gene. Could you please let me know if you have experience with PGD for this condition? We are from Australia and considering travelling to the US for IVF with you. We have two healthy children conceived without IVF.
    Thank you

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 5, 2017 reply

    I have a great deal of experience with PGS but I do not have experience specifically with this condition. However, I am confident that PGS could help identify the specific mutation in the embryos.

    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.

    Caroline - December 5, 2017 reply

    Thank you very much for replying so promptly. We will set up a consultation soon.
    Kind regards

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 5, 2017 reply

    G-d bless!

    Geoff Sher

  • Nathalie - December 4, 2017 reply

    Hello dr,
    Please I need help , I’m confused and need proper advice.
    I recently had ivf done. I’m 36 Had low AMH and irregular periods and have endometriosis.
    I started couple of weeks ago with my clinic for ivf.
    Went on a Monday for a scan and they saw a cyst. On that Wednesday they drained the cyst and did the endometrium scratch. I started stimulation drugs that Friday.
    As my scans went along I was only showing 4 follicles on one uterus and two little ones on the other. The four grew to proper size. They other two grew a little but remained small.
    This last Wednesday ( the 29th November) I went for retrieval. They only got one egg!
    On Thursday they called me and said my egg wasn’t good quality and discovered this as they went to do icis. Failed ivf.

    I don’t understand what happened. What went wrong. Was I not given high enough stim drugs and that’s why only had low amount of follicles? Do I have Pcos ( I had polysistic ovaries when I was younger) ? And that’s why not so many follicles ? Why were the follicles empty?

    Do I go for another round of ivf at the same clinic? Or can another clinic help me better or do a different treatment ? Or is all the same !
    Does this mean I won’t produce more then this and that if I do my eggs will be poor quality?
    Please any help you can give can will be very appreciate it… please
    Nathalie

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 5, 2017 reply

    I truly believe we should talk! 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
    . Endometriosis and Infertily
    • Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF
    • Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
    • Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
    • Early -Endometriosis-related Infertility: Ovulation Induction (with or without Intrauterine Insemination) and Reproductive Surgery Versus IVF
    • Treating Ovarian Endometriomas with Sclerotherapy.
    • Effect of Advanced Endometriosis with Endometriotic cysts (Endometriomas) on IVF Outcome & Treatment Options.

    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

  • Niki - December 4, 2017 reply

    Dear Dr. Sher , I wanted to ask you , I supposed to ship frozen embryos to different state , now the lab told me they don’t do the same process of thaw and I need to pay extra $500 for ordering special solution in order to thaw in them lab . Wanted to ask you if it is s better to do the transfer in the same lab I did last time and succeed or to take the risk and ship them and the solution to the new lab ? Please help me decide ! All I want is to success since I have left with the last 2 embryos. Thank you soooooo much

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 5, 2017 reply

    I don’t understand why there should be an additional charge. Why don’t you stay with the lab you used before.

    Good luck!

    Geoff Sher

  • Melissa - December 4, 2017 reply

    Hi Dr Sher,
    A lap revealed I have endometriosis (silent, asymptomstic) and my fimbrae and tubes are damaged, but the surgeon found nothing around my ovaries. I know you’ve said much of endo is invisible so my question is: in my case, would egg quality for IVF be compromised by silent endo even if surgeon didn’t see anything around my ovaries?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 5, 2017 reply

    Unlikely, but egg quality is not t6he only thing you need to be concerned about with mild endometriosis.

    Endometriosis is a condition that occurs when the uterine lining (endometrium) grows not only in the interior of the uterus but in other areas, such as the fallopian tubes, ovaries and the bowel. Endometriosis is a complex condition where, the lack or relative absence of an overt anatomical barrier to fertility often belies the true extent of reproductive problem(s).
    All too often the view is expounded that the severity of endometriosis-related infertility is inevitably directly proportionate to the anatomical severity of the disease itself, thereby implying that endometriosis causes infertility primarily by virtue of creating anatomical barriers to fertilization. This over-simplistic and erroneous view is often used to support the performance of many unnecessary surgeries for the removal of small innocuous endometriotic lesions, on the basis of such “treatment” evoking an improvement in subsequent fertility.
    It is indisputable that even the mildest form of endometriosis can compromise fertility. It is equally true that, mild to moderate endometriosis is by no means a cause of absolute “sterility”.
    Rather, when compared with normally ovulating women of a similar age who do not have endometriosis, women with mild to moderate endometriosis are about four to six times less likely to have a successful pregnancy.
    Endometriosis often goes unnoticed for many years. Such patients are frequently, erroneously labeled as having “unexplained infertility”, until the diagnosis is finally clinched through direct visualization of the lesions at the time of laparoscopy or laparoscopy. Not surprisingly, many patients with so called “unexplained” infertility, if followed for a number of years, will ultimately reveal endometriosis.

    Women who have endometriosis are much more likely to be infertile. There are several reasons for this:

    • First-Ovulation Dysfunction: In about 25 – 30% of cases, endometriosis is associated with ovulation dysfunction. Treatment requires controlled ovarian stimulation (COS). The problem is that the toxic pelvic environment markedly reduces the likelihood that anything other than IVF will enhance pregnancy potential.
    • Second- Toxic Pelvic environment that compromises Fertilization Endometriosis is associated with the presence of toxins in peritoneal secretions while it is tempting to assert that normally ovulating women with mild to moderate endometriosis would have no difficulty in conceiving if their anatomical disease is addressed surgically or that endometriosis-related infertility is confined to cases with more severe anatomical disease…nothing could be further from the truth. The natural conception rate for healthy ovulating women in their early 30’s (who are free of endometriosis) is about 15% per month of trying and 70% per year of actively attempting to conceive. Conversely, the conception rate for women of a comparable age who have mild or moderate pelvic endometriosis (absent or limited anatomical disease) is about 5-6% per month and 40% after 3 years of trying. As sperm and egg(s) travel towards the fallopian tubes they are exposed to these toxins which compromise the fertilization process. In fact it has been estimated that there is a 5-6 fold reduction in fertilization potential because of these toxins which cannot be eradicated. Frankly, it really does not matter whether an attempt is made to remove endometriosis deposits surgically as this will not improve pregnancy potential. The reason is that for every deposit observed, there are numerous others that are in the process of developing and are not visible to the naked eye and whether visible or not, such translucent deposits still produce toxins. This also explains why surgery to remove visible endometriosis deposits, controlled ovarian stimulation with or without intrauterine insemination will usually not improve pregnancy potential. Only IVF, through removing eggs before they are exposed to the toxic pelvic environment, fertilizing them in-vitro and then transferring the embryos to the uterus represents the only way to enhance pregnancy potential.
    • Third-Pelvic adhesions and Scarring: In its most severe form, endometriosis is associated with scarring and adhesions in the pelvis, resulting in damage to, obstruction or fixation of the fallopian tubes to surrounding structures, thereby preventing the union of sperm and eggs.
    • Fourth-Ovarian Endometriomas, Advanced endometriosis is often associated with ovarian cysts (endometriomas/chocolate cysts) that are filled with altered blood and can be large and multiple. When these are sizable (>1cm) they can activate surrounding ovarian connective tissue causing production of excessive male hormones (androgens) such as testosterone and androstenedione. Excessive ovarian androgens can compromise egg development in the affected ovary (ies) resulting in an increased likelihood of numerical chromosomal abnormalities (aneuploidy) and reduced egg/embryo competency”. In my opinion large ovarian endometriomas need to be removed surgically or rough sclerotherapy before embarking on IVF.
    • Fifth- Immunologic Implantation Dysfunction (IID). Endometriosis, regardless of its severity is associated with immunologic implantation dysfunction linked to activation of uterine natural killer cells (NKa) and cytotoxic uterine lymphocytes (CTL) in about 30 of cases. This is diagnosed by testing the woman’s blood for NKa using the K-562 target cell test or by endometrial biopsy for cytokine analysis, and, for CTL by doing a blood immunophenotype. These NKa attack the invading trophoblast cells (developing “root system” of the embryo/early conceptus) as soon as it tries to gain attachment to the uterine wall. In most cases, this results in death of the embryo even before the pregnancy is diagnosed and sometimes, in a chemical pregnancy or even an early miscarriage. . As such, many women with endometriosis, rather than being infertile, in the strict sense of the word, often actually experience repeated undetected “mini-miscarriages”.

    Advanced Endometriosis: In its most advanced stage, anatomical disfiguration is causally linked to the infertility. In such cases, inspection at laparoscopy or laparoscopy will usually reveal severe pelvic adhesions, scarring and “chocolate cysts”. However, the quality of life of patients with advanced endometriosis is usually so severely compromised by pain and discomfort, that having a baby is often low on the priority list. Accordingly, such patients are usually often more interested in relatively radical medical and surgical treatment options (might preclude a subsequent pregnancy), such as removal of ovaries, fallopian pubis and even the uterus, as a means of alleviating suffering.

    Moderately Severe Endometriosis. These patients have a modest amount of scarring/ adhesions and endometriotic deposits which are usually detected on the ovaries, fallopian tubes, bladder surface and low in the pelvis, behind the uterus. In such cases, the fallopian tubes are usually opened and functional.

    Mild Endometriosis: These patients who at laparoscopy or laparotomy are found to have no significant distortion of pelvic anatomy are often erroneously labeled as having “unexplained” infertility. To hold that the there can only infertility can only be attributed to endometriosis if significant anatomical disease can be identified, is to ignore the fact that, biochemical, hormonal and immunological factors profoundly impact fertility. Failure to recognize this salient fact continues to play havoc with the hopes and dreams of many infertile endometriosis patients.

    TREATMENT:
    The following basic concepts apply to management of endometriosis-related infertility:

    1. Controlled Ovulation stimulation (COS) with/without intrauterine insemination (IUI): Toxins in the peritoneal secretions of women with endometriosis exert a negative effect on fertilization potential regardless of how sperm reaches the fallopian tubes. This helps explain why COS with or without IUI will usually not improve the chances of pregnancy (over no treatment at all) in women with endometriosis. IVF is the only way by which to bypass this problem.
    2. Laparoscopy orLaparotomy Surgery aimed at restoring the anatomical integrity of the fallopian tubes does not counter the negative influence of toxic peritoneal factors that inherently reduce the chances of conception in women with endometriosis four to six fold. Nor does it address the immunologic implantation dysfunction (IID) commonly associated with this condition. Pelvic surgery is relatively contraindicated for the treatment of infertility associated with endometriosis, when the woman is more than 35 years of age. With the pre-menopause approaching, such women do not have the time to waste on such less efficacious alternatives. In contrast, younger women who have time on their side might consider surgery as a viable option. Approximately 30 -40 percent of women under 35 years of age with endometriosis will conceive with in two to three years following corrective pelvic surgery.
    3. Sclerotherapy for ovarian endometriomas.: About 10 years ago I introduced “sclerotherapy”, a relatively non-invasive, safe and effective outpatient method to permanently eliminate endometriomas without surgery being required. Sclerotherapy for ovarian endometriomas involves needle aspiration of the liquid content of the endometriotic cyst, followed by the injection of 5% tetracycline into the cyst cavity. Treatment results in disappearance of the lesion within 6-8 weeks, in more than 75% of cases so treated. Ovarian sclerotherapy can be performed under local anesthesia or under general anesthesia. It has the advantage of being an ambulatory office- based procedure, at low cost, with a low incidence of significant post-procedural pain or complications and the avoidance of the need for laparoscopy or laparotomy
    4. The role of selective immunotherapy Women with antiphospholipid antibodies (APA’s) experience improved IVF birth rates when heparinoids (Clexane/Lovenox) is administered from the onset of ovarian stimulation with gonadotropins until the 10th week of pregnancy.
    a. About Intralipid (IL) and steroid therapy: Intralipid (IL) is a solution of small lipid droplets suspended in water. When administered intravenously, IL provides essential fatty acids, linoleic acid (LA), an omega-6 fatty acid, alpha-linolenic acid (ALA), an omega-3 fatty acid.IL is made up of 20% soybean oil/fatty acids (comprising linoleic acid, oleic acid, palmitic acid, linolenic acid and stearic acid) , 1.2% egg yolk phospholipids (1.2%), glycerin (2.25%) and water (76.5%).IL exerts a modulating effect on certain immune cellular mechanisms largely by down-regulating activated natural killer cells (NKa). This effect is enhanced through the concomitant administration of corticosteroids such as dexamethasone, prednisone, and prednisolone which enhance the therapeutic effect by suppressing cytotoxic/activated T-lymphocytes (CTL). This effect of IL might is likely due to its ability to
    5. In vitro fertilization is the treatment of choice for women with endometriosis. This is especially true for women more than 35 years of age or where surgery and treatment with fertility agents has proven to be unsuccessful. We anticipate that approximately 75 percent of such women will achieve the birth of one or more babies within three IVF attempts performed.
    6.
     suppresses pro-inflammatory cellular (Type-1) cytokines such as interferon gamma and TNF-alpha. In-vitro testing has shown that IL successfully and completely down-regulates activated natural killer cells (NKa) within 2-3 weeks in 78% of women experiencing immunologic implantation dysfunction. In this regard it is just as effective as Intravenous Gamma globulin (IVIg) but at a fraction of the cost and with a far lower incidence of side-effects. Its effect lasts for 4-9 weeks when administered in early pregnancy.

    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.
    • 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
    • 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
    • Endometriosis and Infertily
    • Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF
    • Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
    • Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
    • Early -Endometriosis-related Infertility: Ovulation Induction (with or without Intrauterine Insemination) and Reproductive Surgery Versus IVF
    • Treating Ovarian Endometriomas with Sclerotherapy.
    • Effect of Advanced Endometriosis with Endometriotic cysts (Endometriomas) on IVF Outcome & Treatment Options.
    • Adenomyosis-Related Infertility: A Therapeutic Challenge!

    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.

  • Ana - December 4, 2017 reply

    Hello Doctor, I had a frozen embryo transfer yesterday. 10 days ago I had some uncomfortable feelings around my vaginal area and went to do the tests. Gynaecologist suspected Candida and prescribed me immediate treatment. Today I got the test results back and yes Candida was confirmed, but as well Herpes Simplex 1+2. I’m worried out of my mind now that my FET might not work because of this. I am sure I didn’t have an outbreak as my discomfort was mild.
    Do you have any advice? Can herpes virus be passed to the uterus during the embryo transfer?
    Kind Regards
    Ana

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 4, 2017 reply

    Neither Candida nor Herpes should affect your chance of success!

    Good luck!

    Geoff Sher

    Ana - December 4, 2017 reply

    Fantastic!! Thank you so much for your quick response Dr.Sher!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 4, 2017 reply

    You are most welcome!

    Geoff Sher

  • Cindy - December 3, 2017 reply

    Hi Dr Sher, where would I find your published success rates for each age group for your A/ACP and A/ACEP protocols? I can’t seem to find them anywhere and anything I do find is 7-10 years old. Can you provide the link?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 4, 2017 reply

    I do not have this broken down….Call 800-780-7437 and set up a consultation to discuss.

    Geoff Sher

    Cindy - December 4, 2017 reply

    Hi Dr Sher, it’s $200 to set up a consult. I was just after the success rates per age group.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 4, 2017 reply

    I cannot break down statistics for A/ACP versus non-A/ACP long protocols. I do not have that data. Remember, I reserve the A/ACP in cases where ovarian reserve is diminishing so success rates in those age categories where A/ACP is used cannot be compared with those cases where ovarian reserve is good and a regular long down regulation protocol was used. Also, the more severe the DOR, the higher the stimulation protocol and in spite of best effort, the lower the egg yield. So it is very difficult to quote meaningful statistics in any given age categories.

    If you wish to discuss in detail you will need to set up a consultation.

    Geoff Sher

  • Stella - December 2, 2017 reply

    Hi Dr Sher, I read your article on empty follicle syndrome. I was on a long BCP with lupron overlap cycle and had one empty follicle, is this also likely to be caused by poor protocol? 6 weeks on bcp with 2 days lupron overlap. Period arrived ten days after atopping BCP. Stims started on day 3. Stimmed for 15 days. We did not add luveris.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 3, 2017 reply

    One empty follicle does not alone signify the “syndrome”. Usually many follicles will be empty.

    I would be happy to discus this with you in detail. 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.

    Geoff Sher

  • Tunde - December 2, 2017 reply

    Hi Dr Sher,

    Thank you for the invaluable resource that you provide. I am glad I came across your site before your retirement. I would like to ask why it is that you recommend cetrotide 0.125mg rather than 0.25mg in your A/ACP protocol and if this might increase the risk of a breakthrough LH surge coming towards egg retrieval?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 3, 2017 reply

    125mcg of antagonist in the A/ACP arrangement is in my opinion sufficient to prevent premature luteinization.

    Geoff Sher

    Cherish - December 3, 2017 reply

    The last poster said you were retiring soon? Is this true?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 4, 2017 reply

    Barring unforeseen circumstance, no sooner than the end of 2018.

    Geoff Sher

    Tunde - December 4, 2017 reply

    Hi again, could one use 125mcg during the antagonist protocol starting the antagonist on the first day of the cycle with spontaneous bleeding if A/ACP is not being followed? as I understand your view is that the antagonist is started too late on day 6.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 4, 2017 reply

    Yes!

    Geoff Sher

    Tunde - December 4, 2017

    Thank you for your dedication to helping others. I will always remember your contribution to my IVF journey.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 5, 2017

    Thank you so very much.

    G-d bless!

    Geoff Sher

  • Sonia - December 2, 2017 reply

    Will IL work at all if it was done 7-9 days before embryo transfer? My clinic didn’t time things right, I know you’ve said it’s supossed to be done 10-14 days before.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 2, 2017 reply

    Ideal is 10-14 days before ET. However, anyhing longer than 7 days prior to ET should be OK!

    Geoff Sher

    Sonia - December 2, 2017 reply

    Thank you!!!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 3, 2017 reply

    You are so very welcome!

    Geoff Sher

  • Priyanka - December 1, 2017 reply

    Hi, I have been suffering repeated ivy failure with no apparent reasons. My embryos are perfect, my linning is perfect. Its just the implantation that fails. what should I do, Kindly suggest please. Should I give up the hope of ever having a kid?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 2, 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 .

    *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

  • Stace - December 1, 2017 reply

    Hi Dr Sher, what is your view of splitting Gonal f doses so if you are given 300 IU, instead of taking it in the evening, you split it and take 150iu in the morning and 150iu in the evening 12 hours apart? Would this create more even growth?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 2, 2017 reply

    There would in my opinion be no difference.

    Geoff Sher

  • Mimi - December 1, 2017 reply

    Hello Dr. Sher,
    I just turned 40 years old a week ago. I conceived my two beautiful daughters naturally when I was 31 and 34 years old. This year I also conceived naturally after we tried 6 months, but this pregnancy ended in a miscarriage (Tuner Syndrome) We were devastated and because of my age, we decided to do IVF with PGS. My day three testing result is: AMH 1.31, FSH 8.01, E2 63, LH 2.21 and AFC 7. My baseline E2 was 17 and AFC was 7 after 16 days of birth control pills. I started stimulation with 300iu Follistim and 150iu Menopur from the fourth day after my last BCP. Doctor only found 1 measurable follicle and E2 was 90 on day 4 monitoring. He said it was still too early to tell but he increased the Menopur to 225iu. Today is the day 6 monitoring, still only one measurable follicle 10mm*8mm and E2 is 149. My Menopur dosage is increased again to 300iu and Ganirelix is also added. This Sunday I will do one more monitoring. If there is still nothing going on, this cycle will be cancelled. I will talk with my doctor and nurse about the incoming plan if this cycle is cancelled. They didn’t expected I would have such low response to the medication. What would be your concern and recommendation based on the information I provided? For the next round, what would be your recommendation for the course of action?

    Thank you and Have a wonderful weekend!
    Mimi

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 2, 2017 reply

    You now have diminishing ovarian reserve (DOR) and this requires a very strategic approach to 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
    • 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

  • Anne - December 1, 2017 reply

    Thank you dr Sher and in response to Stella, here is also some more information about my cycle and eggs.
    all 3 of my embryos were Monosomy. One was day 5ab and 2 were day 6 4cc.
    1 was a partial, 1 had two missing chromosomes and third had three missing chromosomes.
    My first beta 13 days post 5 day transfer was 260 and by 15 days it was over 900.
    From those numbers and the sonogram it was pretty clear that all theee implanted!!!
    However only two sacks were growing with viable size and heartbeats.
    So yes mosony’s can implant. And none of these were mosaic.
    Just an FYI – Before my cycle I did a 90 day cleanse of high organic lean protein, no sugar, caffeine, alcohol,minimal amounts of carbs and only whole grains. I did coq10, dhea and royal jelly. Lots of greens, fish, eggs and avocados, nuts and coconut/ fish oils.
    Part of me was determined to implant the embryos simply because I refused to believe such a painful diet would leave me wit nothing. Why not try?
    I wanted to see if maybe the bad cells were pushed to the other layer or I was one of the small percentage of errors.
    My question to you dr Sher is have any of your patients who reached a heartbeat with an abnormal embryo then gone on to miscarry?
    Thank you so much.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 2, 2017 reply

    No! but then I have not had that many cases to be able to quote meaningful statistics.

    Geoff Sher

    Stella - December 2, 2017 reply

    Dear Anne, I would love to stay in contact with you if you would like to email me. I will see if my lab still has my embryo although I suspect they may have discarded it. My email is fairyfloss7676 at gmail dot com.
    Dr Sher, why does the literature out there say monosomy embryos die before implantation? That’s what my clini said!!!!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 2, 2017 reply

    That is true but only if it is meiotic aneuploidy…not mitotic aneuploidy (mosaicism) where it should autocorrect!

    Geoff Sher

    Stella - December 2, 2017 reply

    Hi Dr Sher, how will I know which one it is? I was told it was missing a copy of chromosome 22. Is that meiotic?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 3, 2017

    Unfortunately, in my opinion, you wont know without transferring the embryo to see what happens.

    Geoff Sher

    Ann - December 8, 2017 reply

    Anne – first of all congrats! What exciting news. I don’t know if you ever post on inspire.com (it is a web board that offers a bit more privacy) but if you wanted to connect with others who are in a similar position it’s a good place for that. There are several women who have transferred abnormal pgs embryos that share info there. I follow their journeys as I also have monosomy embryos that I would like to try. If I can find an RE in my area willing to do it.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 8, 2017 reply

    Human embryo development occurs through a process that encompasses reprogramming, sequential cleavage divisions and mitotic chromosome segregation and embryonic genome activation. Chromosomal abnormalities may arise during germ cell and/or pre-implantation embryo development, and represents a major cause of early pregnancy loss. About a decade ago, I and an associate, Levent Keskintepe Ph.D were the first to introduce full embryo karyotyping (identification of all 46 chromosomes) through preimplantation genetic sampling (PGS) as a method by which to selectively transfer only euploid embryos (i.e. those that have a full component of chromosomes) to the uterus. We subsequently reported on a 2-3 fold improvement in implantation and birth rates as well as a significant reduction in early pregnancy loss, following IVF. Since then PGS has grown dramatically in popularity such that it is now widely used throughout the world.
    Most IVF programs that offer PGS services, require that all participating patients consent to all their aneuploid embryos (i.e. those with an irregular quota of chromosomes) be disposed of. However, there is now growing evidence to suggest that following embryo transfer, some aneuploid embryos will in the process of ongoing development, convert to the euploid state (i.e. “autocorrection”) and then go on to develop into chromosomally normal offspring. In fact, I am personally aware of several such cases occurring within our IVF network. So clearly , summarily discarding all aneuploid embryos as a matter of routine we are sometimes destroying some embryos that might otherwise have “autocorrected” and gone on to develop into normal offspring.
    Thus by discarding aneuploid embryos the possibility exists that we could be denying some women the opportunity of having a baby. This creates a major ethical and moral dilemma for those of us that provide the option of PGS to our patients. On the one hand, we strive “to avoid knowingly doing harm” (the Hippocratic Oath) and as such would prefer to avoid or minimize the risk of miscarriage and/or chromosomal birth defects and on the other hand we would not wish to deny patients with aneuploid embryos, the opportunity to have a baby.
    The basis for such embryo “autocorrection” lies in the fact that some embryos found through PGS-karyotyping to harbor one or more aneuploid cells (blastomeres) will often also harbor chromosomally normal (euploid) cells (blastomeres). The coexistence of both aneuploid and euploid cells coexisting in the same embryo is referred to as “mosaicism.” As stated, some mosaic embryos will In the process of subsequent cell replication convert to the normal euploid state (i.e. autocorrect)
    It is against this background, that an ever increasing number of IVF practitioners, rather than summarily discard PGS-identified aneuploid embryos are now choosing to cryobanking (freeze-store) certain of them, to leave open the possibility of ultimately transferring them to the uterus. In order to best understand the complexity of the factors involved in such decision making, it is essential to understand the causes of embryo aneuploidy of which there are two varieties:
    1. Meiotic aneuploidy” results from aberrations in chromosomal numerical configuration that originate in either the egg (most commonly) and/or in sperm, during preconceptual maturational division (meiosis). Since meiosis occurs in the pre-fertilized egg or in and sperm, it follows that when aneuploidy occurs due to defective meiosis, all subsequent cells in the developing embryo/blastocyst/conceptus inevitably will be aneuploid, precluding subsequent “autocorrection”. Meiotic aneuploidy will thus invariably be perpetuated in all the cells of the embryo as they replicate. It is a permanent phenomenon and is irreversible. All embryos so affected are thus fatally damaged. Most will fail to implant and those that do implant will either be lost in early pregnancy or develop into chromosomally defective offspring (e.g. Down syndrome, Edward syndrome, Turner syndrome).
    2. “Mitotic aneuploidy” occurs when following fertilization and subsequent cell replication (cleavage), some cells (blastomeres) of a meiotically euploid early embryo mutate and become aneuploid. This is referred to as mosaicism. Thereupon, with continued subsequent cell replication (mitosis) the chromosomal make-up (karyotype) of the embryo might either comprise of predominantly aneuploid cells or euploid cells. The subsequent viability or competency of the conceptus will thereupon depend on whether euploid or aneuploid cells predominate. If in such mosaic embryos aneuploid cells predominate, the embryo will be “incompetent”). If (as is frequently the case) euploid cells prevail, the mosaic embryo will be “competent” and capable of propagating a normal conceptus.
    Since some mitotically aneuploid (“mosaic”) embryos can, and indeed do “autocorrect’ while meiotically aneuploid embryos cannot, it follows that an ability to differentiate between these two varieties of aneuploidy would be of considerable clinical value. And would provide a strong argument in favor of preserving certain aneuploid embryos for future dispensation.
    Aneuploidy, involves the addition (trisomy) or subtraction (monosomy) of one chromosome in a given pair. As previously stated, some aneuploidies are meiotic in origin while others are mitotic “mosaics”. Certain aneuploidies involve only a single, chromosome pair (simple aneuploidy) while others involve more than a single pair (i.e. complex aneuploidy). Aside from monosomy involving absence of the y-sex chromosome (i.e. XO) which can resulting in a live birth (Turner syndrome) all monosomies involving autosomes (non-sex chromosomes) are lethal and will not result in viable offspring). Some autosomal meiotic aneuploidies, especially trisomies 13, 18, 21, can progress to viable, but severely chromosomally defective babies. All other meiotic autosomal trisomies will almost invariably, either not attach to the uterine lining or upon attachment, will soon be rejected. All forms of meiotic aneuploidy are irreversible while mitotic aneuploidy (“mosaicism) often autocorrects in the uterus. Most complex aneuploidies are meiotic in origin and will almost invariably fail to propagate viable pregnancies.
    There is presently no microscopic or genetic test that can reliable differentiate between meiotic and mitotic aneuploidy. Notwithstanding this, the fact that some “mosaic” embryos can autocorrect in the uterus, makes a strong argument in favor of transferring aneuploid of embryos in the hope that the one(s) transferred might be “mosaic” and might propagate viable healthy pregnancies. On the other hand, it is the fear that embryo aneuploidy might result in a chromosomally abnormal baby that has led many IVF physicians to strongly oppose the transfer of any aneuploid embryos to the uterus.
    While certain meiotic aneuploid trisomies (e.g. trisomies 13, 18, & 21) can and sometimes do result in chromosomally defective babies, no other meiotic autosomal trisomies can do so. Thus the transfer of trisomic embryos in the hope that one or more might be mosaic, should exclude the use of embryos with trisomies 13, 18 or 21. Conversely, no autosomal monosomic embryos are believed to be capable of resulting in viable pregnancies, thereby making the transfer of autosomally monosomic embryos, in the hope that they are “mosaic”, a far less risky proposition. Needless to say, if such action is being contemplated, it is absolutely essential to make full disclosure to the patient (s) , and to insure the completion of a detailed informed consent agreement which would include a commitment by the patient (s) to undergo prenatal genetic testing aimed at excluding a chromosomal defect in the developing baby and/or a willingness to terminate the pregnancy should a serious birth defect be diagnosed.

    Geoff Sher

    Anne - December 9, 2017 reply

    Hi Anne – if you are open to sharing what clinic you are with that was open to exploring the transfer of a monosomy, I would be most grateful. Best wishes for continued success on your pregnancy. My email is ann dot tahini at gmail dot com

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 9, 2017 reply

    Good luck!

    Geoff Sher

  • Cassie - December 1, 2017 reply

    Hi I am doing fet I am on day 12 of my medicated fet cycle and my oestradiol level are 391/poml I start the sending stage in 2 day and have transfer on day 19 my level seem to low

    Cassie - December 1, 2017 reply

    I should also add my lining of womb was 11mm so good

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 1, 2017 reply

    That is fine.

    Geoff Sher

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 1, 2017 reply

    It is on the low side!

    Good luck and G-d bless!

    Geoff Sher

    Cassie - December 1, 2017 reply

    Thanks for your fast response I don’t under why it’s on the low dose as my lining is good can having low oestradiol stop my embryo from implanting thanks again

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 2, 2017 reply

    You only need an E2 of above 100pg/ml (+/-250 pmol/L to produce a thick enough lining. What we are talking about here is the hormonal support needed for optimal stimulation.

    Geoff Sher

  • Dami - December 1, 2017 reply

    Hi Doctor
    Which method of ovulation will you recommend for me..I will be 31 next year April and I have normal BMI, my ovarian reserve too is okay and the only reason I am going for IVF is because of my tubes…which method of stimulation will you advice that I go for long protocol or antagonist?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 1, 2017 reply

    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

  • Kris - December 1, 2017 reply

    Hi Dr. Sher.
    I am scheduled to have a double embryo day 2 transfer tomorrow. I had Chicago tests done in 2015 that showed I had a partial dq alpha match with my husband and nk cells. I have explained to the doctors my concern over putting two back. Will putting two back double the chances of a match and therefore double the chances my body will attack it or will having two put bank give me my best chance? I had two intralipids and am on 5mg prednisolone.
    I’m really confused and greatly appreciate your opinion!
    Thank you.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 1, 2017 reply

    DQa matching is ONLY relevant, requiring treatment, if in addition you have natural killer cell activation. And if (as is mostly the case) this is a partial DQa match (with NKa+) then in my opinion, only 1 embryo should be transferred per cycle, under IL/steroid cover. Also, I believe it to be less than ideal to transfer cleaved embryos. My preference is to transfer only blastocysts.

    Embryo transfer (ET) is undoubtedly a rate limiting factor when it comes to IVF outcome. In fact, in my opinion, it is the single most important procedural step in IVF. Optimal performance of ET takes practice, confidence, dexterity, timing, gentility and skill. Of all the hands-on procedures involved in the IVF process, embryo transfer is by far the most difficult to teach. In fact, any women fail to conceive simply because the practicing physician did (could) not perform this procedure optimally.

    The issue of whether it is better to transfer early (day 2-3,post fertilization) cleaved embryos rather than (day 5-6) blastocysts continues to rage. Here I wish to focus on the reasons why I favor transferring blastocysts.

    Not too long ago, it was believed that the sooner an embryo was transferred into the “natural environment” of the uterus, the greater would be the chance of it implanting and propagating a viable pregnancy. Thus most IVF physicians advocated day 2 or day 3 embryo transfers preferentially. About 20 years ago, we began to realize that there was no validity to the belief that an embryo would develop better and have a greater chance of propagating a baby by being inside the uterus earlier than it would by being allowed to first develop into a blastocyst in an incubator. About a decade later, it was realized that cleaved embryos that fail to develop into blastocysts are with few exceptions numerically chromosomally “incompetent” (aneuploid) such that had they been transferred earlier, they almost certainly would not have developed into blastocysts and would not have propagated a pregnancy anyway. Now most of us practicing in this field believe it to be preferential to selectively transfer blastocysts rather than earlier cleaved embryos. Don’t get me wrong! I am not saying that there is never a place for doing earlier pre-blastocyst transfers. Patients that only have one or two cleaved embryos available might as well transfer them early.

    The recent popularization of full preimplantation genetic sampling (PGS) using methods such as comparative genomic hybridization (CGH), next generation gene sequencing (NGS) and SNP array, now allow us to identify those blastocysts that are the most “competent”. Selective transfer of such embryos improves the implantation rate per embryo by a factor of 2-3.

    It is important to bear in mind that morphologically good looking day 3 embryos/blastocysts that are determined microscopically to be of a “high grade” , are by no means always numerically chromosomally “competent” euploid , and the likelihood of such embryos being “competent” diminishes progressively with advancing age of the woman. Only through the performance of full PGS can his age-related discrepancy be reduced.

    While it would be acceptable to me to transfer 2 PGS-untested blastocysts to women under 39 years, and to transfer 3 to older women, I would not recommend transferring more than 2 PGS-normal embryos at any age.

    The following are arguments in favor of performing blastocysts transfers:
    • By waiting to day 5-6 many unworthy, many aneuploid and “incompetent” embryos can be culled out, thereby allowing for the transfer of fewer embryos and minimizing the risk of high order multiple pregnancies.
    • Diagnostic Advantages:
    o Failure of the expected number of cleaved embryos to advance to the blastocyst stage of development in culture, raises the suspicion of underlying inherent embryo “incompetence”, which is usually (but not exclusively) egg-related rather than due to a sperm factor. While age of the woman is the most important factor involved, it can also be due to the wrong protocol of ovarian stimulation being used).
    o It facilitates the performance of PGS to identify and then selectively transfer only most “competent” (euploid) blastocysts. In such cases, provided there is no underlying uterine implantation dysfunction implantation and pregnancy rate is enhanced significantly.

    Of course, for the treating physician it is far less stressful not have to have to confront a patient with her having no surviving embryos to transfer. The avoidance of this has in my opinion, in the past, been one of the main reasons why IVF practitioners have elected to transfer cleaved embryos rather than blastocysts. But such a policy is usually not in the in the patients’ best interest. In my opinion, it is far better to advise the patient to do a blastocyst transfer since that is almost always in their best interest.

    Geoff Sher

  • Phyllis - December 1, 2017 reply

    Hi Dr Sher, how are you?
    Today is cycle day 17 on a natural cycle. I had an LH surge on CD13 and EWCM between CD12-CD15. Today my internal scan showed a follicle that was 26mm in size. My blood test showed estrogen at 59 pg/ml, progesterone at 0.3 ng/ml and LH at 3.3. There was no sign of the corpus luteum. I have been told I did not ovulate this month. The sonographer didn’t think the follicle was a cyst, it was black and the color doppler suggested so. What do you think it is from your experience? In your opinion, does it sound to you like a simple cyst or a non-functional cyst? if the latter, are they bad? No one seems concerned except me, simply because no one can give me an answer.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 1, 2017 reply

    It sounds like a cystic follicle to me.

    Geoff Sher

    Phyllis - December 1, 2017 reply

    Thanks, Dr Sher. Is a cystic follicle a bad thing? are they quite common for AMA ladies? This has never happened to me before. I always ovulate.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 1, 2017 reply

    They would not yield viable eggs in my opinion.

    Geoff Sher

  • Anne - December 1, 2017 reply

    Hi Dr Sher,
    You had asked me to keep you posted on othe outcome of my abnormal embryo transfer. Today was my six week apt and we saw two sacks and two heat beats. I live hour by hour in fear of a miscarriage. I’ve had healthy pregnancies before and just curious with your experience how many miscarriages vs. live births you’ve seen with abnormal transfers once a heat beat was seen.
    I can find any information on this anywhere you you are the person I know has the most up to date knowledge.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 1, 2017 reply

    This could be good news. I would however recommend prenatal genetic screening (chorionic villus sampling or amnio.

    Good luck and thank you for keeping me updated…Much appreciated!

    Geoff Sher

    Stella - December 1, 2017 reply

    Hi Anne, I, too, am following your story as I, too, have some abnormal embryos I want to transfer, but mine are monosomy and i have been told monosomy embryos do not make it to implantation. Please continue to keep us apprised of developments.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - December 1, 2017 reply

    Human embryo development occurs through a process that encompasses reprogramming, sequential cleavage divisions and mitotic chromosome segregation and embryonic genome activation. Chromosomal abnormalities may arise during germ cell and/or pre-implantation embryo development, and represents a major cause of early pregnancy loss. About a decade ago, I and an associate, Levent Keskintepe Ph.D were the first to introduce full embryo karyotyping (identification of all 46 chromosomes) through preimplantation genetic sampling (PGS) as a method by which to selectively transfer only euploid embryos (i.e. those that have a full component of chromosomes) to the uterus. We subsequently reported on a 2-3 fold improvement in implantation and birth rates as well as a significant reduction in early pregnancy loss, following IVF. Since then PGS has grown dramatically in popularity such that it is now widely used throughout the world.
    Most IVF programs that offer PGS services, require that all participating patients consent to all their aneuploid embryos (i.e. those with an irregular quota of chromosomes) be disposed of. However, there is now growing evidence to suggest that following embryo transfer, some aneuploid embryos will in the process of ongoing development, convert to the euploid state (i.e. “autocorrection”) and then go on to develop into chromosomally normal offspring. In fact, I am personally aware of several such cases occurring within our IVF network. So clearly , summarily discarding all aneuploid embryos as a matter of routine we are sometimes destroying some embryos that might otherwise have “autocorrected” and gone on to develop into normal offspring.
    Thus by discarding aneuploid embryos the possibility exists that we could be denying some women the opportunity of having a baby. This creates a major ethical and moral dilemma for those of us that provide the option of PGS to our patients. On the one hand, we strive “to avoid knowingly doing harm” (the Hippocratic Oath) and as such would prefer to avoid or minimize the risk of miscarriage and/or chromosomal birth defects and on the other hand we would not wish to deny patients with aneuploid embryos, the opportunity to have a baby.
    The basis for such embryo “autocorrection” lies in the fact that some embryos found through PGS-karyotyping to harbor one or more aneuploid cells (blastomeres) will often also harbor chromosomally normal (euploid) cells (blastomeres). The coexistence of both aneuploid and euploid cells coexisting in the same embryo is referred to as “mosaicism.” As stated, some mosaic embryos will In the process of subsequent cell replication convert to the normal euploid state (i.e. autocorrect)
    It is against this background, that an ever increasing number of IVF practitioners, rather than summarily discard PGS-identified aneuploid embryos are now choosing to cryobanking (freeze-store) certain of them, to leave open the possibility of ultimately transferring them to the uterus. In order to best understand the complexity of the factors involved in such decision making, it is essential to understand the causes of embryo aneuploidy of which there are two varieties:
    1. Meiotic aneuploidy” results from aberrations in chromosomal numerical configuration that originate in either the egg (most commonly) and/or in sperm, during preconceptual maturational division (meiosis). Since meiosis occurs in the pre-fertilized egg or in and sperm, it follows that when aneuploidy occurs due to defective meiosis, all subsequent cells in the developing embryo/blastocyst/conceptus inevitably will be aneuploid, precluding subsequent “autocorrection”. Meiotic aneuploidy will thus invariably be perpetuated in all the cells of the embryo as they replicate. It is a permanent phenomenon and is irreversible. All embryos so affected are thus fatally damaged. Most will fail to implant and those that do implant will either be lost in early pregnancy or develop into chromosomally defective offspring (e.g. Down syndrome, Edward syndrome, Turner syndrome).
    2. “Mitotic aneuploidy” occurs when following fertilization and subsequent cell replication (cleavage), some cells (blastomeres) of a meiotically euploid early embryo mutate and become aneuploid. This is referred to as mosaicism. Thereupon, with continued subsequent cell replication (mitosis) the chromosomal make-up (karyotype) of the embryo might either comprise of predominantly aneuploid cells or euploid cells. The subsequent viability or competency of the conceptus will thereupon depend on whether euploid or aneuploid cells predominate. If in such mosaic embryos aneuploid cells predominate, the embryo will be “incompetent”). If (as is frequently the case) euploid cells prevail, the mosaic embryo will be “competent” and capable of propagating a normal conceptus.
    Since some mitotically aneuploid (“mosaic”) embryos can, and indeed do “autocorrect’ while meiotically aneuploid embryos cannot, it follows that an ability to differentiate between these two varieties of aneuploidy would be of considerable clinical value. And would provide a strong argument in favor of preserving certain aneuploid embryos for future dispensation.
    Aneuploidy, involves the addition (trisomy) or subtraction (monosomy) of one chromosome in a given pair. As previously stated, some aneuploidies are meiotic in origin while others are mitotic “mosaics”. Certain aneuploidies involve only a single, chromosome pair (simple aneuploidy) while others involve more than a single pair (i.e. complex aneuploidy). Aside from monosomy involving absence of the y-sex chromosome (i.e. XO) which can resulting in a live birth (Turner syndrome) all monosomies involving autosomes (non-sex chromosomes) are lethal and will not result in viable offspring). Some autosomal meiotic aneuploidies, especially trisomies 13, 18, 21, can progress to viable, but severely chromosomally defective babies. All other meiotic autosomal trisomies will almost invariably, either not attach to the uterine lining or upon attachment, will soon be rejected. All forms of meiotic aneuploidy are irreversible while mitotic aneuploidy (“mosaicism) often autocorrects in the uterus. Most complex aneuploidies are meiotic in origin and will almost invariably fail to propagate viable pregnancies.
    There is presently no microscopic or genetic test that can reliable differentiate between meiotic and mitotic aneuploidy. Notwithstanding this, the fact that some “mosaic” embryos can autocorrect in the uterus, makes a strong argument in favor of transferring aneuploid of embryos in the hope that the one(s) transferred might be “mosaic” and might propagate viable healthy pregnancies. On the other hand, it is the fear that embryo aneuploidy might result in a chromosomally abnormal baby that has led many IVF physicians to strongly oppose the transfer of any aneuploid embryos to the uterus.
    While certain meiotic aneuploid trisomies (e.g. trisomies 13, 18, & 21) can and sometimes do result in chromosomally defective babies, no other meiotic autosomal trisomies can do so. Thus the transfer of trisomic embryos in the hope that one or more might be mosaic, should exclude the use of embryos with trisomies 13, 18 or 21. Conversely, no autosomal monosomic embryos are believed to be capable of resulting in viable pregnancies, thereby making the transfer of autosomally monosomic embryos, in the hope that they are “mosaic”, a far less risky proposition. Needless to say, if such action is being contemplated, it is absolutely essential to make full disclosure to the patient (s) , and to insure the completion of a detailed informed consent agreement which would include a commitment by the patient (s) to undergo prenatal genetic testing aimed at excluding a chromosomal defect in the developing baby and/or a willingness to terminate the pregnancy should a serious birth defect be diagnosed.

    Geoff Sher

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