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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  • nicola - February 1, 2018 reply

    I have just completed the first cycle of a x3 cycles, mild IVF. After seeing 8/9 follicles only 5 were mature enough for collection and all three on the left were empty. Out of the remaining two only one fertilized and that failed to go beyond the 4 cell stage.
    I am 43. A decent ovarian reserve and regular periods. I have mild/moderate Adenomyosis. I had one pregnancy (to 8 weeks) on IUI a year and a half ago. Since then no luck with three further IUIs thus the move to IVF. Any suggestions for the next two cycles?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - February 2, 2018 reply

    Hi Nicola,

    Very respectfully, I am totally against mini-IVF for older women and for thjose with diminished ovarian reserve.Results are very poor!

    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

  • bella - February 1, 2018 reply

    Hello Dr Sher, I saw you advocate the double trigger – would you recommend 2 x Ovitrelle 250mg or a combination of Ovitrelle and another (e.g. Buserelin)? thanks

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - February 2, 2018 reply

    It is NOT a double trigger that I advocate. It is a single trigger with 2X 250mcg ovidrel.

    Geoff Sher

  • Pavani - February 1, 2018 reply

    HCG level of 22.6(2.26mlU) at 15DPO- Should I still be hopeful?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - February 1, 2018 reply

    Repeat in 2 days to see if it doubles.

    Good luck!

    Geoff Sher

  • Katie - February 1, 2018 reply

    Sorry Dr. Sher, one more question: In your experience, how much does BMI affect uterine lining measurement? More specifically could a “healthy” but lower BMI of 19 make it harder to get lining up to 8 mm? I’ve always struggled with my lining (gets to about 7) and wondering if my weight might have something to do with that. I definitely eat well/hearty so I’m not restricting or “dieting” by any means, but if stuffing my face to put on a few pounds will help thicken my lining, I’m definitely open to it. Do you think body weight is a factor here or no?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - February 1, 2018 reply

    Hi Katie,

    If you eat well (no anorexia) and you menstruate regularly, I do not think BMI will play a big role.

    Good luck!

    Geoff Sher

  • Katie - February 1, 2018 reply

    Hey Dr. Sher, what does your clinic recommend as far as “rest” after a frozen embryo transfer? Bed rest or just back to normal activity? Would lifting a 25 pound toddler into and out of his crib (and carrying him around the house when he wants “up”) be detrimental to implantation? I’m not sure how moms with young kids do another transfer– it’s virtually impossible for me to NOT pick him up and I’m worried this is why our last transfer wasn’t successful. If it’s a big deal, don’t want to make the same mistake again.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - February 1, 2018 reply

    Just avoid over-exertion until ultrasound confirmation of a viable pregnancy, and that would include lifting a 25y old toddler, I am afraid.

    Good luck!

    Geoff Sher

    Katie - February 1, 2018 reply

    Ok thank-you! Honestly not sure how it’s possible to not lift my son for 2 weeks (let alone a day!), but I guess you just do the best you can. Putting him in and out of his crib is pretty hard to avoid since my husband leaves at 4 am for work! Eek.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - February 2, 2018 reply

    Do the best you can!

    Geoff Sher

  • Nicole - February 1, 2018 reply

    Hello Dr Sher thank you for your previous prompt responses to my inquiries. My doctor wants me to try the agonist protocol for my ivf schedule and wondering if you think that’s right for my age Im currently38. I tried antagonist but only yielded under 4 follicles so it was cancelled. What are your thoughts ?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - February 1, 2018 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 MD

  • Connie - February 1, 2018 reply

    When doing a natural FET cycle what day is the embryo implanted? It is a blast. Is it LH (or trigger) +7?
    Also in a natural FET when would you start progesterone supplementation? Thanks

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - February 1, 2018 reply

    Usually on the 6th day post-progesterone initiation or post-ovulation.

    Geoff Sher

  • Sheena - February 1, 2018 reply

    Hi Dr Sher, My periods have become very light. They used to last 3-5+ days and now it is only 1.5 days and I could probably use only 1 pad all day. This month my lining was 12mm after ovulation (I only just started my period this cycle so I don’t know if it will be heavier). What could be causing this? How can I find out? My Estrogen is normally on the low side in the luteal phase at around 200-350.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - February 1, 2018 reply

    It is not relevant to implantation. As long as the lining is >8mm on the day of ovulation or the hCG trigger.

    Geoff Sher

    Sheena - February 1, 2018 reply

    Thanks for the reassurance Dr Sher! Can I also get pregnant naturally with the light periods as long as the lining is >8mm? Could the light periods be caused by ablations or scarring? I was told it is not since the lining is thickening and would not thicken if there is scarring … is this correct? Thanks so much in advance!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - February 1, 2018 reply

    Yes you could get pregnant naturally…all other factors being normal.

    Geoff Sher

  • Venessa Laporte - January 31, 2018 reply

    I am 43 and have 3 children. My last one is 5 years old. I would like 1 more but my periods have become irregular. Also I have to use donor sperm so there is no way for me to know if I can concieve naturally. I am currently doing a IUI cycle with injectales. If it does not work should I go straight to IVF.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 31, 2018 reply

    In my opinion, IUI has about a 1:50 chance of resulting in a pregnancy in a woman of 43Y. You need IVF ASAP . Hopefully it is not already too late in the day.

    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

    Venessa Laporte - February 1, 2018 reply

    Hello Dr Sher I just left the Dr. Office I only have 1 lead follicle. I am doing a trigger tomorrow night for my IUI. I told the Dr. that if the IUI does not work that I would like to start a IVF cycle. He said in a IVF cycle I should only get 4 to 5 follicle and that IVF may not be worth it.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - February 1, 2018 reply

    I think IVF is advisable!

    Geoff Sher

  • Michelle - January 31, 2018 reply

    Thank you Dr Sher. Also would a 30minute walk 24hours after embryo transfer be OK? Seems a silly question and I know it says no strenuous exercise but I just wanted to ask.
    Thanks again.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 31, 2018 reply

    I would wait 2 days before doing such!

    Geoff Sher

  • Michelle - January 31, 2018 reply

    Hello Dr Sher,
    Maybe 3 hours after my frozen embryo transfer I had a streak of blood and a bit of discharge on the tissue when I went to the toilet, and nothing after that. I’m a bit worried as it was so soon after the transfer happened…Is this OK?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 31, 2018 reply

    I would not be overly concerned. This was almost certainly not coming from inside the uterus. Most likely it was due to an irritation of the cervix caused by insertion of the catheter.

    Geoff Sher

  • Kara - January 31, 2018 reply

    Hi Dr Sher,
    How soon after a FET should a hatching blastocyst (grade 5AA) implant?
    Thank you

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 31, 2018 reply

    Within 48 hours or so!

    Geoff Sher

  • Mel - January 31, 2018 reply

    Hello Dr Sher,

    In this link
    ( http://drgeoffreysherivf.com/preventing-severe-ovarian-hyperstimulation-syndrome-with-prolonged-coasting/ ) which explains prolonged coasting, Lupron isn’t mentioned. Why is that? I thought Lupron was part of prolonged coasting.

    Thank you

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 31, 2018 reply

    Thanks for this comment. In this article I refer to the use of an “agonist”. Lupron is one of several agonists that can be used. Agonists such as Buserelin and Aminopeptidyl can supplant Lupron. They form an integral part of the “coasting” regime.

    Geoff Sher

    Mel - January 31, 2018 reply

    Thank you

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 31, 2018 reply

    You are most welcome!

    Geoff Sher

    Mel - January 31, 2018 reply

    One additional question regarding that link Dr Sher, since I am really trying to understand prolonged coasting well.

    Based on this sample case you wrote about ( http://haveababy.com/fertility-information/ivf-authority/ovarian-hyperstimulation-syndrome-ohss-prolonged-coasting-can-solution) I thought that prolonged coasting started when the gonadotropin was removed and the agonist kept, and ended by removing the agonist and triggering.

    However, in the original link we were talking about (http://drgeoffreysherivf.com/preventing-severe-ovarian-hyperstimulation-syndrome-with-prolonged-coasting/), which explains prolonged coasting, it says that the agonist and gonadotropin are both stopped at the same time.

    Could you please clarify? thanks so much

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 31, 2018 reply

    No the Lupron continues all the way up to the hCG “trigger”. Central to the optimal execution of the process is to start the coasting preemptively …at the right time. Not too early and not too late. It needs to start when with >25 follicles, >50% of them are 14-16mm and the E2 reaches >2500pg/ml and the 10,000 hCG trigger is implemented as soon as the E2 drops to below 2500 on the down-swing (after coasting has begun). If the coasting lasts >4 days, that is less than optimal as far as egg quality is concerned.

    Good luck!

    Geoff Sher

  • azad - January 30, 2018 reply

    Dear Dr. Sher,
    Thank you so much for you website and all the useful information.
    I’m from middle east .
    40 years old and in IVF cycle with 4 freezed embryos.
    there is a big question in my mind ,
    my doctor Prescribed to use letrozole before transfer embryos .
    why should be Stimulate the ovaries in this part of IVF?
    Is it common or a special strategy ?
    According to my tests I have not any hormone problem except amh= 1
    Do you recommend this strategy?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 30, 2018 reply

    Respectfully,

    In my opinion there is no need for Letrozole here.

    Geoff Sher

  • Nicole - January 30, 2018 reply

    Hi Dr Sher I am 38 with low ovarian reserve which protocol would you recommend I use for Ivf? Thank u!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 30, 2018 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

  • Shahnax - January 30, 2018 reply

    Hi. I am 40

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 30, 2018 reply

    Copy??

    Geoff Sher

  • Eleanore - January 30, 2018 reply

    Hello dr. Sher.
    Can it do harm to take DHEA when the blood result for DHEA, DHEA -S and testosteron are in the normal range?
    Do you have perhaps other tips/ advices for egg maturation?
    Thank you again for your time.
    Kinds regards, Eleanore

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 30, 2018 reply

    Dehydroepiandrosterone (DHEA), is steroid hormone produced by the adrenal glands and ovary. It is involved in producing the male hormones, androstenedione testosterone and also estrogen. DHEA blood levels tend to decline naturally with age.
    Under the effect if luteinizing hormone (LH), DHEA is metabolized to testosterone in ovarian connective tissue (theca/stroma). Thereupon the testosterone is transported to the granulosa cells that form the innermost layer of the ovarian follicles where, under the influence of follicle stimulating hormone (FSH)-induced desmolase and aromatase enzymatic activity the testosterone is converted to estradiol. As this happens, granulosa cells multiply, follicle fluid volume increases along with estrogen output and egg development is promoted.
    It is recognition of the essential/indispensable role that male hormones (mainly testosterone) play in follicle and egg development that prompted the belief that by giving DHEA and boosting ovarian testosterone production might benefit follicle/egg development. This belief was given some credence by an Israeli study that in 2010 reported on improved fertility when a group of infertile women were given the administration of 75mg of oral DHEA for 5 months. However, this study was seriously flawed by the fact that it did not separate out women who had diminished ovarian reserve, older women and those with PCOS, all of whom have increased LH-induced production of testosterone. In fact, we recently completed a study (currently being processed for publication) where we conclusively showed that when follicular fluid testosterone levels exceeded a certain threshold, egg quality was seriously prejudiced as evidenced by a marked increase in the incidence of egg chromosomal defects (aneuploidy).
    Consider the following: Ovarian testosterone is needed for follicular development. However, the amount required is small. Too much ovarian testosterone spills over into the follicular fluid and has a deleterious effect on egg/follicle development. Some women (women with diminished ovarian reserve –DOR, older women and those with polycystic ovarian syndrome-PCOS) who tend to have increased LH biological activity, already over-produce testosterone. To such women, the administration of DHEA to such women, by “adding fuel to the fire” can be decidedly prejudicial, in my opinion. Young women with normal ovarian reserve do not over produce LH-induced ovarian testosterone, and are thus probably not at significant risk from DHEA supplementation. It is noteworthy that to date, none of the studies that suggest a benefit from DHEA therapy have differentiated between young healthy normal women with normal ovarian reserve on the one hand and older women, those with DOR and women with PCOS on the other hand.

    In Some countries DHEA treatment requires a medical prescription and medical supervision. Not so in the U.S.A where it can be bought over the counter. Since DHEA is involved in sex hormone production, including testosterone and estrogen, individuals with malignant conditions that may be hormone dependent (certain types of breast cancer or testicular cancer) should not receive DHEA supplementation. Also, if overdosed with DHEA some “sensitive women” might so increase their blood concentrations of testosterone that they develop increased aggressive tendencies or male characteristics such as hirsuites (increased hair growth) and a deepening voice. DHEA can also interact other medications, such as barbiturates, corticosteroids, insulin and with other oral diabetic medications.
    BUT the strongest argument against the use of routine DHEA supplementation is the potential risk of compromising egg quality in certain categories of women and since there is presently no convincing evidence of any benefit, why take the risk in using it on anyone.
    Finally, for those who in spite of the above, still feel compelled to take DHEA, the best advice I can give is to consult their health care providers before starting the process.

    Addendum: One potential advantage of DHEA therapy if used appropriately came from a study conducted by Washington University School of Medicine in St. Louis, MI and reported in the November 2004 issue of the “Journal of the American Medical Association” which showed that judicious (selective) administration of 50mg DHEA daily for 6 months resulted in a significant reduction of abdominal fat and blood insulin in elderly women.

    Geoff Sher

  • Heather - January 29, 2018 reply

    Dear Dr Sher,
    I’m 43-yrs old, pregnant (13.5 weeks) with donor egg (27-yr old repeated (5X) donor) following FET.
    Based on my donors genetic profile, her risk of Downs is 1/1440, and overall general abnormalities 1/499.
    I just underwent 1st trimester screen, and got puzzling results, which the Dr+counselor weren’t sure how to explain, hence I’m turning to you.
    After NT measurement + PAPP-A/HCG, my Downs risks if 1/90 (adjusted to donor’s age). The Dr isn’t sure whether the tests truly reflect Downs or placental dysfunction due to the following variables:
    -previous complete uterine rupture
    -NT 2.6mm
    -*PAPP-A 0.14 MoM
    -HCG 0.55 MoM
    I asked this Dr if IVF reduces blood test scores but she wasn’t sure.
    This is the 2nd embryo to be transferred : 1st didn’t implant. I only have 3 left and am confused that they’re all ‘abnormal’.
    What do you please think is happening (I’m taking the cell-free blood test next week).
    Thank you very much

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 30, 2018 reply

    I suggest you do an amniocentesis to make absolutely certain all is well!

    Good luck!

    Geoff Sher.

  • Janne - January 29, 2018 reply

    Dr. Sher, I was under IVF/PGS and altogether I got 10 blastos but only 1 out of 10 was euploid (3mosaics). This is the point… after 2 miscarriages from natural conceptión (the heart at the 11th week stopped in both cases…and the biopsy showed aneuploid fetus). On my stims the embryos always present a considerable fragmentation rate and always produces a 6-day blastos. However, my eggs rate maturation is over 90% with the average of 11 oocytes retrieved per stim and with 85% fertilized. The problem comes on day 3/4 when the embryos start to arrest or present more fragmentation. TUNNEL and FISH was already performed and it was negative for SDF. Could you, Dr. Sher, add any light to a diagnosis or how to proceed from now on? In your opinion my case is for egg or sperm donation?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 30, 2018 reply

    Hi Janne,

    I really would need much more information regarding u=your age, your ovarian reserve (AMH) and the exact protocol used for ovarian stimulation to =comment authoritatively. There is little doubt that the most important factors influencing egg/embryo “competency” is the age of the woman and the protocol used.

    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

  • Mahia Keller - January 29, 2018 reply

    Im currently preparing for FET with embryos we made from donor eggs. I’m on cd 75 (which has never happened before) but fsh is always high since i only have half of an ovary. Had large cyst removed November. Had baselines on friday which showed lining of 6 with mild fluid in cul de sac. DHEA 514, testosterone 74.3, lh 63, estrogen 30, prog .7, I cant find anything about all of these numbers showing bad/ok timing for a fet. Im currently on letrezole and lovenox twice a day and go back this friday for recheck. Does dhea have any affect on lining for transfer good or bad and is it true that with a transfer lining is really all that matters as long as prog and estrogen get built in in time? Im so confused.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 30, 2018 reply

    Dehydroepiandrosterone (DHEA), is steroid hormone produced by the adrenal glands and ovary. It is involved in producing the male hormones, androstenedione testosterone and also estrogen. DHEA blood levels tend to decline naturally with age.
    Under the effect if luteinizing hormone (LH), DHEA is metabolized to testosterone in ovarian connective tissue (theca/stroma). Thereupon the testosterone is transported to the granulosa cells that form the innermost layer of the ovarian follicles where, under the influence of follicle stimulating hormone (FSH)-induced desmolase and aromatase enzymatic activity the testosterone is converted to estradiol. As this happens, granulosa cells multiply, follicle fluid volume increases along with estrogen output and egg development is promoted.
    It is recognition of the essential/indispensable role that male hormones (mainly testosterone) play in follicle and egg development that prompted the belief that by giving DHEA and boosting ovarian testosterone production might benefit follicle/egg development. This belief was given some credence by an Israeli study that in 2010 reported on improved fertility when a group of infertile women were given the administration of 75mg of oral DHEA for 5 months. However, this study was seriously flawed by the fact that it did not separate out women who had diminished ovarian reserve, older women and those with PCOS, all of whom have increased LH-induced production of testosterone. In fact, we recently completed a study (currently being processed for publication) where we conclusively showed that when follicular fluid testosterone levels exceeded a certain threshold, egg quality was seriously prejudiced as evidenced by a marked increase in the incidence of egg chromosomal defects (aneuploidy).
    Consider the following: Ovarian testosterone is needed for follicular development. However, the amount required is small. Too much ovarian testosterone spills over into the follicular fluid and has a deleterious effect on egg/follicle development. Some women (women with diminished ovarian reserve –DOR, older women and those with polycystic ovarian syndrome-PCOS) who tend to have increased LH biological activity, already over-produce testosterone. To such women, the administration of DHEA to such women, by “adding fuel to the fire” can be decidedly prejudicial, in my opinion. Young women with normal ovarian reserve do not over produce LH-induced ovarian testosterone, and are thus probably not at significant risk from DHEA supplementation. It is noteworthy that to date, none of the studies that suggest a benefit from DHEA therapy have differentiated between young healthy normal women with normal ovarian reserve on the one hand and older women, those with DOR and women with PCOS on the other hand.

    In Some countries DHEA treatment requires a medical prescription and medical supervision. Not so in the U.S.A where it can be bought over the counter. Since DHEA is involved in sex hormone production, including testosterone and estrogen, individuals with malignant conditions that may be hormone dependent (certain types of breast cancer or testicular cancer) should not receive DHEA supplementation. Also, if overdosed with DHEA some “sensitive women” might so increase their blood concentrations of testosterone that they develop increased aggressive tendencies or male characteristics such as hirsuites (increased hair growth) and a deepening voice. DHEA can also interact other medications, such as barbiturates, corticosteroids, insulin and with other oral diabetic medications.
    BUT the strongest argument against the use of routine DHEA supplementation is the potential risk of compromising egg quality in certain categories of women and since there is presently no convincing evidence of any benefit, why take the risk in using it on anyone.
    Finally, for those who in spite of the above, still feel compelled to take DHEA, the best advice I can give is to consult their health care providers before starting the process.

    Addendum: One potential advantage of DHEA therapy if used appropriately came from a study conducted by Washington University School of Medicine in St. Louis, MI and reported in the November 2004 issue of the “Journal of the American Medical Association” which showed that judicious (selective) administration of 50mg DHEA daily for 6 months resulted in a significant reduction of abdominal fat and blood insulin in elderly women.

    Geoff Sher
    .

  • Kristy - January 29, 2018 reply

    I had IVF after being diagnosed with PCOS and Hydrosalpinx (tubal litigation was done for hydros). I was put on metformin, gonal-f, menopur, lupron, cetrotide, progesterone, and estrace. Anticipated 14 follies going intro retrieval, 8 were retrieved, only 3 were mature (a 4th one they tried to mature but failed), 2 fertilized, and 1 made it to day 5 transfer (we actually did get pregnant but ended up 6 months later with stillborn due to placenta abruption). I’m re-consulting with my RE today, and although I trust him greatly, I was curious to see what your recommendations are for protocol changes that results in more mature eggs?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 30, 2018 reply

    The cause of the stillborn needs to be explained. Can you provide any further information in this regard?

    Geoff Sher

  • Katie - January 29, 2018 reply

    Hey again Dr. Sher. We just had an unsuccessful FET and are gearing up for our next transfer at the end of February. I have hypothalamic amenorrhea and don’t ovulate on my own. I stopped all PIO and estrace last Monday, the 22nd. Day 1 of my cycle was Friday, the 26th.

    I went in or an ultrasound on Day 3 (Sunday) and everything looked fine. Was told to start BCP and I’ll take for just 12 days. Then we’ll go right into estrace in prep for the FET (skipping Lupron since I don’t ovulate). My question is in regards to cycle timing, etc..

    I presume the reason I don’t need to be on BC very long is because I don’t cycle/ovulate on my own? Just felt a little weird to me to “start” what should be mid-cycle. Does it make sense/sound ok to you?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 29, 2018 reply

    If your lining is <5mm you could start without having a period. However, it is important to recognize that hypothalamic amenorrhea is associated with sustained and severe hypo-estrinism and you need sustained estrogen priming to establish estrogen receptor render the endometrium receptive to estrogen stimulation. This is why menopausal women often have a poor uterine lining in spite of short-term estrogen stimulation prior to egg donation-IVF. In my opinion, 2 months ofe E/P cyclical therapy should be considered prior to embarking on ovarian stimulation with or without IVF to build endometrial receptivity to estrogen in advance. If your lining fails to get to 9mm with controlled ovarian stimulation, this could be the reason, in my opinion.

    Good luck!

    Geoff Sher

    Katie - January 29, 2018 reply

    Thanks so much for sharing that. Just so I’m clear, can you elaborate on what “E/P cyclical therapy” entails?

    For reference, our first FET was successful (lining was right around 8mm). Our second was not (lining was around 7 mm). So I definitely want to try to get lining up to 8-9 + this round before transfer. Was considering vaginal viagara after seeing your posts about it, but sounds like you think this might be a better bet?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 30, 2018 reply

    I think a combination of both would be a good idea. Cyclical Estrogen/Progesterone therapy is where you take estrogen for about 25 days and add a progesterone in the last 10 days…then stop for 5 days or so…only to repeat the same cyclically….Discuss with your RE.

    Good luck!

    Geoff Sher

    Katie - January 30, 2018

    Got it. You’re the best, thanks for all your time!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 30, 2018

    You are welcome Katie!

    Geoff Sher

  • Christina - January 29, 2018 reply

    Hi Dr.
    I had a 5th day et In 22 Jan.
    I did my beta HCG today 29 Jan, (day 8 post et).
    HCG level v.low (0.2).
    My Dr. Said I should repeat in 3 or 4 days.
    Is it possible it would raise to normal level?
    Best

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 29, 2018 reply

    It is unlikely (but not impossible) in my opinion.

    Geoff Sher

  • Karen - January 29, 2018 reply

    Eight weeks ago I successfully delivered a beautiful baby girl after FET. This comes after a missed miscarriage some months before. Routine blood work on the placenta showed several clots and I was sent for blood work. Found to have a protein C of 187 and Protein S of 41. Hematologist said no anticoagulation is needed in future pregnancies as I have had one successful pregnancy. I’m wondering if a second opinion is needed. I have only 2 frozen embryos remaining and I want the best chance of carrying them. In your opinion, would you advise anticoagulation in future pregnancies?

    Karen - January 29, 2018 reply

    Sorry, I meant “routine biopsy” of the placenta

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 29, 2018 reply

    Copy!

    Geoff Sher

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 29, 2018 reply

    I would take a 2nd opinion because in my opinion, discretion is the better part of valor and I probably would consider using Lovenox/Clexane.

    Geoff Sher

  • Siri - January 29, 2018 reply

    Hi and a big thank you for writing all the blog posts and answering questions. They are very informative! I hope you have time to answer me as well 🙂

    I am 32 years old and have been trying to conceive for 1,5 years now. The first year naturally, then we went to examinations and everything seemed to be okay. Though they suspect that I might have PCO. My AMH was 11.5, my ovaries have many follicles and I have long cycles (sometimes 40 days). I have thyroid insufficiency to which I take thyroxin.

    First we tried two times with clomifen, then once with letrozole. The cycle was shortened but no pregnancy. Then we tried three times with letrozole, pregnyl and insemination without success.

    We just had our first IVF. They collected 40 follicles, 20 had an egg inside and 17 were mature. Those 17 fertilized, but 10 of them had two or more semen inside them (polyspermy?), so they were abnormal.

    Of the remaining 7, five divided abnormally in the first two days so we lost them as well. One lasted until fourth day, but didn’t make it to blastocyst. One was frozen in Day 2 or 3. We are waiting that to be transferred in the future. We don’t have our hopes high since all the others were bad quality and we fear this will be also.

    What could have caused our poor result and do you have any advise how to proceed with treatment? Do you think we still have hope for our own biological baby?

    Our IVF protocol was as follows:

    Gonal F 100 IU from day 2 to day 13.
    Cetrotide 0,25 mg from day 7 to day 12.
    Gonapeptyl 0,2 mg in day 13 at 10 pm
    The operation was on day 15 at 10 am. We had to freeze all to avoid OHSS.

    Before IVF, I took vitamin D, folic acid, multivitamin (A,D,E,C,B) and Donaferty (myo-inositol, d-chiro-inosito). I have now quit multivitamin since it has vitamin A in it, which I read isn’t good when trying to conceive. Also I took Donaferty only the month when preparing to IVF and I read that I should have taken it from 3 months earlier already. Do you think these might help with the egg quality and is there anything else you could recommend? CoQ10 perhaps?

    Thank you a lot in advance for your reply! We really appreciate your work a lot!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 29, 2018 reply

    Hi Siri,

    While m the supplements you are taking wont do harm , I doubt they alone will impact egg/embryo quality. With PCOS, ot is all about the protocol used for ovarian stimulation and its implementation. It also about the timing and method used for triggering egg maturation prior to ER.

    Polycystic ovary syndrome (PCOS) is a common hormonal system disorder among women affecting between 5% and 10% of women of reproductive age worldwide. Women with PCOS may have enlarged ovaries that contain multiple small collections of fluid (subcapsular microcysts) that are arranged like a “string of pearls” immediately below the ovarian surface (capsule).interspersed by an overgrowth of ovarian connective tissue (stroma). The condition is characterized by abnormal ovarian function (irregular or absent periods, abnormal or absent ovulation and infertility, androgenicity (increased body hair or hirsutism, acne) and increased body weight –body mass index or BMI.
    Women with PCOS are at increased risk that ovarian stimulation with gonadotropins will result in the, of development of severe ovarian hyperstimulation syndrome (OHSS), a life-endangering condition that is often accompanied by a profound reduction in egg “competency” and on fertilization often yield an inordinately high percentage of “incompetent” embryos which have a reduced potential to propagate viable pregnancies.
    Concern and even fear that their PCOS patients will develop of OHSS often leads the treating RE to take measures aimed at reducing the risk of this life-endangering condition. One such measures is to “trigger” egg maturation prematurely in the hope of arresting further follicular growth and the other, is to initiate the “trigger” with a reduced dosage of hCG (i.ed. 5,000U rather than the usual 10,000U of of Pregnyl/Profasi/Novarel, to use or 250mcg rather than 500mcg of Ovidrel or to supplant the hCG “trigger” with a Lupron “trigger” which causes a prompt LH surge from the woman’s pituitary gland to take place. While such measures do indeed reduce the risk of OHSS to the mother, this often comes at the expense of egg quantity and “competency”. Fewer than the anticipated number of eggs are harvested and those that are retrieved are far more likely to be “immature” and chromosomally abnormal (aneuploid”), or “immature” , thereby significantly compromising IVF outcome.
    Against this background, It is my considered opinion that when it comes to performing IVF in women with PCOS, the most important consideration must be the selection and proper implementation of an individualized or customized ovarian stimulation protocol. Thereupon, rather than prematurely initiating the “trigger” to arrest further follicle growth, administering a reduced dosage of hCG or “triggering with a GnRH agonist (e.g. Lupron/Buserelin) that can compromise egg “competency”….. use of one of the following techniques will often markedly reduce the risk of OHSS while at the same time protecting egg quality:
    1. PROLONGED COASTING…my preferred approach: My preferred approach is to use a long pituitary down-regulation protocol coming off the BCP which during the last 3 days is overlapped with the agonist, Lupron/Buserelin/Superfact. The BCP is intended to lower LH and thereby reduce stromal activation (hyperthecosis) in the hope of controlling LH-induced ovarian androgen (predominantly, testosterone) production and release. I then stimulate my PCOS patients using a low dosage of recombinant FSH-(FSHr) such as Follistim/Gonal-F/Puregon. On the 3rd day of such stimulation a smidgeon of LH/hCG (Luveris/Menopur) is added. Thereupon, starting on day 7 of ovarian stimulation, I perform serial blood estradiol (E2) and ultrasound follicle assessments, watching for the number and size of the follicles and the blood estradiol concentration [E2]. 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 concentration daily. The [E2] will almost invariably increase for a few days. I closely monitor the [E2] as it rises, plateaus and then begins to decline. As soon as the [E2] drops below 2500pg/ml (and not before then), I administer a “trigger” shot of 10,000U Profasi/ Novarel/Pregnyl or 500mcg Ovidrel/Ovitrel. This is followed by an egg retrieval, performed 36 hours later. Fertilization is accomplished using intracytoplasmic sperm injection (ICSI) because “coasted” eggs usually have little or no cumulus oophoris enveloping them 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 the blastocyst stage (up to day 5- 6 days) and thereupon are either vitrified and preserved for subsequent transfer in later hormone replacement cycles or (up to 2) blastocysts are transferred to the uterus, transvaginally under transabdominal ultrasound guidance. The success of this approach depends on precise timing of the initiation and conclusion of “prolonged coasting”. If started too early, follicle growth will arrest and the cycle will be lost. If commenced too late, too many follicles will be post-mature/cystic (>22mm) and as such will usually harbor abnormal or dysmature eggs. Use of “Coasting” almost always prevents the development of severe OHSS, optimizes egg/embryo quality and avoids unnecessary cycle cancellation. If correctly implemented, the worst you will encounter is moderate OHSS and this too is relatively uncommon.
    2. EMBRYO FREEZING AND DEFERMENT OF EMBRYO TRANSFEDR (ET): OHSS is always a self-limiting condition. In the absence of continued exposure to hCG, symptoms and signs as well as the risk of severe complications will ultimately abate. Thus, in the absence of pregnancy, all symptoms, signs and risks associated with OHSS will disappear within about 10-14 days of the hCG trigger. Conversely, since early pregnancy is always accompanied by a rapid and progressive rise in hCG , the severity of OHSS will increase until about the 9th or tenth gestational week whereupon a transition from ovarian to placental hormonal dominance occurs, the severity of OHSS rapidly diminishes and the patient will be out of risk. Accordingly, in cases where in spite of best effort to prevent OHSS, the woman develops symptoms and signs of progressive overstimulation prior to planned ET, all the blastocysts should be vitrified and cryostored for FET in a subsequent hormone replacement cycle. In this way women with OHSS can be spared the risk of the condition spiraling out of control.
    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.
    · Egg Maturation in IVF: How Egg “Immaturity”, “Post-maturity” and “Dysmaturity” Influence IVF Outcome:
    · Commonly Asked Question in IVF: “Why Did so Few of my Eggs Fertilize and, so Many Fail to Reach Blastocyst?”
    · 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?
    · Taking A Fresh Look at Ovarian Hyperstimulation Syndrome (OHSS), its Presentation, Prevention and Management
    · Preventing Severe Ovarian Hyperstimulation Syndrome (OHSS) with “Prolonged Coasting”
    · Understanding Polycystic Ovarian Syndrome (PCOS) and the Need to Customize Ovarian Stimulation Protocols.
    · “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?
    • .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.
    • Implications of “Empty Follicle Syndrome and “Premature Luteinization”
    • Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
    • Preventing Severe Ovarian Hyperstimulation Syndrome (OHSS) with “Prolonged Coasting”

    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

    Siri - January 29, 2018 reply

    From 17 fertilized embryos, only one was good enough to be frozen and it was frozen quite early (day2 or 3). Do you think the poor result could be because of the IVF protocol we used? Do you think we still have hope with another IVF done differently (prolonged coasting method)?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 30, 2018 reply

    Hi Siri,

    In my opinion, the age of the woman, her ovarian reserve ad the protocol used for ovarian stimulation are tghe most important factors determining egg/embryo “competency” mand nthus outcome with IVF.

    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

  • atena - January 29, 2018 reply

    hi doctor
    i am pco with 15.4 amh my Uterus cavity and endometrium is normal. my husband has sperm issues rapid progressive(a)= 2 , progressive (b)=18, total progressive=50, non motile=50. and sperm count 50 million. morphology is 2.
    does my spouse need to do SDFA (DNA fragmentation index (DFI)) SPERM TEST FOR ivf ? i have had no pregnancy for 14 months. i took 5 cycles of letrozol.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 29, 2018 reply

    It could be beneficial.

    Geoff Sher

  • Renda Shadowen - January 29, 2018 reply

    I have read alot of reveiws and some woman said they would have a neg hcg until almost 8 weeks pregnant is that possible or no

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 29, 2018 reply

    impossible!

    Geoff Sher

    Christina - January 29, 2018 reply

    Dr. Geoffrey,
    Hi again,
    Your response (Impossible), is for my question, or for Renda (the next commenter).
    Thx

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 29, 2018 reply

    OK!

    Geoff Sher

  • Maria Ana Rocha Caixe - January 29, 2018 reply

    We would like to discuss to doctor Sher about our final prognosis, after 2 miscarriages (from natural conception) and 1 IVF cycle (7 stims which provided around 43 matures eggs but only 10 bad qualities blastos, which were under PGS, resulting 1 euploid embryo (FET performed but bfn); 3 mosaics (they are now frozen for further reflexion) and 6 aneuploids embryos out of those previous 10. Nowadays, we put our former infertility clinic,in Helsinki, in stand by about the transfer of the mosaics and we moved, then, into a renowned clinic in Spain. First thing in the new clinic: they analyzed DH’s sperm in a molecular level by TUNNEL and FISH. No SDF was found. Despite that, they still think the infertility is a male factor once the fragmentation and embryos arrest were always seen from day 3/4 from those previos stims. In resume, according to the first clinic (finnish clinic) the infertility issue is a female factor, advising for a egg donation. On the other hand, the new clinic are going to try one stim. to check the lab factor, otherwise they advise for sperm donation!!! it means: 2 clinics, 2 completly opposite diagnosis. what Dr. Sher shall add?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 29, 2018 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

    Maria Ana Rocha Caixe - January 29, 2018 reply

    Thank you for The long coment, but, with all due respect, I can not find in this general reply, althoug very consistent, of course (I have read the same answer to another patient with diferent question approach) not much that could bright my questions, unfortunatly … as you can see, Dr. Sher, I have already submited my embryos to PGS… but only 1 out of 10 was euploid. This is the point… after 2 miscarriages from natural conceptión (the heart at the 11th week stopped in both cases…and the biopsy showed aneuploid fetus). On my stims the embryos always present a considerable fragmentation rate and always produces a 6-day blastos. However, my eggs rate maturation is over 90% with the average of 11 oocytes retrieved per s tim and with 85% fertilized. The problem comes on day 3/4 when the embryos start to arrest or present more fragmentation. TUNNEL and FISH was already performed and it was negative for SDF. Could you, Dr. Sher, add any light to an diagnosis or how to proceed from now on?

  • Renda Shadowen - January 29, 2018 reply

    How did a gestation sac get into my uterus if the only tube i have left showed blocked in 2012

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 29, 2018 reply

    If indeed there is a gestational sac then at least one tube must have a small opening. W

    Geoff Sher

  • Nicole - January 28, 2018 reply

    Hi Dr Sher I have been taking ubiquinol and royal jelly for a year now.
    Does this help the quality of eggs?
    Thanks

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 28, 2018 reply

    There is no data to that effect but it possibly could have a benefit…in my opinion.

    Geoff Sher

  • Renda Shadowen - January 28, 2018 reply

    I had my tubrs cut tied and burned after my 4th child they were tied for 13 years i had a reversal in march 2012 6 months later i was pregnant in was an ectopic in my left fube so at 8 weeks along they removed my tube so a couple months later i had an hsg done and it showed my right tube blocked at the top i had a vaginal ultra sound yesterday due to alot of pain they said i have a fibroid tumor on my uterus and they said there is a gestational sac in my uterus but they ran a hcg blood test and it was negitive so im at a loss what does this mean and if my tube is blocked how does a sac even get into my uterus and does it mean its empty or that im not pregnant because the blood test is negitive

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 28, 2018 reply

    If the hCG is negative you are not pregnant. The fibroid and the tubal condiytion must be assessed separately.

    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
    • The Role of IVF in Cases of Tubal Damage
    • Case Study: Treating Hydrosalpinx by Surgical Removal (Salpingectomy) as a Prelude to IVF
    • Ectopic (Tubal) Pregnancy and IVF
    • Fibroid uterus

    If you are interested in my advice or medical 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.
    Also, 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

  • Jessica - January 28, 2018 reply

    Hi Dr Sher,
    I am starting an IVF shortly but am unclear on the impact my LH day 2 should have on the protocol.
    My most recent day 2 blood details below: (husbands sperm is excellent).
    Amh: 2.8
    Afc: 16
    FSH: 7.5
    LH: 12.1
    Estradiol: 31
    Progesterone: <1

    My proposed protocol is 225 Gonal-f and 75 Menopur; cetrotide (assuming this will start being administered on around day 6) and a 10,000 iu HCG trigger. I am trying to understand some of the literature on higher than normal LH at start of cycle but not making head or tail of it.
    Should I get a second opinion on this protocol ie should I be requesting a down regulation first and then not be using menopur and only sticking with the recombinant FSH (Gonal-f)?

    Thank you!
    Jessica

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 28, 2018 reply

    I do not believe the LH on day 2 is relevant. What I do not understand is why your stimulation is only starting on day 6. late…

    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

    Leena - January 29, 2018 reply

    My RE doesnt add the LH at all for this protocol. What effect, if any, does leaving luveris or menopur out and using just FSH have? I get good blasts on this cycle but not when I add LH…?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 29, 2018 reply

    Hi Leena,

    Depending on the protocol used, your age and your hormonal profile, you could be providing enough pituitary LH to meet the need for egg development.

    This having been said, the only way I can comment authoritatively would be if I knew much more about your case. Feel free to call Julie at 702-533-2691 to set up a Skype consultation so we can discuss in detail.

    Geoff Sher

  • Nicki - January 27, 2018 reply

    Dear Dr Sher

    I’d be interested to hear your opinion on my recent IVF experience, I’m 41 and egg reserves are low Ive tried IUI in the past but this was my first IVF attempt, All was going as good as could be expected for my age, 5 possibilities of eggs, at the trigger injection it started to go a bit wrong the liquid leaked as I mixed it and then the same as I injected it leaked from the join between the needle head and the sering losing some down my tummy, tricky to know how much, I took it off and tried to get it as tight as I can but it still leaked, surely it should do that? 4 eggs were harvested then the purchased donor sperm when thawed was not great only 3% swimming the clinic offered ICSI to help fertilisation, only 2 eggs matured to have ICSI, one was abnormal and the second shows no signs of fertilisation, I just wondered in your profession opinion if the two events totally out of my control had a big impact on the outcome? Many Thanks

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 28, 2018 reply

    The older a woman becomes, the more likely it is that her eggs will be chromosomally/genetically “incompetent” (not have the potential upon being fertilized and transferred, to result in a viable pregnancy). That is why, the likelihood of failure to conceive, miscarrying and of giving birth to a chromosomally defective child (e.g. with Down Syndrome) increases with the woman’s advancing age. In addition, as women age beyond 35Y there is commonly a progressive diminution in the number of eggs left in the ovaries, i.e. diminished ovarian reserve (DOR). So it is that older women as well as those 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 age-related effect on the woman’s “biological clock, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can 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 older women and those 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 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

  • Ayesha - January 27, 2018 reply

    Hi Dr

    Its my 9th day of missed period. Note that my pms cycle is very regular. I did home pregnancy test that came out to be positive with one dark line and one light pink line. Now ive experienced bright red spotting thrice a day. My doctor suggested dupahstan 10 mg twice a day and adfolic 300mg once a day. Is this spotting normal? Im worried so please reply

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 27, 2018 reply

    Vaginal bleeding occurs in about 25% of all pregnancies. When it happens, it almost invariably raises the concern of pregnancy loss (miscarriage). Bleeding can also be a sign of a tubal (ectopic) pregnancy, and in cases where the distended Fallopian tube ruptures it can precipitate a life-threatening crises. However, a small amount of painless vaginal bleeding can also be the result of normal embryo implantation (i.e. implantation bleeding) or it can result a local erosion of the vagina or cervix and/or trauma during intercourse.
    Notwithstanding, in virtually all cases the occurrence of early pregnancy vaginal bleeding congers concerns or even alarm regarding the possibility of miscarriage. And when this happens to women who conceived following infertility treatment, the alarm often turns into panic. However, the truth is that in most such cases the bleeding soon stops and the pregnancy proceeds unabated to the birth of a healthy baby. However, because some do progress and end in miscarriage, and in most cases, only time will tell how things will ultimately turn out, we use the term “threatened miscarriage” to describe such early bleeding. The term “inevitable miscarriage” is used once symptoms and signs confirm a miscarriage is in progress. The term “complete miscarriage” is used if all products of conception are passed, leaving the uterus “empty”. An “incomplete miscarriage” refers to cases where some products

    Good luck!

    Geoff Sher

  • Irina - January 27, 2018 reply

    Dear Dr. Sher,
    I am not sure that I can ask this kind of question here, but I will try.
    I just need a little advice.
    My case: PCOS, AMH 8,9, Fsh 5.5, LH 8,5. Anti TPO 1000, insulin resistence, PAI trombofilia 4g/5g. NK cells from endometrium negative (4,5), from blood – high level active T lymphocites.
    Terapy: euthyrox 25 mcg, glucophage 850 2 x1, Profertil Female, Inofolic.
    I had 3 failed IUI.
    1st IVF : BC pills one month, Puregon 150 j, 9 days and no Pregnil because of OHSS (E2 over 6000), 24 cells, 18 fertilized, the result : 6 blasts, all freezed.
    1st FET – BP
    2nd FET – bhcg 0. ( including Prednison and Fraxiparin). Both times I had preparation with estrogen pills to avoid ovulation, but even than I had high level of LH – 14 day of cycle around 17, but no ovulation.
    Now I will have my second IVF. My doctor gave me a protocol: from 18th day of my cycle 2 x 1 Estrogen pills. No BC pills this time. Second day will have ultrasound and blood test for LH and Pg. If LH is high, I will receive Antagonists tree days and than again Puregon. My doctor wants to get less cells but with better quality, and to have oportunity to give me Pregnil this time and to be able to do transfer.
    I am so scared that I will get OHSS again. Please tell me your opinion is this protocol with estrogen and no BC pills good for my case. Thank you very much in advance.
    Best regards,
    Irina

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 27, 2018 reply

    Two issues! 1) The relationship between thyroid disease and immunologic implantation dysfunction (IID) and, 2) PCOS, egg quality and preventing OHSS.

    1. Thyroid:

    Between 2% and 5% of women of the childbearing age have reduced thyroid hormone activity (hypothyroidism). Women with hypothyroidism often manifest with reproductive failure i.e. infertility, unexplained (often repeated) IVF failure, or recurrent pregnancy loss (RPL). The condition is 5-10 times more common in women than in men. In most cases hypothyroidism is caused by damage to the thyroid gland resulting from of thyroid autoimmunity (Hashimoto’s disease) caused by damage done to the thyroid gland by antithyroglobulin and antimicrosomal auto-antibodies.
    The increased prevalence of hypothyroidism and thyroid autoimmunity (TAI) in women is likely the result of a combination of genetic factors, estrogen-related effects and chromosome X abnormalities. This having been said, there is significantly increased incidence of thyroid antibodies in non-pregnant women with a history of infertility and recurrent pregnancy loss and thyroid antibodies can be present asymptomatically in women without them manifesting with overt clinical or endocrinologic evidence of thyroid disease. In addition, these antibodies may persist in women who have suffered from hyper- or hypothyroidism even after normalization of their thyroid function by appropriate pharmacological treatment. The manifestations of reproductive dysfunction thus seem to be linked more to the presence of thyroid autoimmunity (TAI) than to clinical existence of hypothyroidism and treatment of the latter does not routinely result in a subsequent improvement in reproductive performance.
    It follows, that if antithyroid autoantibodies are associated with reproductive dysfunction they may serve as useful markers for predicting poor outcome in patients undergoing assisted reproductive technologies.
    Some years back, I reported on the fact that 47% of women who harbor thyroid autoantibodies, regardless of the absence or presence of clinical hypothyroidism, have activated uterine natural killer cells (NKa) cells and cytotoxic lymphocytes (CTL) and that such women often present with reproductive dysfunction. We demonstrated that appropriate immunotherapy with IVIG or intralipid (IL) and steroids, subsequently often results in a significant improvement in reproductive performance in such cases.
    The fact that almost 50% of women who harbor antithyroid antibodies do not have activated CTL/NK cells suggests that it is NOT the antithyroid antibodies themselves that cause reproductive dysfunction. The activation of CTL and NK cells that occurs in half of the cases with TAI is probably an epiphenomenon with the associated reproductive dysfunction being due to CTL/NK cell activation that damages the early “root system” (trophoblast) of the implanting embryo. We have shown that treatment of those women who have thyroid antibodies + NKa/CTL using IL/steroids, improves subsequent reproductive performance while women with thyroid antibodies who do not harbor NKa/CTL do not require or benefit from such treatment.

    2. PCOS, OHSS and egg-embryo quality:

    Polycystic ovary syndrome (PCOS) is a common hormonal system disorder among women affecting between 5% and 10% of women of reproductive age worldwide. Women with PCOS may have enlarged ovaries that contain multiple small collections of fluid (subcapsular microcysts) that are arranged like a “string of pearls” immediately below the ovarian surface (capsule).interspersed by an overgrowth of ovarian connective tissue (stroma). The condition is characterized by abnormal ovarian function (irregular or absent periods, abnormal or absent ovulation and infertility, androgenicity (increased body hair or hirsutism, acne) and increased body weight –body mass index or BMI.
    Women with PCOS are at increased risk that ovarian stimulation with gonadotropins will result in the, of development of severe ovarian hyperstimulation syndrome (OHSS), a life-endangering condition that is often accompanied by a profound reduction in egg “competency” and on fertilization often yield an inordinately high percentage of “incompetent” embryos which have a reduced potential to propagate viable pregnancies.
    Concern and even fear that their PCOS patients will develop of OHSS often leads the treating RE to take measures aimed at reducing the risk of this life-endangering condition. One such measures is to “trigger” egg maturation prematurely in the hope of arresting further follicular growth and the other, is to initiate the “trigger” with a reduced dosage of hCG (i.ed. 5,000U rather than the usual 10,000U of of Pregnyl/Profasi/Novarel, to use or 250mcg rather than 500mcg of Ovidrel or to supplant the hCG “trigger” with a Lupron “trigger” which causes a prompt LH surge from the woman’s pituitary gland to take place. While such measures do indeed reduce the risk of OHSS to the mother, this often comes at the expense of egg quantity and “competency”. Fewer than the anticipated number of eggs are harvested and those that are retrieved are far more likely to be “immature” and chromosomally abnormal (aneuploid”), or “immature” , thereby significantly compromising IVF outcome.
    Against this background, It is my considered opinion that when it comes to performing IVF in women with PCOS, the most important consideration must be the selection and proper implementation of an individualized or customized ovarian stimulation protocol. Thereupon, rather than prematurely initiating the “trigger” to arrest further follicle growth, administering a reduced dosage of hCG or “triggering with a GnRH agonist (e.g. Lupron/Buserelin) that can compromise egg “competency”….. use of one of the following techniques will often markedly reduce the risk of OHSS while at the same time protecting egg quality:
    1. PROLONGED COASTING…my preferred approach: My preferred approach is to use a long pituitary down-regulation protocol coming off the BCP which during the last 3 days is overlapped with the agonist, Lupron/Buserelin/Superfact. The BCP is intended to lower LH and thereby reduce stromal activation (hyperthecosis) in the hope of controlling LH-induced ovarian androgen (predominantly, testosterone) production and release. I then stimulate my PCOS patients using a low dosage of recombinant FSH-(FSHr) such as Follistim/Gonal-F/Puregon. On the 3rd day of such stimulation a smidgeon of LH/hCG (Luveris/Menopur) is added. Thereupon, starting on day 7 of ovarian stimulation, I perform serial blood estradiol (E2) and ultrasound follicle assessments, watching for the number and size of the follicles and the blood estradiol concentration [E2]. 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 concentration daily. The [E2] will almost invariably increase for a few days. I closely monitor the [E2] as it rises, plateaus and then begins to decline. As soon as the [E2] drops below 2500pg/ml (and not before then), I administer a “trigger” shot of 10,000U Profasi/ Novarel/Pregnyl or 500mcg Ovidrel/Ovitrel. This is followed by an egg retrieval, performed 36 hours later. Fertilization is accomplished using intracytoplasmic sperm injection (ICSI) because “coasted” eggs usually have little or no cumulus oophoris enveloping them 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 the blastocyst stage (up to day 5- 6 days) and thereupon are either vitrified and preserved for subsequent transfer in later hormone replacement cycles or (up to 2) blastocysts are transferred to the uterus, transvaginally under transabdominal ultrasound guidance. The success of this approach depends on precise timing of the initiation and conclusion of “prolonged coasting”. If started too early, follicle growth will arrest and the cycle will be lost. If commenced too late, too many follicles will be post-mature/cystic (>22mm) and as such will usually harbor abnormal or dysmature eggs. Use of “Coasting” almost always prevents the development of severe OHSS, optimizes egg/embryo quality and avoids unnecessary cycle cancellation. If correctly implemented, the worst you will encounter is moderate OHSS and this too is relatively uncommon.
    2. EMBRYO FREEZING AND DEFERMENT OF EMBRYO TRANSFEDR (ET): OHSS is always a self-limiting condition. In the absence of continued exposure to hCG, symptoms and signs as well as the risk of severe complications will ultimately abate. Thus, in the absence of pregnancy, all symptoms, signs and risks associated with OHSS will disappear within about 10-14 days of the hCG trigger. Conversely, since early pregnancy is always accompanied by a rapid and progressive rise in hCG , the severity of OHSS will increase until about the 9th or tenth gestational week whereupon a transition from ovarian to placental hormonal dominance occurs, the severity of OHSS rapidly diminishes and the patient will be out of risk. Accordingly, in cases where in spite of best effort to prevent OHSS, the woman develops symptoms and signs of progressive overstimulation prior to planned ET, all the blastocysts should be vitrified and cryostored for FET in a subsequent hormone replacement cycle. In this way women with OHSS can be spared the risk of the condition spiraling out of control.
    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.
    · Egg Maturation in IVF: How Egg “Immaturity”, “Post-maturity” and “Dysmaturity” Influence IVF Outcome:
    · Commonly Asked Question in IVF: “Why Did so Few of my Eggs Fertilize and, so Many Fail to Reach Blastocyst?”
    · 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?
    · Taking A Fresh Look at Ovarian Hyperstimulation Syndrome (OHSS), its Presentation, Prevention and Management
    · Preventing Severe Ovarian Hyperstimulation Syndrome (OHSS) with “Prolonged Coasting”
    · Understanding Polycystic Ovarian Syndrome (PCOS) and the Need to Customize Ovarian Stimulation Protocols.
    · “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?
    • .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.
    • Implications of “Empty Follicle Syndrome and “Premature Luteinization”
    • Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
    • • 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
    • 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!

    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

  • Sally - January 27, 2018 reply

    I transferred a partially compacting morula on day 5. On day 3 it was 8 cells, <5% fragmentation. At 13dpo I started to bleed brown/pink, then on 14dpo it got a bit heavier with dark maroon/red blood. It started to get a bit lighter on 15dpo.
    At 14dpo my HCG was 5, progesterone was 35, oestrogen was 49, FSH was 9 and LH was 2.6.
    At 16dpo my HCG was 15.6, progesterone was 25, oestrogen was 65, FSH was 18 and LH was 3.9.

    I stopped taking the progesterone as in my heart I didn't think it was going to be viable and I am keen to start another cycle.

    I'm still bleeding. It's light bleeding but it is fresh red blood. My HCG has a doubling time of 1.3 days. My RE is telling me he hopes it's not ectopic!!! The RE nurse says she doesn't believe it's ectopic because my progesterone levels are ok. I'm really quite scared. I have NO pain and it looks like my FSH, LH and E2 are trying to grow a follicle for this cycle.

    In your years of experience, what could be the reason for the period and high FSH and oestrogen? If miscarrying, shouldn't HCG be trying to go down? Is this sounding like an ectopic or a miscarriage or something else? My clinic likes to see HCG at over 80 on 14dpo. Mine is too low and I am not feeling confident. I have started my progesterone back again, even though I know this won't end well. Please tell me your opinion.. would love to hear it as I am so worried. I don't want to lose a tube..

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 27, 2018 reply

    If the hCG is still rising appropriately this could still be a viable pregnancy. I would continue the progesterone and keep measuring hCG every 2-4 days and provided it is rising appropriately, I would do an US when it reaches >2,000 at which time the US should be definitive. All along you should be on the lookout for symptoms of sudden pain, Rt shoulder tip pain and lightheadedness . If any of these occur you should go immediately to an emergency room as it could be an ectopic.

    Good luck!

    Please keep me in the loop!

    Geoff Sher

    Sally - January 27, 2018 reply

    Thank you so much for your kindness in replying and your care in wanting to know how I get on. I’ll keep you updated. For now, I have resumed the progesterone pressaries and the prometrium progesterone capsules and will wait and see what transpires. Thank you so much for your view, it is most appreciated! xx

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 27, 2018 reply

    Youn are very welcome, Sally.

    Good luck and G-d bless!

    Geoff Sher

  • Don - January 27, 2018 reply

    Dear Dr. Sher,

    We would first and foremost like to say THANK YOU on the blog titled “Recurrent Unexplained IVF Failure with “Good Quality” Embryos” that you did regarding about the couple trying to conceive but failed on several tries on IVF even with healthy embryos. Today we just received the horrible news that our recent frozen embryo transfer (FET) was negative. My wife is 31 years old, HEALTHY (5’4 and 115lbs), with good endometrial lining at the time of FET. She did already have a laparoscopic procedure to remove her endometriosis in 2016. We previously in the past also performed 3 unsuccessful IUI with healthy size follicles. As mentioned before regarding the FET procedure it was our second attempt. All the eggs transferred were high grade and even went through Pre-genetic screening. We are now desperate to get answers as to what is causing these failed transfers. It crushes me every time my wife asked me of what is wrong with her, why can’t she get pregnant? I don’t have those answers. All I can do is be supportive to her. We hope you provide us some enlightenment because right at this very moment we are in the dark.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 27, 2018 reply

    Endometriosis can be associated with an immunologic implantation dysfunction in about 1/3 of cases. More than half of women who have endometriosis harbor antiphospholipid antibodies (APA) that can compromise development of the embryo’s root system (trophoblast). In addition and far more serious, is the fact that in about one third of cases endometriosis, regardless of its severity is associated with NKa and cytotoxic uterine lymphocytes (CTL) which can seriously jeopardize implantation. This immunologic implantation dysfunction (IID) is diagnosed by testing the woman’s blood for APA, for NKa (using the K-562 target cell test or by endometrial biopsy for cytokine activity) and, for CTL (by a blood immunophenotype). Activated NK cells 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 rejection of the embryo even before the pregnancy is diagnosed and sometimes, in a chemical pregnancy or 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”.
    Women who harbor APA’s often experience improved IVF birth rates when heparinoids (Clexane/Lovenox) are administered from the onset of ovarian stimulation with gonadotropins until the 10th week of pregnancy. NKa is treated with a combination of 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 NKa.
    The therapeutic effect of IL/steroid therapy is likely due to an ability to suppress pro-inflammatory cellular (Type-1) cytokines such as interferon gamma and TNF-alpha. IL/steroids down-regulates NKa within 2-3 weeks of treatment the vast majority of women experiencing immunologic implantation dysfunction. In this regard IL 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.
    The toxic pelvic environment caused by endometriosis, profoundly reduces natural fertilization potential. As a result normally ovulating infertile women with endometriosis and patent Fallopian tubes are much less likely to conceive naturally, or by using fertility agents alone (with or without intrauterine (IUI) insemination. The only effective way to bypass this adverse pelvic environment is through IVF. I am not suggesting here that all women who have endometriosis require IVF! Rather, I am saying that in cases where the condition is further compromised by an IID associated with NKa and/or for older women(over 35y) who have diminished ovarian reserve (DOR) where time is of the essence, it is my opinion that IVF is the treatment of choice.

    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

  • Danielle - January 27, 2018 reply

    Dear Dr Sher, I wish we found your blog earlier) because I am suppose to start the estrogen patch right after I ovulate, probably next week.  Right now I am on cycle day 8.  So it’s kind of urgent.  Thank you for reading this.
     
    My husband, 42 years old, has non-obstructive azoospermia and therefore we have to do TESE Surgery and I have to do IVF. I was told I was perfectly normal.  No red-flags. 
    I completed one cycle of IVF at a large known NYC RE-Center. Like I said, I was told everything was perfect and didn’t find out till the second week (randomly from another doctor monitoring) that I have low AMH. 
    I didn’t respond to IVF and had one egg which was retrieved on day 18.
    I started IVF on November 25th, 2017 and did the trigger shot December 10 and on December 12th was egg retrieval. They tried to fertilize my one egg with a fresh sperm they retrieved when my husband ejaculated that day.  TESE was canceled the day before retrieval because they only had one egg  (first it showed  he had zero sperm in his semen sample but after further analysis they found one in the sample. We are not sure on the quality of that one.) We are not sure if it was the sperm or the egg, but the egg did not fertilize.  
     
    My protocol was one week on birth control before starting IVF
    (to control my cycle to synchronize with my husband’s TESE surgery which only takes place during certain dates) 
    Then every day 150 Menopure and 300 Gonal F. 
    The last five days I had to take Citrotide.
    On day 16 I did the trigger shot. 5000 HCG and 80 iu of Lupron
     
    I had one egg which was 14 and one which was 21.  I lost the egg which was 14 the day before, and they retrieved the egg which was 21.
     
     
    The doctor said in retrospect it failed because of the birth control.  I left this RE center l and am now I am starting at a new clinic.  My AMH has gone up from .017  to .031 in this blood work.
    My FSH has remained at 2.5.  I’m not sure if my AMH went up in these two months because my vitamin D was in it’s 30’s and now it’s 107 (so I have to stop taking the supplement) or it’s just a different test and this isn’t a big difference.  Never the less I just asked for my vitamin D to be taken again and I am going to closely monitor it so it remains high but not over 100.  
     
    The new doctor (at a boutique RE center in NY)(also feels the birth control messed up the cycle and has wrote the following protocol for my next IVF cycle:
    Estrogen Patch right after I ovulate, change patch every 48 hours.
    Clomid for 5 Days
    Then Gonal F 225 iu and Menopure 225 iu  and continue on clomid throughout
    Then trigger with Lupron and hcg
     
     
    I just turned 33 years.  I don’t fear that I’m not able to get pregnant naturally given my age, my family history,  I have no symptoms of a problem and given that I’ve never tried naturally.  
    I’ve gotten my period every 21 days since I’ve gotten my period when I was 12.  
    My period lasts 4-6 days. The only possibly sign could have been my period every three weeks.  
    I feel that my body just hates IVF.  Maybe that’s naive thinking but it doesn’t matter because I need IVF to work for me and I need my body to respond to it for my husbands TESE surgery. I would like to know what you think of this protocol for me and if you think I can successfully do IVF in New York. 

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 27, 2018 reply

    Danielle,

    You clearly have severe prematurely diminishing ovarian reserve. Aside from the obvious need for TESE/ICSI, your stimulation protocol needs to be carefully reviewed and revised…in my opinion.

    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

    Danielle - January 27, 2018 reply

    Dear Dr Sher,
    Thank you very much for your helpful response.
    I will definitely schedule an appointment with you.
    Regarding my LH values throughout my previous (and first) IVF cycle, these are here:

    (please note that I was on a birth control pill for 7 days, until 2 days before cycle day one)

    Cycle Day LH Value
    2 2.3 (FSH 2.3)
    3
    4 6.08
    5
    6 6.4
    7
    8 7.9
    9
    10 4.2
    11
    12 2.8
    13
    14 2.6
    15 3.9
    16 8.1 Trigger Shot
    17 11.1

    Does this in any way change your view?

    Best,
    Danielle

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 27, 2018 reply

    No! It does not!

    Geoff Sher

  • Kate Larson - January 26, 2018 reply

    Hey Dr. Sher, how important is timing an FET with the menstrual cycle? Looks like I’m going to skip Lupron (I don’t ovulate on my own) and start estrogen on Monday, but that’ll be day 4 of my menstrual cycle. Is it crucial to start stimulation (estrogen) on day 2 or 3 or do you think day 4 will be ok?

    Also, we’ve had issues with my lining in the past. Any concerns with extending estrogen an extra few days if lining isn’t thick enough or is it important to transfer before a certain day in the cycle? (If, so what day do you usually draw the cut off?)

    Thanks again so much for your time and expertise.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 27, 2018 reply

    I do not think tat starting on day 4 would be a serious impediment. However, the issue of the endometrial thickness is very important.

    Eighteen years ago years ago, after reporting on the benefit of vaginal Sildenafil (Viagra) for to women who had implantation dysfunction due to thin endometrial linings I was proud to announce the birth of the world’s first “Viagra baby.” Since the introduction of this form of treatment, thousands of women with thin uterine linings have been reported treated and many have gone on to have babies after repeated prior IVF failure.

    For those of you who aren’t familiar with the use of Viagra in IVF, allow me to provide some context. It was in the 90’s that Sildenafil (brand named Viagra) started gaining popularity as a treatment for erectile dysfunction. The mechanism by which it acted was through increasing penile blood flow through increasing nitric oxide activity. This prompted me to investigate whether Viagra administered vaginally, might similarly improve uterine blood flow and in the process cause more estrogen to be delivered to the basal endometrium and thereby increase endometrial thickening. We found that when Viagra was administered vaginally it did just that! However oral administration was without any significant benefit in this regard. We enlisted the services of a compound pharmacy to produce vaginal Viagra suppositories. Initially, four (4) women with chronic histories of poor endometrial development and failure to conceive following several advanced fertility treatments were evaluated for a period of 4-6 weeks and then underwent IVF with concomitant Viagra therapy. Viagra suppositories were administered four times daily for 8-11 days and were discontinued 5-7 days prior to embryo transfer in all cases.

    Our findings clearly demonstrated that vaginal Viagra produced a rapid and profound improvement in uterine blood flow and that was followed by enhanced endometrial development in all four cases. Three (3) of the four women subsequently conceived. I expanded the trial in 2002 and became the first to report on the administration of vaginal Viagra to 105 women with repeated IVF failure due to persistently thin endometrial linings. All of the women had experienced at least two (2) prior IVF failures attributed to intractably thin uterine linings. About 70% of these women responded to treatment with Viagra suppositories with a marked improvement in endometrial thickness. Forty five percent (45%) achieved live births following a single cycle of IVF treatment with Viagra The miscarriage rate was 9%. None of the women who had failed to show an improvement in endometrial thickness following Viagra treatment achieved viable pregnancies.

    Following vaginal administration, Viagra is rapidly absorbed and quickly reaches the uterine blood system in high concentrations. Thereupon it dilutes out as it is absorbed into the systemic circulation. This probably explains why treatment is virtually devoid of systemic side effects

    It is important to recognize that Viagra will NOT be effective in improving endometrial thickness in all cases. In fact, about 30%-40% of women treated fail to show any improvement. This is because in certain cases of thin uterine linings, the basal endometrium will have been permanently damaged and left unresponsive to estrogen. This happens in cases of severe endometrial damage due mainly to post-pregnancy endometritis (inflammation), chronic granulomatous inflammation due to uterine tuberculosis (hardly ever seen in the United States) and following extensive surgical injury to the basal endometrium (as sometimes occurs following over-zealous D&C’s).

    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.
    • 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.
    • Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
    • A Thin Uterine Lining: Vaginal Viagra is Often the Answer (update)
    • 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

    If you are interested in my advice or medical 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.
    Also, 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

  • Anonymous - January 26, 2018 reply

    Hi, we have been on menopur and gonal for the last 10 days and centrotide for 7 last one this morning. We are supposed to trigger tonight for egg retrieval Sunday morning. This mornings lh level was 24.6 mIU/mL and progesterone was .76 my/ml. Lh has been 3 or under up until today. Are we too late has ovulation already started? Thank you for your time and opinion.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 26, 2018 reply

    It sounds as if you might be having premature luteinization coming. Recheck the progesterone level tomorrow.

    Good luck!

    Geoff Sher

  • SriRam - January 26, 2018 reply

    First would like to thank you for providing so much of good information. My wife is 32 and she just completed her first cycle of IVF and 5 day embryo transferred post pgs. Her first beta hcg came positive and the value is 199.8. Post 48 hours we took second level beta hcg test and it came 357.8. Hope this is good sign. I heard that the count should double every two days. So was curious to check everything is fine.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 26, 2018 reply

    Looks very promising!

    Good luck!

    Geoff Sher

  • Alison - January 26, 2018 reply

    Hi Dr. Sher,
    I am 39 and have had two rounds of IVF (antagonist protocol with 150 Gonal-F and just 75 of Menopur as my LH is a bit higher than my FSH). Both times I had very few eggs collected (5 and 4) but they transferred two Grade A 3-day embryos each time. The first time one implanted but I had a very low beta hCG from the start, and although it doubled well the embryo stopped developing at about week 6. The second time neither of the embryos implanted. Before the third round they decided to do some clotting and antibody tests. All antibodies were negative but I found out I am homozygous for the C677T mutation and my C protein functional was 55%. All other results were normal.

    I have been reading about the c667t mutation and thrombophilia, but I’m still not sure whether this is a factor in implantation failure and very early pregnancy loss, or if my results definitely indicate that I am thrombophilic. Most of the information I have found points to miscarriage later on in the pregnancy.

    I guess my questions for you are:
    1) Can clotting disorders be related to implantation failure and very early pregnancy loss?
    2) Do my results indicate thrombophilia, and do you think they should do something different this time round (e.g. different protocol, heparin, etc.)?
    3) With a homozygous C677T mutation, should I be taking folic acid (I have read some advice saying this should be avoided) or is it better to take L-Methylfolate combined with vitamin b12? Should I be taking any other supplements? About ten years ago I had a vitamin b-12 deficiency (levels at 165 pg/mL) but since then I have been taking a vitamin b1-b6-b12 supplement with 500 mcg of b12 every two weeks, which has raised the levels to 700 or so.

    Thank you so much for taking the time to answer, and for any help you can give!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 26, 2018 reply

    1) Can clotting disorders be related to implantation failure and very early pregnancy loss?

    A: It is in my opinion very unlikely that a thrombophilia will cause implantation to fail or result in early miscarriage. It probably does cause later miscarriages and can compromise placentation though.

    2) Do my results indicate thrombophilia, and do you think they should do something different this time round (e.g. different protocol, heparin, etc.)?

    A: Yes to both those questions….but I do not believe the thrombophilia is responsible for IVF failure.

    3) With a homozygous C677T mutation, should I be taking folic acid (I have read some advice saying this should be avoided) or is it better to take L-Methylfolate combined with vitamin b12? Should I be taking any other supplements? About ten years ago I had a vitamin b-12 deficiency (levels at 165 pg/mL) but since then I have been taking a vitamin b1-b6-b12 supplement with 500 mcg of b12 every two weeks, which has raised the levels to 700 or so.

    A: This is controversial but it is still my opinion that Lovenox + folate may be the way to go.

    Good luck!

    Geoff Sher

  • Nicole - January 26, 2018 reply

    Hi Dr Sher I am 38 and have a 3 and half year old son who I got pregnant easily and had him at age 34 and had miscarriage at 36&1/2 and now gone through 4 unsuccessful IUIs and now approaching IVF, I have unexplained secondary infertility and low ovarian reserve. Hoping for another little one soon. Any advice for me?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 26, 2018 reply

    It is one thing for a woman who has never been able to conceive (primary infertility) to come to grips with undergoing In Vitro Fertilization. It is quite another matter for someone who has successfully achieved a pregnancy in the past having to come to terms with a subsequent inability to conceive (secondary infertility). When this happens, it raises issues of guilt, a declining sense of self-worth and ultimately self-recrimination. The ramifications often impact family relationships involving partners and siblings. The truth is that secondary infertility can be just as difficult for individuals and family to deal with as primary infertility.
    There are many factors that contribute to the problem of secondary infertility. These include:
    Social and marital factors: In this modern day and age where at least one in two marriages ends in divorce, it is not surprising that there would be an inevitable hiatus in childbearing. This often results in a considerable delay in re-initiating family building. Since the biological clock keeps on ticking in the interim, advancing age can, and often does, have a profound affect on a woman’s ability to subsequently conceive and successfully complete a pregnancy. In my experience, this is one of the most common reasons for secondary infertility. In addition, by the time a decision is made to enter a new relationship, many men and women will have undergone a prior sterilization procedure which now needs to be addressed. To make matters worse, many such men and women first opt for surgical reversal of their occlusive surgery, only to learn in the end that the procedures were not successful, and they now need to consider in vitro fertilization (IVF) in one form or another.
    Financial factors: Here, the cost of raising a child often weighs heavily, especially in this present tough economic climate. This is becoming more of an issue as women playing an ever increasing role as a primary bread winner.
    Career demands: There can be little doubt that when it comes to climbing the career ladder, women are considerably disadvantaged by the fact that pregnancy and the immediate demands of child rearing take away from their ability to compete with men. As such, many women choose to delay having another child until such time as they have been able to make up for prior lost opportunity.
    Medical barriers to fertility: Certain common medical conditions, while not absolutely precluding pregnancy, make it much more difficult to conceive.
    Endometriosis: It is not uncommon for women with endometriosis to achieve a pregnancy, but find difficulty in doing so again at a later date. The reason for this is that while most women with endometriosis have patent fallopian tubes, the environment surrounding their tubes is compromised due to pelvic toxins that are produced by the endometriotic implants. These toxins compromise egg fertilization potential, making it more difficult for sperm in the fallopian tube to fertilize the egg upon its arrival there. As such, endometriosis is one of the commonest causes of secondary infertility.
    Tubal damage due to prior pelvic inflammatory disease: In first world countries, the early and often indiscriminate use of antibiotics for the slightest symptom has led to the point where an acute attack of pelvic inflammatory disease is often masked. As such, less than 30% of American women with tubal damage have knowledge that their tubes are compromised and that they might have subsequent difficulty in conceiving. Since, in many such cases the tubal damage will not have totally blocked both tubes, some of the women so affected might experience a pregnancy but have difficulty in conceiving again later down the line.
    Dysfunctional ovulation: Since ovulation as well as normal hormonal support of the early implanting embryo are both essential for a healthy pregnancy to occur, it follows that women with irregular or dysfunctional ovulation (e.g., polycystic ovarian syndrome – PCOS, persistent follicular luteal phase deficiencies or post birth control pill ovulatory problems) might sporadically conceive and thereupon find it difficult to do achieve another pregnancy later on.
    Immunologic Implantation Dysfunction (IID): has become ever more apparent that immunologic factors play an important role in achieving healthy implantation. Women with endometriosis (regardless of its severity), those with a personal or family history of autoimmune diseases such as lupus erythematosus, rheumatoid arthritis and thyroid autoimmunity (TAI), and some cases where the man and the woman share certain genetic similarities (alloimmune implantation dysfunction), will have activated CTL/NK cells that can inhibit or compromise healthy implantation. This is an often overlooked cause of secondary infertility. Most such autoimmune/alloimmune cases require selective immunotherapy and IVF.
    Antisperm Antibodies: Although infrequent, some cases of secondary infertility might also be caused by the woman harboring antisperm antibodies. In such cases IVF is mandated.
    Previous post-pregnancy uterine infection: Retention of products of conception after the birth of a child, miscarriage, or abortion can so damage the uterine lining as to result in subsequent implantation failure. Unless specifically looked for, this will usually be unknown to the patient, who will simply present with secondary infertility. Treatment is often difficult because such patients might not respond adequately to surgical removal of intrauterine scar tissue or to hormonal or Viagra therapy
    Male immunologic factors: Most men who have undergone a previous vasectomy more than 10 years earlier, will have antisperm antibodies that will interfere with fertilization. Such cases require IVF with intracytoplasmic sperm injection (ICSI). Here we offer a few words of caution to men who are considering undergoing surgical reversal of vasectomy. Always first have a test done to exclude the presence of circulating antisperm antibodies, because in such cases, even if the reversal is successfully performed, they will not be able to initiate a pregnancy without IVF/ICSI.
    Whatever the cause, secondary infertility often affects older couples disproportionately, creating a sense of urgency and even desperation in achieving a viable pregnancy before time runs out. It is for this reason that IVF becomes the treatment of choice in such cases. However, even IVF becomes progressively less successful with advancing age of the woman (whose eggs are being fertilized). In such cases it is important for the couple to be realistic with regard to their expectations. Here, options that include embryo banking and egg donation should be carefully considered.
    Another important point is that whenever a regularly ovulating younger woman (under 36 years of age) with patent fallopian tubes is diagnosed with secondary infertility, it is essential to consider underlying endometriosis or non-obstructive tubal disease as a possible cause. In such cases, IVF is again the treatment of choice.

    If you are interested in my advice or medical 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.
    Also, 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.

  • Christina - January 25, 2018 reply

    Hi I’m 12 day past transfer of a 5day already hatching embryo my first beta was at 10dpt andmy hcg was 25 now today it is 30 while I know this is low they want to recheck everything in 4 days instead of 2 is there any hope that this may go on to be a viable pregnancy even with the low rising betas??

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 26, 2018 reply

    Hi Christina,

    Sadly, this does not look very promising.

    Geoff Sher

  • Demi - January 25, 2018 reply

    Dear Mr. Sher,
    I’m very grateful that you provide this kind of support to all of us worldwide- I can easily say that I have gained most valuable knowledge through your webpage.I have an urgent question hope that you can support.
    Me and my husband (F 41 age, M 44 age) we are married since 8 years. My husband has advanced varicosele, both sides. He never wanted to try naturally (he believed his sperm morphology will cause miscarriages). He also didn’t agree on varicosele operation. Instead, after many years of waiting, in 2016 we have started our IVF journey. But during this period (one of the reason was his alcohol addiction and smoking) sperm count went to just around 1ml, 0% motility and 0% morphology.
    We both started using a lot of supplements (to ensure egg quality and sperm count) and planned for ICSI, microchip techniques. In total we have done 4 rounds of egg retrieval (in just 9 months) each time between 9 and 17 eggs collected, and his sperm count and motility seems to be increased, but still 0% morphology. Each round we have got several blastocyst embryos and these were sent to NGS (next generation sequencing for embryos). We endup with just 1 embryo all 24 chromosomes normal, 1 monosomy 14 and all the others with more advances issues.
    Now I’m preparing for the first time embryo transfer for next week. We have done hysteroscopy (even though no issue shown on HGS), ERA and endometrium biopsy (CD56 is normal).
    My RE recommended to transfer the normal embryo together with the other embryo with monosomy 14. I guess he is worried a bit about the quality of the normal one. Both of them are from the same cycle. During that cycle we had 3 blast embryos were sent to NGS test. He said he will not know about the quality until the transfer day which is next week.

    I have read some articles about monosomic embryos. They may correct if they implant (unless the issue is on the X-Y chromosome, ours is monosomy 14). My question is that if we will transfer it together with the chromosomally normal one do we decrease the chance for implementation for the normal one? Is it better to transfer just the normal one?

    Thanks a lot,
    Demi

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 25, 2018 reply

    I agree with the strategy to transfer both. If you do conceive I strongly would advocate that you do CVS or amniocentesis to asses the chromosomal integrity of the conceptus!

    Good luck!

    Geoff Sher

  • Adina - January 25, 2018 reply

    Dear Dr. Sher,
    Thank you so much for you website and all the great information.
    I have done 5 cycles of traditional IVFs for egg retrieval. I got 18 eggs total, 7 embryos an did genetic testing. 3 came back normal. 2 of them day-5 grade good and one day-6 grade fair.
    They transferred the day-6 embryo and it didn’t work.
    To me it was an odd choice for them to choose the less quality embryo.
    We decided not to touch the left embryos in a fear of losing them.
    Our hope is to try to see if we can get more embryos and if not we use a surrogate for the left embryos.
    I was told that mini IVF might be a better route for me as I have low egg quantity (3-4 each cycle)
    I am 37 years old with stage 4 endo and AMH 0.4
    Do you think mini IVF is a better choice and might help getting better quality eggs?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 25, 2018 reply

    Respectfully, I do not advocvate mini-IVF. Thew number and quality of eggs/embryos so propagated will likely be less than opytimal. In addition, endometriosis is also a “red flag.”.

    Endometriosis and implantation dysfunction:

    More than half of women who have endometriosis harbor antiphospholipid antibodies (APA) that can compromise development of the embryo’s root system (trophoblast). In addition and far more serious, is the fact that in about one third of cases endometriosis, regardless of its severity is associated with NKa and cytotoxic uterine lymphocytes (CTL) which can seriously jeopardize implantation. This immunologic implantation dysfunction (IID) is diagnosed by testing the woman’s blood for APA, for NKa (using the K-562 target cell test or by endometrial biopsy for cytokine activity) and, for CTL (by a blood immunophenotype). Activated NK cells 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 rejection of the embryo even before the pregnancy is diagnosed and sometimes, in a chemical pregnancy or 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”.
    Women who harbor APA’s often experience improved IVF birth rates when heparinoids (Clexane/Lovenox) are administered from the onset of ovarian stimulation with gonadotropins until the 10th week of pregnancy. NKa is treated with a combination of 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 NKa.
    The therapeutic effect of IL/steroid therapy is likely due to an ability to suppress pro-inflammatory cellular (Type-1) cytokines such as interferon gamma and TNF-alpha. IL/steroids down-regulates NKa within 2-3 weeks of treatment the vast majority of women experiencing immunologic implantation dysfunction. In this regard IL 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.
    The toxic pelvic environment caused by endometriosis, profoundly reduces natural fertilization potential. As a result normally ovulating infertile women with endometriosis and patent Fallopian tubes are much less likely to conceive naturally, or by using fertility agents alone (with or without intrauterine (IUI) insemination. The only effective way to bypass this adverse pelvic environment is through IVF. I am not suggesting here that all women who have endometriosis require IVF! Rather, I am saying that in cases where the condition is further compromised by an IID associated with NKa and/or for older women(over 35y) who have diminished ovarian reserve (DOR) where time is of the essence, it is my opinion that IVF is the treatment of choice.

    Mini-IVF

    Mini-IVF is a procedure that involves ovarian stimulation using low dosage medications (often oral drugs like clomiphene and letrozole) under the premise that it is a “safer” and less expensive than conventional gonadotropin stimulation regimes while yielding comparable success. …….. Nothing could be further from the truth. The fact is that success rates per fresh mini-IVF cycle ranges between 10% and 12%s (i.e., about one third of that which reported national average for conventional IVF performed on women under 39y of age) ). And when it comes to older women and those with diminished ovarian reserve (DOR), the success rate with mini-IVF is usually much lower still.
    There can be little doubt that aside from a woman’s age, the method used for ovarian stimulation represents the most important determinant of egg/embryo quality and thus of IVF outcome. There is no single stimulation protocol that is suitable for all IVF patients. It must be individualized…. especially when it comes to women who, regardless of their age have diminished ovarian reserve (DOR) and for women over >40y of age. The reason for this is that in such cases, the pituitary gland often over-produces LH which in turn causes the ovarian stroma/theca (connective tissue) to thicken (stromal hyperplasia/hyperthecosis) and over-produce male hormones (mainly testosterone). This in turn adversely influences egg and follicle growth, resulting in poor egg/embryo “competency” and compromised IVF outcome.
    So let us examine the validity of the claims made in support of mini-IVF:

    1. Milder stimulation using oral agents such as clomiphene, letrozole (alone or in combination with low dosage gonadotropins (Follistim/Gonal-F/Puregon/Menopur) reduces stress on the ovaries and overall risk associated with IVF. This argument while perhaps having some merit when applied to mini-IVF conducted in younger women who also have normal ovarian reserve, does not hold water for older women and those with DOR who (s stated above) often already have excessive LH-induced ovarian testosterone production. Furthermore, addition of clomiphene and letrozole by further increasing pituitary LH (and thus ovarian testosterone) only serves to add “fuel to the fire” in such cases and Menopur which contains both LH and hCG ( that both have similar effects on ovarian testosterone production), if administered in large amounts (>75U per day) can also do harm in my opionion.

    2. Women with DOR will respond better to “milder stimulation” and egg quality will so be enhanced. This assertion borders on the ridiculous. It is like saying that applying less force to a heavier object will increase the likelihood of moving it”. That is simply not how FSH stimulates follicle development. You see…the cell membranes that envelop the follicular granulosa cells that line the inside surface of ovarian follicles have on their surfaces, a finite number of FSH receptors. FSH molecules attach to these receptors and mediate intracellular events that lead to granulosa cell proliferation with production of estradiol and the concurrent development of the egg (oogenesis) that is attached to the inner wall of the follicle. Once all the FSH receptors on the cell membranes are saturated, any residual FSH is discarded. This is why, when it comes to older women and women with DOR whose granulose cell membranes harbor fewer FSH receptors, it is virtually impossible to overstimulate them. Excessive FSH will simply be rejected and discarded.

    3. Use of fewer drugs translates into lower cost. This would be true, were it not for the fact that success rates with mini-IVF across the board are much lower than with conventional ovarian stimulation. More important is the fact that the cost of IVF should be expressed in terms of “the cost of having a baby” rather than “cost per cycle of treatment”. When this is taken into account the cost associated with mini-IVF will b be significantly higher than conventional IVF. Then there is the additional emotional cost associated with a much higher IVF failure rate with mini-IVF.
    4. Mini-IVF is less technology driven, less stressful and easier to execute. This assertion is in my opinion also without merit. Aside from reduced cost of medications, the same monitoring and laboratory procedures are needed for mini-IVF as with conventional treatment.

    What is the best approach? When it comes to older women and those with DOR, it is in my opinion preferable to use a long pituitary down-regulation protocol with conversion from an I.M agonist (e.g. Lupron or Buserelin) to an antagonist such as Cetrotide/Orgalutron or Ganirelix (the agonist/antagonist conversion protocol) augmented with human growth hormone (HGH) and/or estrogen priming and combing this “embryo banking” over several cycles. In such cases preimplantation genetic screening (PGS) can be incorporated to help select the most “competent” embryos for transfer.

    What about younger women with normal or increased ovarian reserve? If mini-IVF has any role at all, it could be in young women who have normal or increased ovarian reserve. I do not o not advocate aggressively stimulating the ovaries of younger women who have normal or increased ovarian reserve (as assessed by basal FSH, AMH and estradiol) simply to try and access more eggs. In fact, such an approach is neither safe nor acceptable. In such women it is often wiser to use lower dosage stimulation to try and prevent the development of severe ovarian hyperstimulation syndrome (OHSS) which aside from putting the woman at severe risk of (sometimes) life-endangering complications, can also compromise egg/embryo quality. However, it is my fervent belief that in such women, the preferred approach to ovarian stimulation is through the use of low dosage FSHr-dominant gonadotropins (rather than oral agents such as clomiphene or letrozole and/or high dosage Menopur). This approach is referred to as Micro-I

    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.
    • 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
    • Why did my IVF Fail
    • 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
    • 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
    • A Thin Uterine Lining: Vaginal Viagra is Often the Answer (update)
    • 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
    • How Many Embryos should be transferred: A Critical Decision in IVF.
    • Avoiding High Order Multiple Pregnancies (Triplets or Greater) with IVF
    • The Role of Nutritional Supplements in Preparing for IVF
    • Endometriosis and Infertily
    • 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 my advice or medical 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.
    Also, 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

  • Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 25, 2018 reply

    In my opinion, such testing is to your advantage because it would help decide whether/how to proceed with ET to your uterus.

    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 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!
    • 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
    • How Many Embryos should be transferred: A Critical Decision in IVF.
    If you are interested in my advice or medical 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.
    Also, 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

  • Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 25, 2018 reply

    In my opinion and others might not concur), I definitely would advise testing for alloimmune factors such as DQ alpha/HLA matching. If there were to be a match I would yse IL+prednisone therapy and do s single blastocyst transfer of a PGS-normal blastocyst.

    If you are interested in my advice or medical 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.
    Also, 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

  • Diana - January 25, 2018 reply

    Dr Sher, what’s the benefit of BCP with lupron overlap over of d21 lupron start? Do they achieve the exact same baseline hormone levels before menses or is one better than the other? Just curious the reason for your preference.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 25, 2018 reply

    Most important is that it allows for timing of the onset of stimulation to the benefit and convenience of all and it does so without any down-side….in my opinion. In addition, by lowering ovarian LH-induced male hormone (predominantly testosterone activity) for longer, it could (in my opinion) enhance egg quality, especially oin women with DOR.

    One often hears the expressed opinion that the BCP suppresses response to ovarian stimulation. This is not the case, provided that the BCP is overlapped with administration of an agonist (e.g. Lupron, Buserelin, Superfact) for several days leading up to the start of menstruation and the initiation of ovarian stimulation cycle with gonadotropin drugs. If the latter precaution is not taken, and the cycle of stimulation is initiated coming directly off the BCP the response will often be blunted and subsequent egg quality could be adversely affected. The explanation for this is that in natural (unstimulated) as well as in cycles stimulated with fertility drugs, the ability of follicles to properly respond to FSH stimulation is dependent on their having developed FSH-responsive receptors . Pre-antral follicles (PAF) do not have such primed FSH receptors and thus cannot respond properly to FSH stimulation with gonadotropins. The acquisition of FSH receptor responsivity requires that the pre-antral follicles be exposed to FSH, for a number of days (5-7) during which time they attain “FSH-responsivity” and are now known as antral follicles (AF). These AF’s are now able to respond properly to stimulation with administered FSH-gonadotropins. In regular menstrual cycles, the rising FSH output from the pituitary gland insures that PAFs convert tor AF’s. The BCP (as well as prolonged administration of estrogen/progesterone) suppresses FSH. This suppression needs to be countered by artificially causing blood FSH levels to rise in order to cause PAF to AF conversion prior to COS commencing, otherwise pre-antral-to –antral follicle conversion will not take place in an orderly fashion, the duration of ovarian stimulation will be prolonged and both follicle and egg development may be compromised. GnRH agonists (e.g. Lupron, Buserelin, Superfact) , cause an immediate surge in release of FSH by the pituitary gland thus causing conversion from PAF to SAF. This is why, women who take a BCP to launch a cycle of COS need to have an overlap of the BCP with an agonist. By overlapping the BCP with an agonist for a few days prior to menstruation the early recruited follicles are able to complete their developmental drive to the AF stage and as such, be ready to respond appropriately to optimal ovarian stimulation. Using this approach, the timing of the initiation of the IVF treatment cycle can readily and safely be regulated and controlled by varying the length of time that the woman is on the BCP.
    Since optimizing follicular response to COS requires that prior to stimulation with gonadotropins, FSH-induced conversion from PAF to AF’s first be completed and the BCP suppresses FSH, it follows when it comes to women launching COS coming off a BCP something needs to be done to cause a rise in FSH for 5-7 days prior to menstruation heralding the cycle of CO S.This is where overlapping the BCP with an agonist (e.g. Lupron/Superfact/Buserelin) comes in. The agonist causes FSH to be released by the pituitary gland and if overlapped with the BCP for several days and this will (within 2-5 days) facilitate PAF to AF conversion…. in time to start COS with the onset of menstruation. Initiating ovarian stimulation in women taking a BCP, without doing this is suboptimal
    I believe it to be essential regardless of the protocol of COS protocol being contemplated, for women who launching ovarian stimulation coming off a BCP to overlap with an agonist for several days in advance of initiating ovarian stimulation with the onset of menstruation,

    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.
    • Human Growth Hormone Administration in IVF: Does it Enhances
    • 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

    If you are interested in my advice or medical 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.
    Also, 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

  • Cherie - January 25, 2018 reply

    Hiya, are you still a proponent of human growth hormone for DOR women? If so, is it best to start taking HGH on day 1 of stims?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 25, 2018 reply

    I am and there are differing protocols for its use. I prefer starting it later (either with agonist down-regulation or with the stimulation start.

    A woman’s reproductive potential is very much influenced affected by her “biological clock” which comprises two components:
    1. Age: Advancing age is inevitably accompanied by a progressive reduction in the number of eggs in the ovaries (“ovarian reserve”). As a diminution in ovarian reserve (DOR) ultimately passes a theoretical “threshold” the woman becomes progressively more resistant to stimulation with fertility drugs. This is accompanied by a fall in blood AMH levels and a rise in basal blood FSH. After several years of progressive DOR, the ovarian reserve is ultimately depleted, and ovulation as well as cyclical menstruation ceases (menopause).
    2. “Egg Competency” The second component of the biological clock is an inevitable age-related decline in egg competency (the ability of an egg, upon fertilization, to propagate a healthy embryo) . The most important manifestation of this age-related occurrence is an inevitable and rapid increase in the percentage of eggs that have numerical chromosome irregularities (aneuploidy). By way of example, at age 30Y, about one out of every two human eggs will be aneuploid while at 45Y more than nine out of ten are so afflicted. Aneuploid eggs cannot propagate healthy babies. Most will not even fertilize and those that do, will usually be lost as early miscarriages or go on to produce a birth defect such as Down syndrome.
    It is important to understand is that e the two components of the biological clock (i.e. ovarian reserve and age) represent variables which while they are often interrelated and inter-dependent can often exist independently. By way of example, some older women in their mid-forties have excellent ovarian reserve while some young women in their thirties have DOR. Yet while they produce fewer eggs, the potential competency of the eggs they produce is largely tied to their age. However, the ovarian hormonal environment brought about by DOR and the protocol used for ovarian stimulation, is readily affected by the protocol used for ovarian stimulation. Selection of the wrong stimulation protocol can adversely influence egg competency. Conversely, an individualized and optimal protocol for ovarian stimulation by favorably regulating the ovarian hormonal environment, can improve the potential for optimal follicle and egg development thereby minimizing the risk of egg aneuploidy. The problem is that it becomes progressively more difficult to optimally regulate the intra-ovarian hormonal environment in older women, and in those with DOR, and it is here that the use of human growth hormone can play a valuable role.
    Several researchers have shown that the administration of human growth hormone (HGH), as an adjunct to ovarian stimulation, enhances follicle response in older women and those with DOR and so can help optimize egg quality. It is thought that HGH hormone by increasing the production of insulin-like growth factor 1 (IGF-1), improves follicle development, estrogen hormone production and egg maturation. Two basic mechanisms have been proposed: 1) improving the response to gonadotropin therapy by up-regulating the FSH receptors on the granulosa cells that form the inner lining of follicles and, 2) through a direct enhancing effect of HGH on the egg’s mitochondrial activity. While human eggs do have HGH receptors, those retrieved from older women show decreased expression of such receptors (as well as a reduction in the number of functional mitochondria) as compared with those derived from younger women. In fact, it has recently been shown that older women treated with HGH showed a marked increase in functional mitochondria in their eggs along with improved egg quality.
    My own experience in selectively prescribing HGH as an adjuvant to women with DOR, older women and those with unexplained egg quality deficits, is that if used in combination with individualized protocols of ovarian stimulation it does indeed enhance egg quality and ovarian response, culminating in improved IVF outcome.

    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.
    • Use of the BCP
    • 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

    If you are interested in my advice or medical 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.
    Also, 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

Alert ! - Dr. Sher will not have access to the internet, and will therefore be out of reach, from June 5 until June 25. Please re-submit this comment after that date. Until then, please explore the Sher IVF website and his Facebook videos archived on his page.

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