Ask Our Doctors – Archive

Our Medical Directors are outstanding physicians that you will find to be very personable and compassionate, who take care to ensure that you have the most cutting-edge fertility treatments at your disposal. This is your outlet to ask your questions to the doctors.

19,771 Comments

  1. I just began a natural cycle for an upcoming FET with DE. I have had several failed IVF attempts over the past 4 years with my OE and twice with DE. I am going to be proceeding with Intralipid infusions for NK cells in this cycle. I was introduced to intralipids on the recommendation of a previous clinic (I’m at my 3rd clinic now, although this 3rd clinic doesn’t believe/recommend intralipids, the Dr. wrote the prescription for me anyways to use with a home health nursing group—they come to me). I’m seeking your advice about the frequency to start the intralipids. I believe, from my own research, to do an infusion 2 weeks before the FET, the day of the FET, again with a positive beta, and then 2 more, each a month apart. Does this sound correct?

    • Yes! It sounds correct!

      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 15y 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
      e.Ureaplasma Urealyticum (UU) Infection of cervical mucous and the endometrial lining of the uterus, can sometimes present as unexplained early pregnancy loss or unexplained failure following intrauterine insemination or IVF. The infection can also occur in the man, (prostatitis) and thus can go back and forth between partners, with sexual intercourse. This is the reason why both partners must be tested and if positive, should be treated contemporaneously.
      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?
      ______________________________________________________
      ADDENDUM: PLEASE READ!!
      INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
      Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.

      If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).

      PLEASE SPREAD THE WORD ABOUT SFS!

      Geoff Sher

  2. Hi Dr Sher,

    Thanks for running this blog. Your replies are really so helpful in answering so many questions we will have on IVF.

    My husband is born without Vas DF and we went through 3 retreivals & transfers, all failed. Really looking for a opinion now on how to move forward from here.
    I believe all of my stimulation cycles are short protocols.

    Cycle 1 (Frozen Sperm)
    Start Simulation using 300 menopur for 11 days on Day 2 of cycle,start orgalutran at around day 6 of stimms
    Lupron Trigger
    16 eggs, 5 mature eggs and 3 fertilized normally. Frozen Sperm.
    At Day 5, transfered 2 remaining embroyos, Sadly there were only at 9 cell and compacting morula stage.
    No embroyos left to freeze, Negative beta test done 14 days after transfer
    My period actually starts 2 days before my beta test

    Cycle 2 (Frozen Sperm)
    Start Simulation using 250 Puregon for 7 days on Day 3 of cycle,start orgalutran at around day 6 of stimms
    HCG Trigger
    23 eggs, 11 mature eggs and only 4 fertilized. 3 eggs was frozen at Day 2 at 6,7,8 cells.
    Start Frozen Embroyo Cycle down regulated with Triptorelin with 2mgx2 progyonova twice daily and nearer to transfer start cyclogest twice daily
    Transfer date – The lab defroze the 3 embroyos 2 days before the transfer. At transfer day, 2 embroyos was transfer 2 morulas (1 cavitating/1 cavitaed)
    Negative beta test done 14 days after transfer, My period starts 2 days after

    Cycle 3: (Fresh Sperm)
    Start Simulation using 175 Gonal-F for 6 days on Day 2 of cycle,
    At day 7 of stimms,start orgalutran dosage increase to Gonal F 250 for another 4 days before adding 75 menopur to it.
    Both HCG Trigger AND ovidrel Trigger used
    16 eggs, 7 mature eggs and only 4 fertilized using fresh sperm.
    2 blastocysts was frozen – 1 DAy 5 4BB grade , 1 Day 6 blasts 4BC grade’

    Start Frozen Embroyo Cycle down regulated, with 8mg progyonova a day and nearer to transfer start cyclogest twice daily
    Transfer date – PIO jab given before transfer, Both blastocysts thawed successfully, assisted hatching used due to thick zona.
    Continue with 8mg progyonova a day and nearer to transfer start cyclogest twice daily + duphaston twice daily, PIO Jab given day 4 post transfer

    Day 10 – Beta of 16.7

    There are comment from the lab of poor egg quality. Would want to seek if a long cycle would help with egg quality? And also do you suggest if my husband should still go through another sperm retrieval to use fresh? He still have some frozen left enough for the next cycle.

    Feeling lost. Thanks. Poa

    • I would require much more information to comment on the influence of the protocols used for ovarian stimulation, versus a sperm related issue.

      Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
      It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
      1.Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
      2.Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
      We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about 15y 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
      e.Ureaplasma Urealyticum (UU) Infection of cervical mucous and the endometrial lining of the uterus, can sometimes present as unexplained early pregnancy loss or unexplained failure following intrauterine insemination or IVF. The infection can also occur in the man, (prostatitis) and thus can go back and forth between partners, with sexual intercourse. This is the reason why both partners must be tested and if positive, should be treated contemporaneously.
      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?
      ______________________________________________________
      ADDENDUM: PLEASE READ!!
      INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
      Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.

      If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).

      PLEASE SPREAD THE WORD ABOUT SFS!

      Geoff Sher

  3. Hi Dr SHER

    I’m questioning my new clinics protocol for FET. I was on BCP for 2 months after my hysteroscopy in prep for FET. They had me do baseline the last day of my pill and start estrogen 4 days later- regardless if I got my period. This seemed odd since I thought I’m supposed to confirm lining shed prior to E2. My baseline was 6.6 mm and I never got my period but started E2 as instructed. Period never came and now my ultrasounds are showing a decreasing lining to 5.8 then 5.2. What do you make of this? I’m not bleeding or spotting since starting E2 and my blood levels are high.

    Thank you

    • Adding that my baseline E2 was below 55 pmol/L

    • I respectfully do not personally begin hormone therapy until a period starts.

      Geoff Sher

  4. Hi Dr Sher

    Thank you v much for providing this invaluable service.

    My husband and I have been TTC since 2012 – I was 30 when we started and I am now 38. Our official diagnosis is unexplained infertility, although IVF revealed there is a problem with my eggs. I’m a high responder – we get lots of eggs (19-32, depending on the protocol) and usually have 10-12 ‘good’ day 3 embryos, but very poor blastocyst conversion. We did six rounds of IVF with my eggs, and managed to make a handful of good looking blastocysts with our most recent clinic. But despite transferring 5 ‘good’ expanded A/B grade blasts (although not PGSd) over three cycles, I never had a hint of implantation.

    My husband’s semen analysis is fine. We actually tried fertilising my eggs with donor sperm to see if perhaps there was a ‘hidden’ issue, and ended up with one average-looking blast which is currently frozen.

    After this we made the decision to try donor eggs, and ended up with six great quality blasts from 10 eggs and my husband’s sperm. None of them stuck 🙁

    We have had every test under the sun – including immunes and ERA – and have found nothing. We are now pursuing donor eggs and surrogacy as I can’t just keep throwing embryos and hoping they will stick – I have had 10 transfers in total.

    About me – my ovaries are ‘mildly polycystic’ although I don’t have PCOS. My cycles are generally regular, if a little on the short side at 26 days – ovulation on day 15 and an 11 day luteal phase. Blood glucose normal and my BMI is 20.

    I’m also happy with our clinic and the protocols used.

    I just wondered if you might have any insight on our situation, which to me, doesn’t seem typical. I regret not getting our embryos screened but I can’t go back in time… The dramatic improvement in quality when we took my eggs out of the equation seemed to speak for itself. But now I’m wondering whether the problem was with them or my uterus. Maybe one or two of the blasts we made with my eggs were ok, but something about my endometrium stopped them from sticking? Is it possible that whatever ovarian dysfunction is affecting my eggs could also be interfering with implantation?

    Very best wishes

    Katie

    • One of the commonest questions asked by patients undergoing IVF relates to the likelihood of their eggs fertilizing and the likely “quality of their embryos. This is also one of the most difficult questions to answer. On the one hand many factors that profoundly influence egg quality; such as the genetic recruitment of eggs for use in an upcoming cycle, the woman’s age and her ovarian reserve, are our outside of our control. On the other hand the protocol for controlled ovarian stimulation (COS) can also profoundly influence egg/embryo development and this is indeed chosen by the treating physician.
      First; it should be understood that the most important determinant of fertilization potential, embryo development and blastocyst generation, is the numerical chromosomal integrity of the egg (While sperm quality does play a role, in the absence of moderate to severe sperm dysfunction this is (moderate or severe male factor infertility a relatively small one). Human eggs have the highest rate of numerical chromosomal irregularities (aneuploidy) of all mammals. In fact only about half the eggs of women in their twenties or early thirties, have the required number of chromosomes (euploid), without which upon fertilization they cannot propagate a normal pregnancy. As the woman advances into and beyond her mid-thirties, the percentage of eggs euploid eggs declines progressively such that by the age of 40 years, only about one out of seven or eight are likely to be chromosomally normal and by the time she reaches her mid-forties less than one in ten of her eggs will be euploid.
      Second; embryos that fail to develop into blastocysts are almost always aneuploid and not worthy of being transferred to the uterus because they will either not implant, will miscarry or could even result in a chromosomally abnormal baby (e.g. Down syndrome). However, it is incorrect to assume that all embryos reaching the blastocyst stage will be euploid (“competent”). ). It is true that since many aneuploid embryos are lost during development and that those failing to survive to the blastocyst stage are far more likely to be competent than are earlier (cleaved) embryos. What is also true is that the older the woman who produces the eggs, the less likely it is that a given blastocyst will be “competent”. As an example, a morphologically pristine blastocyst derived from the egg of a 30-year-old woman would have about a 50:50 chance of being euploid and a 30% chance of propagating a healthy, normal baby, while a microscopically comparable blastocyst-derived through fertilization of the eggs from a 40-year-old, would be about half as likely to be euploid and/or propagate a healthy baby.
      While the effect of species on the potential of eggs to be euploid at ovulation is genetically preordained and nothing we do can alter this equation, there is, unfortunately, a lot we can (often unwittingly) do to worsen the situation by selecting a suboptimal protocol of controlled ovarian stimulation (COS). This, by creating an adverse intraovarian hormonal environment will often disrupt normal egg development and lead to a higher incidence of egg aneuploidy than otherwise might have occurred. Older women, women with diminished ovarian reserve (DOR) and those with polycystic ovarian syndrome are especially vulnerable in this regard.

      During the normal, ovulation cycle, ovarian hormonal changes are regulated to avoid irregularities in production and interaction that could adversely influence follicle development and egg quality. As an example, small amounts of androgens (male hormones such as testosterone), that are produced by the ovarian stroma (tissue surrounding ovarian follicles) during the pre-ovulatory phase of the cycle enhance late follicle development, estrogen production by the granulosa cells (that line the inner walls of follicles), and egg maturation. However, over-production of testosterone can adversely influence the same processes. It follows that COS protocols should be individualized and geared toward optimizing follicle growth and development time while avoiding excessive ovarian androgen (testosterone) production and that the hCG “trigger shot” should be carefully timed.
      In summary, it is important to understand the influence species, age of the woman as well as the effect of the COS protocol can have on egg/embryo quality and thus on IVF outcome. The selection of an individualized protocol for ovarian stimulation is one of the most important decisions that the RE has to make and this becomes even more relevant when dealing with older women, those with DOR and women with PCOS. Such factors will in large part determine fertilization potential, the rate of blastocyst generation and indeed IVF outcome.
      I strongly recommend that you visit http://www.SherIVF.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
      •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.
      •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)
      •Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
      •Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
      •Optimizing Response to Ovarian Stimulation in Women with Compromised Ovarian Response to Ovarian Stimulation: A Personal Approach.
      •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?
      •Staggered IVF
      •Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of 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.
      •IVF: Selecting the Best Quality Embryos to Transfer
      •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
      •IVF outcome: How Does Advancing Age and Diminished Ovarian Reserve (DOR) Affect Egg/Embryo “Competency” and How Should the Problem be addressed.

      ______________________________________________________
      ADDENDUM: PLEASE READ!!
      INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
      Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.

      If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).

      PLEASE SPREAD THE WORD ABOUT SFS!

      Geoff Sher

  5. Hi Dr Sher I have been doing a lot of reading on your blog and convinced my fertility specialists to use your protocol because I got dysmature eggs before and after checking my labs lh and progesterone did show it. My question is if I do two weeks of birth control then overlap with lucerin will my cycle day 1 labs be accurate when measuring LH and progesterone? You said it’s a stairway affect so I just want to make sure it’s accurate before I start the second part with the cetrorelix and the rest. Two weeks birth control then lucerin will be enough to turn off my pituitary gland I am hoping?

    • Yes! It will in my opinion, would be sufficient!

      Geoff Sher