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. Hi There. I am 42 year old with 4 failed cycles, two with my own eggs and two with donor eggs. My issue is implantation, out of all these 4 failed cycles none of the embryos implanted. In one cycle doctor even put the PGS tested embryo but that also failed. I have done all the tests available like Yale biopsy, receptivity test, NK cells test. All test results came fine. My uterine lining is also great like 10mm-11mm everytime.Can you please advise what should I do different so that my embryo can implant. I am also considering using Embryo glue but not sure if that would change anything. Kindly advise.

    • 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
      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?

      Geoff Sher

      ADDENDUM:

      Sher-Fertility Solutions (SFS) will be officially launched in April 2019. Through SFS I will provide fertility consultations (via SKYPE) to an ever-growing number of patients (from >40 countries) with complex Reproductive Dysfunction (RD) who seek access to my input and guidance.

      In the past, I have limited my consultations with patients from afar to those who expressed a willingness to travel to Las Vegas for treatment by me. But now with the “birth” of SFS, all this is about to change. With one notable exception I will, as of April, 2019, no longer be conducting and performing hands-on IVF treatments. Rather, I will focus on providing SKYPE consultations and guidance to as many patients as possible. The one important exception will apply to approximately 1,000 existing patients who, following IVF previously performed by me, have remaining eggs or embryos stored (cryopreserved) at SIRM-LV and wish for me to perform their Frozen Embryo Transfers (FETs). I have agreed to accommodate such patients…..but only through August, 2019.

      Patients will have ready access online, to SFS: by going to http://www.SherIVF.com; by phone (1-800-780-7437 or 702-533-2691) and via email (sher@sherivf.com or concierge@sherIVF.com). A onetime fee of $400.00, will provide enrollees with access to: a full review of all their medical records (+ assistance in requisitioning additional records, as needed); a comprehensive initial 1 hour, SKYPE consultation with me; additional SKYPE consultations (as might be required); a written medical report (which will include a recommended plan of action) that you can share with a Physician(s) of choice. I would, subject to your approval and a request by such Physician(s), also be willing to discuss your case with him/her/them. I will in due course post on my website, a list of Fertility Physicians in key locations all over the United States and abroad, whom I endorse and to whom I would be willing to direct SFS patients for subsequent treatment.

      I have good news for those of you who are interested in traveling to Las Vegas for IVF. Dr Russel Foulk, Medical Director of SIRM-LV has expressed a willingness to be receptive to, treatment plans that I recommend for SFS patients Moreover, Dr Foulk has graciously agreed to interact with me during such treatments. I highly recommend Dr Foulk to those of you who, following consultation with me, wish to have me remain involved in the implementation of your treatment. This having been said, the final say in any management decision is always up to the treating physician.

      It is both my objective and commitment to serve as a resource to SFS patients on complex RD issues such as: Unexplained IVF failure; Recurrent Pregnancy loss (RPL); Immunologic Implantation Dysfunction-IID; Genetic/chromosomal issues; effects of Diminished Ovarian Reserve (DOR) and advancing age on reproductive performance, etc.

      I hope to ultimately expand the National and International reach of SFS, through my website (www.sherIVF.com) , through online webinars as well as Town hall- type consumer-based seminars, workshops and through social media. At the same time I will continue blogging on my website and doing bi-weekly Live-feed Facebook presentations (at “Dr Geoffrey Sher”) on a variety of subjects and topical issues.
      For me this is a very exciting venture. Please become part of the SFS family and help spread the word!

      I was very recently greatly honored in receiving an award by the prestigious; International Association of Top Professionals (IAOTP). For more information, go to the press release on my website, http://www.sherIVF.com .

  2. Dear Mr Sher,
    I am almost 37 and 4 months ago I discovered I have low AMH, around 0.9ng/ml. I never tried to conceive and currently do not have a partner. I do not want to miss any chance of having a baby and although I know it is already too late I want to do whatever I can do to improve my chances.
    1. Does my AMH show that I am near menopause?
    2. I was taking yasmin contraceptives for 6weeks to change my cycle and would start stimulation some days ago but another doctor told me that it will be difficult to retrieve eggs after first withdrawal, that my ovaries are very small and I cancelled it. Is it true? I would get two injections of daronda for the 1st and 2nd day of cycle and then stimulation. Now I will start in 1.5 months again. Do you think I did the right thing?
    3. Do you have any suggestions for me? I saw that you do not recommend egg freezing after 35y

    • 1. Does my AMH show that I am near menopause?

      AQ: You certainly have diminishing ovarian reserve (see below)

      2. I was taking yasmin contraceptives for 6weeks to change my cycle and would start stimulation some days ago but another doctor told me that it will be difficult to retrieve eggs after first withdrawal, that my ovaries are very small and I cancelled it. Is it true?

      A: Not necessarily so

      Women who (regardless of age) have diminished ovarian reserve (DOR) have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production, and/or biological activity, of LH. This can result in excessive ovarian male hormone (predominantly testosterone) production. This 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, www. SherIVF.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
      ______________________________________________________
      ADDENDUM:

      Sher-Fertility Solutions (SFS) will be officially launched in April 2019. Through SFS I will provide fertility consultations (via SKYPE) to an ever-growing number of patients (from >40 countries) with complex Reproductive Dysfunction (RD) who seek access to my input and guidance.

      In the past, I have limited my consultations with patients from afar to those who expressed a willingness to travel to Las Vegas for treatment by me. But now with the “birth” of SFS, all this is about to change. With one notable exception I will, as of April, 2019, no longer be conducting and performing hands-on IVF treatments. Rather, I will focus on providing SKYPE consultations and guidance to as many patients as possible. The one important exception will apply to approximately 1,000 existing patients who, following IVF previously performed by me, have remaining eggs or embryos stored (cryopreserved) at SIRM-LV and wish for me to perform their Frozen Embryo Transfers (FETs). I have agreed to accommodate such patients…..but only through August, 2019.

      Patients will have ready access online, to SFS: by going to http://www.SherIVF.com; by phone (1-800-780-7437 or 702-533-2691) and via email (sher@sherivf.com or concierge@sherIVF.com). A onetime fee of $400.00, will provide enrollees with access to: a full review of all their medical records (+ assistance in requisitioning additional records, as needed); a comprehensive initial 1 hour, SKYPE consultation with me; additional SKYPE consultations (as might be required); a written medical report (which will include a recommended plan of action) that you can share with a Physician(s) of choice. I would, subject to your approval and a request by such Physician(s), also be willing to discuss your case with him/her/them. I will in due course post on my website, a list of Fertility Physicians in key locations all over the United States and abroad, whom I endorse and to whom I would be willing to direct SFS patients for subsequent treatment.

      I have good news for those of you who are interested in traveling to Las Vegas for IVF. Dr Russel Foulk, Medical Director of SIRM-LV has expressed a willingness to be receptive to, treatment plans that I recommend for SFS patients Moreover, Dr Foulk has graciously agreed to interact with me during such treatments. I highly recommend Dr Foulk to those of you who, following consultation with me, wish to have me remain involved in the implementation of your treatment. This having been said, the final say in any management decision is always up to the treating physician.

      It is both my objective and commitment to serve as a resource to SFS patients on complex RD issues such as: Unexplained IVF failure; Recurrent Pregnancy loss (RPL); Immunologic Implantation Dysfunction-IID; Genetic/chromosomal issues; effects of Diminished Ovarian Reserve (DOR) and advancing age on reproductive performance, etc.

      I hope to ultimately expand the National and International reach of SFS, through my website (www.sherIVF.com) , through online webinars as well as Town hall- type consumer-based seminars, workshops and through social media. At the same time I will continue blogging on my website and doing bi-weekly Live-feed Facebook presentations (at “Dr Geoffrey Sher”) on a variety of subjects and topical issues.
      For me this is a very exciting venture. Please become part of the SFS family and help spread the word!

      I was very recently greatly honored in receiving an award by the prestigious; International Association of Top Professionals (IAOTP). For more information, go to the press release on my website, http://www.sherIVF.com .

  3. You’ve said before that you don’t believe in the ERA test. Could you explain your thoughts on ERA and why you are not a fan?
    Thanks!

    • With ERA you are attempting to evaluate endometrial receptivity in one cycle and using this to predict receptivity in another. I know of no convincing evidence that this premise holds true.

      Geoff Sher

  4. Hello and thanks for this question board!
    I am 37 (so is my husband). He has CABVD so we have to do IVF. Neither of us have had pregnancies before. My BMI is 25 and due to changes in cycles and a history of intermittent ovarian cysts I have been evaluated for PCOS many times since I was a teen. I was always told “maybe borderline”. For the last year my periods were regular, q33-37 days with predictable positive OPKs. My fsh/oh wasn’t impressive, normal testosterone and high end of normal estrogen. I do not have any androgen-excess symptoms. I do have a fmhx of DM2 however. My AMH is 9.24 which seems to point to PCOS. I just finished my first IVF which unfortunately was not successful. I was on 3 weeks of OCPs then started 225 of Follistim with 75u of Menopur at night. I also was on Femara 5mg in AM b/c I have migraines with auras and trying to prevent super high estrogen levels related to that. About Day 7 I added Ganirelix in Am and increased FSH to 300. I was told I had 24 follicles that were growing at that time the largest being 12mm. I also had one pre-cycle cyst about 2cm prior as well.
    I keep on this until day 11 when I triggered with HCG and Lupron. I was never told what my estrogen levels were. Retrieval day 13-had 27 eggs, 25 mature, 18 fertilized with ICSI (his thawed sperm from PESA). I was told 7 days later none of them made it. The clinic does not do updates in between those days and I was not told what day they arrested on. I was bloated but did not have OHSS.

    My questions are related to my (suspected) poor egg quality and my (suspected) PCOS. What protocol changes would you recommend to potentially improve egg quality (quality over quantity) Regarding egg quality I started CoQ10 and am trying to work on weight and sugar. I am continuing a low carb diet however should I ask about metformin? (I have very mild IR with A1C around 5.5 and occasional FBS of low 100s. )

    Thank you in advance for your help!

    • 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 small collections of fluid — called follicles — located in each ovary as seen during an ultrasound. 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. The ovaries of women with PCOS characteristically contain multiple micro-cysts often arranged like a “string of pearls” immediately below the ovarian surface (capsule).interspersed by an overgrowth of ovarian connective tissue (stroma).

      PCOS is one of the most common causes of menstrual irregularities, infertility, and hirsutism, Despite an enormous effort to define its cause, the etiology of PCOS remains unclear, and there is no definite cure at this time. PCOS is clearly a heterogeneous disorder which often has a familial (genetic) basis. Infertility associated with PCOS has been attributed to numerous factors, including dysfunctional gonadotropin pituitary secretion, peripheral insulin resistance, elevated adrenal and/or ovarian androgen (male hormone) levels, and dysfunction of several growth factors. Women with this condition are often obese and insulin resistant. The compensatory hyperinsulinemia further stimulates ovarian androgen production which may be detrimental to egg maturation and there is a clear link between the degree of insulin resistance and anovulation. PCOS is also a significant long-term health risk for women, thus necessitating vigilance through regular annual examinations (non-insulin dependent diabetes mellitus, hypertension, hypercholesterolemia, cardiovascular disease and endometrial cancer). Whereas PCOS-related infertility is usually manageable through the use of fertility drugs, lifestyle changes (diet and exercise) remain a mainstay of long-term therapy. More recently, ovulation rates, circulating androgens, pregnancy rates and perhaps even first-trimester miscarriage rates have been shown to improve when insulin sensitizers like metformin are used to correct the underlying insulin resistance.

      Most patients with PCOS are young and have excellent pregnancy rates with oral clomiphene. Those that require more aggressive treatments with injectable medications probably represent a subgroup of PCOS patients with severe ovarian dysfunction. These women often have explosive response to gonadotropins which can result in serious complications like Severe Ovarian Hyperstimulation Syndrome (OHSS…see below) and high order multiple births. In those women, the ability to perform “prolonged coasting” (see below) and selectively transfer fewer embryos during IVF offers a clear advantage over standard gonadotropin injections.

      Egg quality in PCOS

      The potential for a woman’s eggs to undergo orderly maturation, successful fertilization and subsequent progression to “good quality embryos” is in large part genetically determined. However, the expression of such potential is profoundly susceptible to numerous influences, especially intra-ovarian hormonal changes during the pre-ovulatory phase of the cycle. Proper follicular stimulation as well as precise timing of egg maturation with LH (Luteinizing Hormone) or hCG (human chorionic gonadotropin) is crucial to optimal egg maturation, fertilization and ultimately embryo quality. Both pituitary gonadotropins, LH and FSH (follicle stimulating hormone) play a pivotal but different role in follicular development. The action of FSH is mainly directed toward granulosa cell (cells lining the inside of the follicle) proliferation and estrogen production (E2). LH, on the other hand, acts primarily on the ovarian stroma (the connective tissue that surrounds the follicle) to produce androgens. While small amounts of ovarian androgens, such as testosterone, enhance egg and follicle development, over-exposure to them can have a deleterious effect. Furthermore, excessive ovarian androgens can also compromise estrogen-induced endometrial growth and development.

      Suppressing pituitary secretion of LH with gonadotropin releasing hormone (GnRH) agonists such as Lupron®, is particularly useful in PCOS. In that condition, serum LH levels are elevated, leading to stromal overgrowth, follicular arrests (so-called cysts) and high levels of androgens synthesis. It is therefore not surprising that these follicles often yield poorly developed (“immature”) eggs” at the time of egg retrieval (ET) and that “poor egg/embryo quality”, inadequate endometrial development and high miscarriage rates are common features of this condition. However, contrary to popular belief, this is not due to an intrinsic deficit in “egg quality”. Stimulation protocols geared toward optimizing follicle and egg development and avoiding over exposure to androgens correct these problems ad result in pregnancy rates similar to those of non-PCOS women. Whereas the overuse of LH-containing preparations such as Menopur® and Luveris® further aggravates this effect. In conclusion, to maximize ultimate oocyte maturation, we strongly recommend against the exclusive use of such products in PCOS patients, preferring FSH-dominant products such as Folistim®, Gonal F® or Bravelle® over a period of at least 9 days following pituitary suppression with Lupron®.

      PCOS women often have a family history of diabetes and demonstrable insulin resistance (evidenced by high blood insulin levels and an abnormal 2-hour glucose tolerance test).This underlying Diabetes mellitus tendency could play a role in the development of PCOS and contribute to the development of obesity, an abnormal blood lipid profile, and a predisposition to coronary vascular disease. Women with PCOS are slightly more at risk of developing uterine, ovarian and possibly also breast cancer in later life and accordingly should be evaluated for these conditions on a more frequent basis than would ordinarily be recommended to non-PCOS women.

      Most women with PCOS either do not ovulate at all or they ovulate irregularly. As a consequence thereof they in addition usually experience delayed, absent or irregular menstruation. In addition, an inordinate percentage of the eggs produced by PCOS women following ovulation induction, tend to be chromosomally abnormal (aneuploid). Rather than being due to an intrinsic egg defect being inherent in PCOS women, the poor egg quality more than likely the result of over-exposure to male hormones (predominantly, testosterone) produced by the ovarian stroma. These two factors (ovulation dysfunction and poor egg quality) are the main reasons for the poor reproductive performance (infertility and an increased miscarriage rate) in PCOS women.

      PCOS patients are at an inordinate risk of severely over-responding fertility drugs, both oral varieties (e.g. Clomiphene, Serophene & Femara) and especially the injectables (e.g. Follistim, Puregon, Gonal F, Menopur and Bravelle) by forming large numbers ovarian follicles. This can lead to life endangering complications associated with sever ovarian hyperstimulation (OHSS). In addition PCOS women receiving fertility drugs often experience multiple ovulations putting them at severe risk (40%+) of high order multiple pregnancy (i.e. triplets or greater) with often devastating consequences.

      VARIETIES OF POLYCYSTIC OVARIAN SYNDROME:

      1) Hypothalamic-pituitary-PCOS: This is the commonest form of PCOS and is often genetically transmitted and is characteristically associated with a blood concentration of Luteinizing Hormone (LH) that is uncharacteristically much higher than the Follicle Stimulating Hormone (FSH) level (FSH is normally higher than the LH concentration) as well as high-normal or blood androgen ( male) hormone concentrations (e.g. androstenedione, testosterone and dehydroepiandrosterone -DHEA).Hypothalamic-pituitary-ovarian PCOS is also often associated with insulin resistance and in about 40%-50% of the cases.

      2) Adrenal PCOS: Here the excess of male hormones are derived from overactive adrenal glands rather than from the ovaries. Blood levels of testosterone and/or androstenedione raised but here, but here, the blood level of dehydroepiandrosterone (DHEAS) is also raised, clinching the diagnosis.

      3) Severe pelvic adhesive disease secondary to severe endometriosis, chronic pelvic inflammatory disease and/or extensive pelvic surgery: Women who have this type of PCOS tend to less likely to hyperstimulate in response to ovulation induction . Their. DHEAS is also is not raised.

      TREATMENT OF INFERTILITY DUE TO ASSOCIATED OVULATION DYSFUNCTION:

      Hypothalamic-pituitary-/ovarian PCOS: Ovulation induction with fertility drugs such as clomiphene citrate, Letrozole (Femara) or gonadotropins, with or without intrauterine insemination (IUI) is often highly successful in establishing pregnancies in PCOS women. However, IVF is fast becoming a treatment of choice (see below).

      In about 40% of cases, 3-6 months of oral Metformin (Glucophage) treatment results in a significant reduction of insulin resistance, lowering of blood androgen levels, an improvement in ovulatory function, and/or some amelioration of androgenous symptoms and signs.

      Surgical treatment by “ovarian drilling” of the many small ovarian cysts lying immediately below the envelopment (capsule) of the ovaries, is often used, but is less successful than alternative non-surgical treatment and is only temporarily effective. The older form of surgical treatment, using ovarian wedge resection is rarely used any longer as it can produce severe pelvic adhesion formation.

      Adrenal PCOS is treated with steroids such as prednisone or dexamethasone which over a period of several weeks will suppress adrenal androgen production, allowing regular ovulation to take place spontaneously. This is often combined with clomiphene, Letrozole and/or gonadotropin therapy to initiate ovulation.

      PCOS attributable to Pelvic Adhesive Disease is one variety which often is associated with compromised ovarian reserve, a raised FSH blood level and ovarian resistance to fertility drugs. In many such cases, high dosage of gonadotropins (FSH-dominant) with “estrogen priming” will often elicit an ovarian response necessary for successful ovulation induction and/or IVF. Neither steroids nor Metformin are helpful in the vast majority of such cases.

      PCOS women undergoing ovulation induction usually release multiple eggs following the hCG trigger and are thus at inordinate risk of twin or higher order multiple pregnancies. They are also at risk of developing OHSS. Many now believe that IVF should be regarded as a primary and preferential treatment for PCOS. The reason is that it is only through this approach that the number of embryos reaching the uterus can be controlled and in this manner the risk of high-order multiples can be minimized and it is only in the course of IVF treatment that a novel treatment method known as “prolonged coasting” ( see below) which prevents OHSS, can be implemented

      SEVERE OVARIAN HYPERSTIMULATION SYNDROME (OHSS):

      As indicated above, there is an inordinate propensity for women with PCOS to hyper-respond to gonadotropin fertility drugs and in the process produce large numbers of ovarian follicles. If left unchecked this can lead to OHSS, a potentially life endangering condition. The onset of OHSS is signaled by the development of a large number of ovarian follicles (usually more than 25 in number). This is accompanied by rapidly rising plasma estradiol (E2) levels, often exceeding 3000pg/ml within 7 or 9 days of stimulation, often rapidly peaking above 6,000 pg/ml prior to hCG administration. When this happens, the risk of OHSS developing is above 80%.

      Symptoms and signs of OHSS include: abdominal distention due to fluid collection (ascites), fluid in the chest cavity (hydrothorax), rapid weight gain (of a pound or more per day) due to tissue fluid retention, abdominal pain, lower back ache, nausea, diarrhea, vomiting, visual disturbances such as blurred vision and spots in front of the eyes (scotomata), a rapidly declining urine output, cardiovascular collapse and failure of blood to clot which sometimes results in severe bruising (echymosis) and frank bleeding. These symptoms and signs may appear before pregnancy can be diagnosed. If pregnancy occurs, the condition is likely to worsen progressively over a period of 3-5 weeks whereupon it rapidly resolves spontaneously over a few days. If no pregnancy occurs, the symptoms and signs all disappear spontaneously within 10-12 days of the hCG injection.

      When increasing fluid collection in the abdominal cavity (ascites) starts to compromise breathing raising the head of the bed rose slightly by placing a 4-6 inch block at the base of each head post and using a few additional pillows, will sometimes help ameliorate the problem. In cases where this does not help or symptoms become severe, all or most of the fluid can readily and safely be drained through t transvaginal sterile needle aspiration (vaginal paracentesis-performed once or sometimes twice a week) can be performed once or twice weekly . The problem will usually self corrects within 10-12 days of the hCG shot if pregnancy does not occur or, by the 8th week of pregnancy.

      Urine output should be monitored daily to see if it drops below about 500ml a day (about two cups and a half). A chest X-ray, to evaluate for fluid collection in the chest and around the heart should be done weekly along with blood tests for hematocrit, BUN, electrolytes, creatinine, platelet count and fibrin split products (FSP). If indicated on the basis of a deteriorating clinical situation, hospitalization might be needed for close observation and if necessary, to provide intensive care.

      In all case of OHSS, the ovaries will invariably be considerably enlarged. This is irrelevant to the final outcome, unless ovarian torsion (twisting of the ovary on its axis), an extremely rare complication occurs. The latter would usually require surgical emergency surgical intervention.

      It is important to know that symptoms and signs of OHSS are severely aggravated by rising hCG levels. Thus such patients should not receive additional hCG injections.

      Does PCOS cause poor egg/embryo quality? It is an undeniable fact that women with PCOS undergoing IVF are commonly found to have poorly developed (“dysmorphic”) eggs, with reduced fertilization potential and yielding “poor quality embryos”. However, in the author’s opinion (which admittedly runs contrary to popular opinion), this is unlikely to be due to an intrinsic deficit in egg quality. Rather, it more likely relates to intra-ovarian hormonal changes brought about by hyperstimulation and which compromise egg development. This effect, in the author’s opinion, can often be significantly reduced through implementation of an individualized or customized ovarian stimulation protocols that minimize exposure of the developing follicles and eggs to excessive LH-induced ovarian androgens. This can be best achieved by limiting the use of LH-containing gonadotropins such as Menopur through selective institution of “prolonged coasting” (see below).

      In the past, the onset of OHSS, heralded by the presence of large numbers of developing ovarian follicles and rapidly rising plasma estradiol levels often led the treating physician to prematurely administer hCG in an attempt to abruptly arrest the process and prevent escalation of risk to the patient. However the premature administration of hCG, while abruptly arresting further proliferation of estrogen producing granulosa cells in the follicles, unfortunately also prematurely arrests egg development. Since the ability of an egg to achieve optimal maturation upon hCG triggering is largely predicated upon it having achieved prior optimal development, the untimely administration of hCG which triggers meiosis, probably increases the risk of numerical chromosomal abnormalities (aneuploidy) of the egg. This in turn would lead to reduced fertilization potential, poor egg/embryo quality and low embryo implantation potential.

      In women with PCOS the connective tissue that surrounding the follicles (ovarian stroma) is often characteristically overgrown (stromal hyperplasia). It is the stroma that produces androgens (mainly testosterone) in response to LH. It is this, coupled with the fact that PCOS women also often have elevated blood LH concentrations (see above) results in the excessive production of androgen hormones, which is so characteristic in PCOS. While excessive exposure of developing eggs to ovarian androgens compromises follicle and egg growth it also impairs endometrial response to estrogen, which could explain the common finding of poor endometrial thickening in many PCOS women undergoing IVF.
      .

      The obvious remedy for these adverse effects on egg and endometrial development is to employ stimulation protocols that limit ovarian over-exposure to LH and allowing the time necessary for the follicles/eggs to develop optimally, prior to administering hCG through the judicious implementation of “Prolonged coasting” (PC).

      “PROLONGED COASTING”:

      In the early 90’s we were the first to report on “prolonged coasting” (PC), a novel approach that protects egg quality while preventing the development of OHSS. PC has since, gained widespread acceptance as a method of choice for preventing OHSS and has established itself as the “standard of care”. It involves withholding gonadotropin therapy while continuing the administration of the GnRHa and waiting until the plasma estradiol concentration drops below 2,500 pg/ml. Thereupon hCG is administered. In such cases, regardless of the number of developed follicles or the number of eggs retrieved, these women rarely, if ever develop OHSS. It has been reported that while PC virtually eliminates the risk of life-endangering complications associated with OHSS, there are reports in the literature that “the price to pay with PC” is often a poorer fertilization rate and reduced embryo implantation potential, compromising the pregnancy”. It is the author’s opinion an experience in the development of PC that egg/embryo quality deficit likely has little to do with the process of PC, itself and can be explained as follows: When PC is initiated too early, follicle growth and development may cease (as evidenced by the estradiol level plateauing or falling immediately, rather than showing an initial continued increase), and when PC is started too late, the follicles will often become cystic, measuring >21mm by the time the estradiol level falls below the safe threshold of 250000pg/ml, and so harbor dysmorphic eggs. Thus precise timing of the initiation of PC is critical. It should in pact be initiated preemptively in all cases when there are more than 25 follicles and the plasma estradiol reaches or exceeds 2,500pg/ml in association, provided that at least 50% of the follicles measuring 14-16mm in mean diameter. Not a day sooner or a day later. If PC is initiated with precise timing, it will usually be followed by a further progressive rise in the estradiol concentration. After a few days, the estradiol level will plateau and then it will start to fall (often rapidly). The temptation to trigger with hCG before the estradiol level falls below 3000picogtrams per milliliter must be resisted …even if the level falls below 1,000pg/ml by the time hCG is given.

      Since when using agonist ( Cetrotide/Ganirelix/Orgalutron) pituitary suppression throughout the stimulation phase with gonadotropins, the plasma estradiol level often under expressed follicle growth, this method of pituitary blockade should not be used in cases ( such as with PCOS) where PC might be required.,

      Prolonged coasting prevents canceled cycles and with it, canceled dreams.

      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.
      •A Fresh Look at the Indications for IVF
      •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.
      •Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
      •IVF and the use of Supplementary Human Growth Hormone (HGH) : Is it Worth Trying and who needs it?
      •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
      •Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
      •Embryo Transfer: The “Holy Grail in IVF.
      •IVF: Approach to Selecting the Best Embryos for Transfer to the Uterus.
      •Fresh versus Frozen Embryo Transfers (FET) Enhance IVF Outcome
      •Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
      •Genetically Testing Embryos for IVF
      •Staggered IVF
      •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?
      •Sher Fertility Solutions (SFS): An Exciting New Chapter….
      •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
      •Ovarian Hyperstimulation Syndrome (OHS): Its Evolution & Reducing itsIncumbent Risks
      •Taking A Fresh Look at Ovarian Hyperstimulation Syndrome (OHSS), its Presentation, Prevention and Management
      •Preventing Severe Ovarian Hyperstimulation Syndrome (OHSS) with “Prolonged Coasting”
      •IVF Outcome in Patients with Polycystic Ovarian Syndrome (PCOS): Minimizing the Risk of Severe Ovarian Hyperstimulation Syndrome (OHSS) and optimizing Egg/Embryo Quality.
      •Understanding Polycystic Ovarian Syndrome (PCOS) and the Need to Customize Ovarian Stimulation Protocols.
      •IVF & Polycystic Ovarian Syndrome (PCOS): Reducing the Risk of Severe Ovarian Hyperstimulation Syndrome (OHSS), Improving Egg Quality and Optimizing Outcome.

      Geoff Sher

      Sher-Fertility Solutions (SFS) will be officially launched in April 2019. Through SFS I will provide fertility consultations (via SKYPE) to an ever-growing number of patients (from >40 countries) with complex Reproductive Dysfunction (RD) who seek access to my input and guidance.

      In the past, I have limited my consultations with patients from afar to those who expressed a willingness to travel to Las Vegas for treatment by me. But now with the “birth” of SFS, all this is about to change. With one notable exception I will, as of April, 2019, no longer be conducting and performing hands-on IVF treatments. Rather, I will focus on providing SKYPE consultations and guidance to as many patients as possible. The one important exception will apply to approximately 1,000 existing patients who, following IVF previously performed by me, have remaining eggs or embryos stored (cryopreserved) at SIRM-LV and wish for me to perform their Frozen Embryo Transfers (FETs). I have agreed to accommodate such patients…..but only through August, 2019.

      Patients will have ready access online, to SFS: by going to http://www.SherIVF.com; by phone (1-800-780-7437 or 702-533-2691) and via email (sher@sherivf.com or concierge@sherIVF.com). A onetime fee of $400.00, will provide enrollees with access to: a full review of all their medical records (+ assistance in requisitioning additional records, as needed); a comprehensive initial 1 hour, SKYPE consultation with me; additional SKYPE consultations (as might be required); a written medical report (which will include a recommended plan of action) that you can share with a Physician(s) of choice. I would, subject to your approval and a request by such Physician(s), also be willing to discuss your case with him/her/them. I will in due course post on my website, a list of Fertility Physicians in key locations all over the United States and abroad, whom I endorse and to whom I would be willing to direct SFS patients for subsequent treatment.

      I have good news for those of you who are interested in traveling to Las Vegas for IVF. Dr Russel Foulk, Medical Director of SIRM-LV has expressed a willingness to be receptive to, treatment plans that I recommend for SFS patients Moreover, Dr Foulk has graciously agreed to interact with me during such treatments. I highly recommend Dr Foulk to those of you who, following consultation with me, wish to have me remain involved in the implementation of your treatment. This having been said, the final say in any management decision is always up to the treating physician.

      It is both my objective and commitment to serve as a resource to SFS patients on complex RD issues such as: Unexplained IVF failure; Recurrent Pregnancy loss (RPL); Immunologic Implantation Dysfunction-IID; Genetic/chromosomal issues; effects of Diminished Ovarian Reserve (DOR) and advancing age on reproductive performance, etc.

      I hope to ultimately expand the National and International reach of SFS, through my website (www.sherIVF.com) , through online webinars as well as Town hall- type consumer-based seminars, workshops and through social media. At the same time I will continue blogging on my website and doing bi-weekly Live-feed Facebook presentations (at “Dr Geoffrey Sher”) on a variety of subjects and topical issues.

      For me this is a very exciting venture. Please become part of the SFS family and help spread the word!

      I was very recently greatly honored in receiving an award by the prestigious; International Association of Top Professionals (IAOTP). For more information, go to the press release on my website, http://www.sherIVF.com .

  5. Dear Mr. Sher,

    I am so happy that I could get some information about sperm antibodies through your website as this is really difficult to find (beside some very basic stuff) – so thank you for that. My question is concerning exactly those antibodies. My husband has them (lg(G): 98% and lg(A): 15%) and we had trouble with the blastocyst development. 1. ICSI (GONAL-F 150): We did 6 of my eggs with IVF (none fertilized) and the 8 with ICSI (7 fertilized). All looked good until day 3, we froze 6 eggs as the clinic did not work on the weekend (one got transferred) – that is why they were developed to blastocysts after unfreezing. Only 1 was of a good enough quality (but also only 2 AB). No pregnancy. 2. ICSI – we were hopeful, because we changed clinic which works also on the weekend so that we had the chance for seeing how they develop without the freezing (old clinic said there was no egg issue). Unfortunately, 2. ICSI (Pergoveris: 1. day 225 2. day 150 from day 7 187.5) my follicles were from the beginning on very unequal (some bigger, some smaller) and that’s why we got only 9 mature eggs out of 19 as the other ones were just too small. 8 eggs fertilized and all looked good again until day 3… we ended up with one blastocyst (fair quality grade 4 2 2). Another one was grade 232 but was not frozen. The doctor said my eggs looked like having particles in it and was wondering if it is an egg quality as my AMH-value is low for my age – soon 28 years old- (though still normal 1.6 ug/l as well as the FSH 7.1 IU/l ). I need to say in the 3 month before the 2. ICSI I took antibiotics for the vagina, had 1 mammography and 1 röntgen of the back (just 1 day apart from each other). I was reinsured it would not matter – maybe it did? In other words, I am confused, panicked and I do not know whether I should put hope into a new ICSI with my own eggs. The big question I just have is how much the antibodies of my husband are impacting all of this? However, I am extremely stressed for a longer period of time (unemployment, living abroad, infertility) so that could have an impact as well?!

    Thanks a lot for taking the time to answer!

    • Hi Alina,

      Respectfully, ICSI will overcome the effects of spem antibodies. I think the likely explanation for your egg/embryo quality issue relates more to the protocol used for ovarian stimulation than anything else.

      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 the 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:

      Sher-Fertility Solutions (SFS) will be officially launched in April 2019. Through SFS I will provide fertility consultations (via SKYPE) to an ever-growing number of patients (from >40 countries) with complex Reproductive Dysfunction (RD) who seek access to my input and guidance.

      In the past, I have limited my consultations with patients from afar to those who expressed a willingness to travel to Las Vegas for treatment by me. But now with the “birth” of SFS, all this is about to change. With one notable exception I will, as of April, 2019, no longer be conducting and performing hands-on IVF treatments. Rather, I will focus on providing SKYPE consultations and guidance to as many patients as possible. The one important exception will apply to approximately 1,000 existing patients who, following IVF previously performed by me, have remaining eggs or embryos stored (cryopreserved) at SIRM-LV and wish for me to perform their Frozen Embryo Transfers (FETs). I have agreed to accommodate such patients…..but only through August, 2019.

      Patients will have ready access online, to SFS: by going to http://www.SherIVF.com; by phone (1-800-780-7437 or 702-533-2691) and via email (sher@sherivf.com or concierge@sherIVF.com). A onetime fee of $400.00, will provide enrollees with access to: a full review of all their medical records (+ assistance in requisitioning additional records, as needed); a comprehensive initial 1 hour, SKYPE consultation with me; additional SKYPE consultations (as might be required); a written medical report (which will include a recommended plan of action) that you can share with a Physician(s) of choice. I would, subject to your approval and a request by such Physician(s), also be willing to discuss your case with him/her/them. I will in due course post on my website, a list of Fertility Physicians in key locations all over the United States and abroad, whom I endorse and to whom I would be willing to direct SFS patients for subsequent treatment.

      I have good news for those of you who are interested in traveling to Las Vegas for IVF. Dr Russel Foulk, Medical Director of SIRM-LV has expressed a willingness to be receptive to, treatment plans that I recommend for SFS patients Moreover, Dr Foulk has graciously agreed to interact with me during such treatments. I highly recommend Dr Foulk to those of you who, following consultation with me, wish to have me remain involved in the implementation of your treatment. This having been said, the final say in any management decision is always up to the treating physician.

      It is both my objective and commitment to serve as a resource to SFS patients on complex RD issues such as: Unexplained IVF failure; Recurrent Pregnancy loss (RPL); Immunologic Implantation Dysfunction-IID; Genetic/chromosomal issues; effects of Diminished Ovarian Reserve (DOR) and advancing age on reproductive performance, etc.

      I hope to ultimately expand the National and International reach of SFS, through my website (www.sherIVF.com) , through online webinars as well as Town hall- type consumer-based seminars, workshops and through social media. At the same time I will continue blogging on my website and doing bi-weekly Live-feed Facebook presentations (at “Dr Geoffrey Sher”) on a variety of subjects and topical issues.
      For me this is a very exciting venture. Please become part of the SFS family and help spread the word!

      I was very recently greatly honored in receiving an award by the prestigious; International Association of Top Professionals (IAOTP). For more information, go to the press release on my website, http://www.sherIVF.com .